PMID-sentid Pub_year Sent_text compound_name comp_offset prot_official_name organism prot_offset 16681037-0 2006 Chemical modification of the human ether-a-go-go-related gene (HERG) K+ current by the amino-group reagent trinitrobenzene sulfonic acid. Trinitrobenzenesulfonic Acid 107-136 potassium voltage-gated channel subfamily H member 2 Homo sapiens 63-67 16681037-1 2006 We investigated the effects of trinitrobenzene sulfonic acid (TNBS), an amino-group reagent, on the human ether-a-go-go-related gene (HERG) K+ channels expressed in Xenopus oocytes. Trinitrobenzenesulfonic Acid 31-60 potassium voltage-gated channel subfamily H member 2 Homo sapiens 134-138 16681037-1 2006 We investigated the effects of trinitrobenzene sulfonic acid (TNBS), an amino-group reagent, on the human ether-a-go-go-related gene (HERG) K+ channels expressed in Xenopus oocytes. Trinitrobenzenesulfonic Acid 62-66 potassium voltage-gated channel subfamily H member 2 Homo sapiens 134-138 16681037-3 2006 External application of TNBS at 10 mM for 5 min irreversibly shifted the curves for currents at the end of the pulse and tail currents of HERG to a more negative potential and decreased the maximal amplitude of the I(tail) curve (I(tail,max)). Trinitrobenzenesulfonic Acid 24-28 potassium voltage-gated channel subfamily H member 2 Homo sapiens 138-142 16681037-5 2006 TNBS shifted the time constant curves of both activation and deactivation of the HERG current to a more hyperpolarized potential; TNBS"s effect was greater on channel opening than channel closing. Trinitrobenzenesulfonic Acid 0-4 potassium voltage-gated channel subfamily H member 2 Homo sapiens 81-85 16681037-5 2006 TNBS shifted the time constant curves of both activation and deactivation of the HERG current to a more hyperpolarized potential; TNBS"s effect was greater on channel opening than channel closing. Trinitrobenzenesulfonic Acid 130-134 potassium voltage-gated channel subfamily H member 2 Homo sapiens 81-85 16614986-2 2006 The aim of this study was to evaluate leukocyte-endothelium interaction and colitis activity after applying the selective cyclooxygenase-2 inhibitor NS-398 in a rat trinitrobenzene sulfonic acid (TNBS) colitis model. Trinitrobenzenesulfonic Acid 196-200 prostaglandin-endoperoxide synthase 2 Rattus norvegicus 122-138 16314851-2 2006 Administration of the GSK-3beta inhibitor TDZD-8 (0.1, 0.33 or 1.0 mg kg-1, s.c., b.i.d., for 3 days) caused a dose-dependent reduction in the colonic inflammation induced by intracolonic TNBS assessed after 3 days, both as the area of macroscopic involvement and as a score using 0-10 scale. Trinitrobenzenesulfonic Acid 188-192 glycogen synthase kinase 3 beta Rattus norvegicus 22-31 16549770-1 2006 Intracolonic administration of trinitrobenzene sulfonic acid in mice causes inflammation in the colon that is accompanied by increased expression of proinflammatory cytokines and of the substance P (SP), neurokinin 1 receptor (NK-1R) in the proximal mesenteric fat depot. Trinitrobenzenesulfonic Acid 31-60 tachykinin 1 Mus musculus 186-197 16549770-1 2006 Intracolonic administration of trinitrobenzene sulfonic acid in mice causes inflammation in the colon that is accompanied by increased expression of proinflammatory cytokines and of the substance P (SP), neurokinin 1 receptor (NK-1R) in the proximal mesenteric fat depot. Trinitrobenzenesulfonic Acid 31-60 tachykinin 1 Mus musculus 199-201 16549770-1 2006 Intracolonic administration of trinitrobenzene sulfonic acid in mice causes inflammation in the colon that is accompanied by increased expression of proinflammatory cytokines and of the substance P (SP), neurokinin 1 receptor (NK-1R) in the proximal mesenteric fat depot. Trinitrobenzenesulfonic Acid 31-60 tachykinin receptor 1 Mus musculus 204-225 16549770-1 2006 Intracolonic administration of trinitrobenzene sulfonic acid in mice causes inflammation in the colon that is accompanied by increased expression of proinflammatory cytokines and of the substance P (SP), neurokinin 1 receptor (NK-1R) in the proximal mesenteric fat depot. Trinitrobenzenesulfonic Acid 31-60 tachykinin receptor 1 Mus musculus 227-232 16314851-5 2006 The increase in myeloperoxidase activity, an index of neutrophil infiltration into the TNBS-induced inflamed colon, was significantly inhibited by both TDZD-8 and SB 415286 at each dose level. Trinitrobenzenesulfonic Acid 87-91 myeloperoxidase Rattus norvegicus 16-31 16314851-7 2006 The elevated levels of the transcription factor NF-kappaB subunit p65, as determined by Western blot in the nuclear extracts from the TNBS-provoked inflamed colonic tissue, were dose-dependently reduced by TDZD-8 or SB 415286 treatment. Trinitrobenzenesulfonic Acid 134-138 synaptotagmin 1 Rattus norvegicus 66-69 16332442-5 2006 Moreover, treatments with matrine (10 and 20 mg kg(-1)) decreased the up-regulated mRNA and protein levels of tumour necrosis factor-alpha (TNF-alpha) caused by TNBS. Trinitrobenzenesulfonic Acid 161-165 tumor necrosis factor Mus musculus 140-149 16332442-6 2006 Our findings suggest that matrine improves TNBS-induced colitis in mice and the therapeutic mechanism might be related to the reduction of up-regulated colonic TNF-alpha production caused by TNBS. Trinitrobenzenesulfonic Acid 191-195 tumor necrosis factor Mus musculus 160-169 17077645-0 2006 Interleukin-6 genetic ablation protects from trinitrobenzene sulfonic acid-induced colitis in mice. Trinitrobenzenesulfonic Acid 45-74 interleukin 6 Mus musculus 0-13 17077645-6 2006 METHODS: Acute colitis was induced in wild-type and IL-6-deficient (Il-6(-/-)) mice by intracolonic administration of TNBS. Trinitrobenzenesulfonic Acid 118-122 interleukin 6 Mus musculus 68-72 16120757-6 2006 2,4,6-Trinitrobenzene sulphonic acid (TNBS) induced colitis was induced in SOCS1Tg mice and severity was compared with control littermates by measurement of survival rates. Trinitrobenzenesulfonic Acid 38-42 suppressor of cytokine signaling 1 Mus musculus 75-80 16120757-9 2006 Young SOCS1Tg mice less than 15 weeks of age, before the onset of colitis, were susceptible to TNBS induced colitis. Trinitrobenzenesulfonic Acid 95-99 suppressor of cytokine signaling 1 Mus musculus 6-11 17077645-5 2006 OBJECTIVE: It was the aim of this study to investigate the role of genetic IL-6 deficiency in trinitrobenzene sulfonic acid (TNBS)-mediated colitis, an experimental model inflammation that shares several features with Crohn"s disease in humans. Trinitrobenzenesulfonic Acid 94-123 interleukin 6 Homo sapiens 75-79 17077645-8 2006 RESULTS: In wild-type mice, TNBS administration increased both IL-6 serum levels and local expression of IL-6 by 36 and 9 fold, respectively, compared with control, vehicle-injected mice. Trinitrobenzenesulfonic Acid 28-32 interleukin 6 Mus musculus 63-67 17077645-8 2006 RESULTS: In wild-type mice, TNBS administration increased both IL-6 serum levels and local expression of IL-6 by 36 and 9 fold, respectively, compared with control, vehicle-injected mice. Trinitrobenzenesulfonic Acid 28-32 interleukin 6 Mus musculus 105-109 17077645-5 2006 OBJECTIVE: It was the aim of this study to investigate the role of genetic IL-6 deficiency in trinitrobenzene sulfonic acid (TNBS)-mediated colitis, an experimental model inflammation that shares several features with Crohn"s disease in humans. Trinitrobenzenesulfonic Acid 125-129 interleukin 6 Homo sapiens 75-79 17077645-9 2006 Compared with the wild-type mice, the Il-6(-/-) mice had significantly reduced intestinal inflammation as evidenced by epithelial damage, neutrophil infiltration, colon thickness and proinflammatory cytokine expression, following treatment with TNBS. Trinitrobenzenesulfonic Acid 245-249 interleukin 6 Mus musculus 38-42 17077645-6 2006 METHODS: Acute colitis was induced in wild-type and IL-6-deficient (Il-6(-/-)) mice by intracolonic administration of TNBS. Trinitrobenzenesulfonic Acid 118-122 interleukin 6 Mus musculus 52-56 16306767-14 2005 A significant increase in IL-10, IFN-gamma, and PGE2 was noted in the Adex+TNBS group compared with the sham+TNBS group. Trinitrobenzenesulfonic Acid 75-79 interleukin 10 Mus musculus 26-31 16306767-14 2005 A significant increase in IL-10, IFN-gamma, and PGE2 was noted in the Adex+TNBS group compared with the sham+TNBS group. Trinitrobenzenesulfonic Acid 75-79 interferon gamma Mus musculus 33-42 16306767-15 2005 Splenic CD4 lymphocytes decreased in the sham+TNBS and Adex+TNBS groups as compared with control groups (Adex and naive). Trinitrobenzenesulfonic Acid 46-50 CD4 antigen Mus musculus 8-11 16306767-15 2005 Splenic CD4 lymphocytes decreased in the sham+TNBS and Adex+TNBS groups as compared with control groups (Adex and naive). Trinitrobenzenesulfonic Acid 60-64 CD4 antigen Mus musculus 8-11 16306767-16 2005 The CD8/CD4 ratio was significantly higher in the Adex+TNBS compared with the sham+TNBS group. Trinitrobenzenesulfonic Acid 55-59 CD4 antigen Mus musculus 8-11 16306767-16 2005 The CD8/CD4 ratio was significantly higher in the Adex+TNBS compared with the sham+TNBS group. Trinitrobenzenesulfonic Acid 83-87 CD4 antigen Mus musculus 8-11 16105891-2 2005 The authors have previously demonstrated that oral administration of recombinant CT-B (rCT-B) is able to prevent and cure the Crohn"s disease (CD)-like trinitrobenzene sulfonic acid (TNBS) mediated colitis. Trinitrobenzenesulfonic Acid 152-181 phosphate cytidylyltransferase 1B, choline Homo sapiens 81-85 16105891-2 2005 The authors have previously demonstrated that oral administration of recombinant CT-B (rCT-B) is able to prevent and cure the Crohn"s disease (CD)-like trinitrobenzene sulfonic acid (TNBS) mediated colitis. Trinitrobenzenesulfonic Acid 152-181 phosphate cytidylyltransferase 1B, choline Rattus norvegicus 87-92 16105891-2 2005 The authors have previously demonstrated that oral administration of recombinant CT-B (rCT-B) is able to prevent and cure the Crohn"s disease (CD)-like trinitrobenzene sulfonic acid (TNBS) mediated colitis. Trinitrobenzenesulfonic Acid 183-187 phosphate cytidylyltransferase 1B, choline Homo sapiens 81-85 16105891-2 2005 The authors have previously demonstrated that oral administration of recombinant CT-B (rCT-B) is able to prevent and cure the Crohn"s disease (CD)-like trinitrobenzene sulfonic acid (TNBS) mediated colitis. Trinitrobenzenesulfonic Acid 183-187 phosphate cytidylyltransferase 1B, choline Rattus norvegicus 87-92 16105891-4 2005 METHODS: TNBS treated mice were fed with rCT-B, and IFN-gamma and IL-12 production by colonic lamina propria mononuclear cells (LPMC) was examined by ELISA. Trinitrobenzenesulfonic Acid 9-13 phosphate cytidylyltransferase 1B, choline Rattus norvegicus 41-46 16105891-7 2005 RESULTS: rCT-B significantly reduced IL-12 and IFN-gamma secretion by LPMC from TNBS treated mice. Trinitrobenzenesulfonic Acid 80-84 phosphate cytidylyltransferase 1B, choline Rattus norvegicus 9-14 16105891-7 2005 RESULTS: rCT-B significantly reduced IL-12 and IFN-gamma secretion by LPMC from TNBS treated mice. Trinitrobenzenesulfonic Acid 80-84 interferon gamma Mus musculus 47-56 16213481-4 2005 caused a dose-dependent reduction in macroscopic damage, inhibition of the TNBS-provoked elevation of both colonic myeloperoxidase and tumour necrosis factor-alpha (TNF-alpha), and a reduction in the histologically assessed increase in mucosal and submucosal thickness and neutrophil infiltration. Trinitrobenzenesulfonic Acid 75-79 myeloperoxidase Rattus norvegicus 115-130 16239967-5 2005 administration of decoy ODNs encapsulated in a viral envelope prevented and treated a model of acute trinitrobenzene sulfonic acid-induced (TNBS-induced) colitis, as assessed by clinical course and effect on Th1 cytokine production. Trinitrobenzenesulfonic Acid 101-130 negative elongation factor complex member C/D, Th1l Mus musculus 208-211 16239967-5 2005 administration of decoy ODNs encapsulated in a viral envelope prevented and treated a model of acute trinitrobenzene sulfonic acid-induced (TNBS-induced) colitis, as assessed by clinical course and effect on Th1 cytokine production. Trinitrobenzenesulfonic Acid 140-144 negative elongation factor complex member C/D, Th1l Mus musculus 208-211 16213481-4 2005 caused a dose-dependent reduction in macroscopic damage, inhibition of the TNBS-provoked elevation of both colonic myeloperoxidase and tumour necrosis factor-alpha (TNF-alpha), and a reduction in the histologically assessed increase in mucosal and submucosal thickness and neutrophil infiltration. Trinitrobenzenesulfonic Acid 75-79 tumor necrosis factor Rattus norvegicus 165-174 16210467-6 2005 RESULTS: After treated with TNBS/ethanol, the extent of CMDI and HS, the levels of MPO, MDA, and NO in the model group, were higher than that in the control group; melatonin ameliorated these parameters effectively. Trinitrobenzenesulfonic Acid 28-32 myeloperoxidase Rattus norvegicus 83-86 16185315-6 2005 The decrease in myenteric neurones was not associated with a decrease in any given subpopulation of neurones, but the proportion of VIP-immunoreactive neurones increased 6 days following TNBS administration and returned to the control range at the 56 days. Trinitrobenzenesulfonic Acid 187-191 VIP peptides Cavia porcellus 132-135 16237764-9 2005 RESULTS: In TNBS rats, the distal colon showed severe histological lesions and a high MPO activity, while the DUMC exhibited normal histology and MPO activity. Trinitrobenzenesulfonic Acid 12-16 myeloperoxidase Rattus norvegicus 86-89 16015023-3 2005 METHODS: Using cultured human KCs, the effects of FK506 on the production of IL-1alpha treated with chemicals (trinitrobenzene sulfonic acid sodium salt, TNBS) plus hydrocortisone were analyzed by ELISA and mRNA expression of IL-1alpha using RT-PCR. Trinitrobenzenesulfonic Acid 111-152 interleukin 1 alpha Homo sapiens 77-86 16133967-4 2005 TNF-alpha mRNA expression in the colon was significantly higher in all TNBS-administered groups than in controls. Trinitrobenzenesulfonic Acid 71-75 tumor necrosis factor Mus musculus 0-9 15908024-1 2005 The present study was aimed to investigate the effect of ACE inhibition on trinitrobenzene sulphonic acid (TNBS)-induced colonic inflammation in rats by using captopril and lisinopril. Trinitrobenzenesulfonic Acid 107-111 angiotensin I converting enzyme Rattus norvegicus 57-60 15857940-4 2005 Our study demonstrates, by using a trinitrobenzene sulfonic acid-induced colitis model of Crohn"s disease, the constitutive expression and the up-regulation of TLR2 and -4 at messenger and protein levels in colon extracts, as well as in macrophages, dendritic cells, and lymphocytes from mesenteric lymphoid nodes. Trinitrobenzenesulfonic Acid 35-64 toll like receptor 2 Homo sapiens 160-164 15973123-2 2005 A healing effect of vasoactive intestinal peptide (VIP) in the murine model of CD based on 2,4,6-trinitrobencene sulfonic acid (TNBS) administration has been previously shown. Trinitrobenzenesulfonic Acid 128-132 vasoactive intestinal polypeptide Mus musculus 51-54 15879003-1 2005 We have previously shown that complement factor 5a (C5a) plays a role in the pathogenesis of 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis in rats by using the selective, orally active C5a antagonist AcF-[OP(d-Cha)WR]. Trinitrobenzenesulfonic Acid 93-128 complement C5 Rattus norvegicus 52-55 15879003-1 2005 We have previously shown that complement factor 5a (C5a) plays a role in the pathogenesis of 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis in rats by using the selective, orally active C5a antagonist AcF-[OP(d-Cha)WR]. Trinitrobenzenesulfonic Acid 93-128 complement C5 Rattus norvegicus 198-201 15879003-1 2005 We have previously shown that complement factor 5a (C5a) plays a role in the pathogenesis of 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis in rats by using the selective, orally active C5a antagonist AcF-[OP(d-Cha)WR]. Trinitrobenzenesulfonic Acid 130-134 complement C5 Rattus norvegicus 52-55 15879003-1 2005 We have previously shown that complement factor 5a (C5a) plays a role in the pathogenesis of 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis in rats by using the selective, orally active C5a antagonist AcF-[OP(d-Cha)WR]. Trinitrobenzenesulfonic Acid 130-134 complement C5 Rattus norvegicus 198-201 15778124-2 2005 In this study we compared the efficacy of a potent, new and highly selective inhibitor of group IIa human sPLA(2) enzyme (5-(4-benzyloxyphenyl)-4S-(7-phenylheptanoylamino)-pentanoic acid; sPLA(2)I), with that of sulfasalazine, in a rat model of trinitrobenzene sulfonic acid (TNBS)-induced colitis. Trinitrobenzenesulfonic Acid 245-274 phospholipase A2 group IIA Rattus norvegicus 106-113 15876425-13 2005 Our results also suggest that the activation of the PPARgamma pathway reduces COX-2 overexpression, returns the increased PGD(2) values to basal levels and induces a significant increase of TNBS-induced apoptosis. Trinitrobenzenesulfonic Acid 190-194 peroxisome proliferator-activated receptor gamma Rattus norvegicus 52-61 15857607-6 2005 Colonic nitrite and nitrate levels and protein expression of inducible nitric oxide synthase (iNOS) were also lower in the treated groups in comparison to the TNBS control. Trinitrobenzenesulfonic Acid 159-163 nitric oxide synthase 2, inducible Mus musculus 61-92 15905700-6 2005 CONCLUSIONS: TNFalpha signaling through TNFR1 is protective in the trinitrobenzene sulfonic acid mouse model of inflammatory bowel disease. Trinitrobenzenesulfonic Acid 67-96 tumor necrosis factor Mus musculus 13-21 15905700-6 2005 CONCLUSIONS: TNFalpha signaling through TNFR1 is protective in the trinitrobenzene sulfonic acid mouse model of inflammatory bowel disease. Trinitrobenzenesulfonic Acid 67-96 tumor necrosis factor receptor superfamily, member 1a Mus musculus 40-45 15905702-0 2005 Hepatocyte growth factor facilitates the repair of large colonic ulcers in 2,4,6-trinitrobenzene sulfonic acid-induced colitis in rats. Trinitrobenzenesulfonic Acid 75-110 hepatocyte growth factor Rattus norvegicus 0-24 15778124-2 2005 In this study we compared the efficacy of a potent, new and highly selective inhibitor of group IIa human sPLA(2) enzyme (5-(4-benzyloxyphenyl)-4S-(7-phenylheptanoylamino)-pentanoic acid; sPLA(2)I), with that of sulfasalazine, in a rat model of trinitrobenzene sulfonic acid (TNBS)-induced colitis. Trinitrobenzenesulfonic Acid 276-280 phospholipase A2 group IIA Rattus norvegicus 106-113 15778124-6 2005 This study supports a role for the group IIa sPLA(2) enzyme in pathology associated with the TNBS rat model of IBD, and suggests a possible therapeutic application for selective inhibitors of group IIa sPLA(2) inhibitors in the treatment of IBD. Trinitrobenzenesulfonic Acid 93-97 phospholipase A2 group IIA Rattus norvegicus 45-52 15749854-2 2005 In the present study, we analyzed the regulatory cytokine and cell response to probiotic (VSL#3) administration in the context of the Th1 T cell colitis induced by trinitrobenzene sulfonic acid treatment of SJL/J mice. Trinitrobenzenesulfonic Acid 164-193 negative elongation factor complex member C/D, Th1l Mus musculus 134-137 15550554-2 2005 We studied the effects of HGF in mice with trinitrobenzene sulfonic acid-induced colitis, which shows clinical and molecular resemblance to Crohn"s disease. Trinitrobenzenesulfonic Acid 43-72 hepatocyte growth factor Mus musculus 26-29 15887108-4 2005 The aim of this study was to investigate the immunomodulatory activity of a nitric oxide-releasing derivative of mesalamine (NCX-456), as compared with standard mesalamine, in 2,4,6-trinitrobenzene sulfonic acid-induced colitis in mice. Trinitrobenzenesulfonic Acid 176-211 T cell leukemia, homeobox 2 Mus musculus 125-128 15554929-5 2004 In wild-type mice, TNBS treatment resulted in colonic ulceration and marked apoptosis, which was associated with decreased colon content of the antiapoptotic protein Bcl-2, whereas the proapoptotic Bax was unchanged. Trinitrobenzenesulfonic Acid 19-23 B cell leukemia/lymphoma 2 Mus musculus 166-171 15685552-10 2005 Administration of follistatin also reduced the histologic score and tissue myeloperoxidase activity in established TNBS and DSS colitis and reduced the severity of the colitis in IL-10 -/- mice. Trinitrobenzenesulfonic Acid 115-119 myeloperoxidase Mus musculus 75-90 15591506-6 2005 The therapeutic potency of rAS3 was evaluated in the 2,4,6-trinitrobenzene sulphonic acid (TNBS) induced colitis model of the rat. Trinitrobenzenesulfonic Acid 91-95 PDS5 cohesin associated factor B Rattus norvegicus 27-31 15649029-3 2005 The arm consists of a flexible biotinylated DNA oligonucleotide base specifically modified with a dye and terminating in a TNB recognition element, which is an analogue of TNT. Trinitrobenzenesulfonic Acid 123-126 chromosome 16 open reading frame 82 Homo sapiens 172-175 15554929-5 2004 In wild-type mice, TNBS treatment resulted in colonic ulceration and marked apoptosis, which was associated with decreased colon content of the antiapoptotic protein Bcl-2, whereas the proapoptotic Bax was unchanged. Trinitrobenzenesulfonic Acid 19-23 BCL2-associated X protein Mus musculus 198-201 15178552-5 2004 Intracolonic TNBS induced c-fos mRNA expression in brain nuclei involved in the autonomic, behavioral, and neuroendocrine response to a stimulus (PVN, amygdala, locus coeruleus, parabrachial nucleus, nucleus of the solitary tract) and in circumventricular organs (lamina terminalis, subfornical organ, area postrema). Trinitrobenzenesulfonic Acid 13-17 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 26-31 15665574-6 2004 In control, nNOS immunoreactivity was present in the mucosa, submucosa, lamina propria, and ganglion cells of the myenteric plexus, while after TNBS treatment, reduced nNOS cells were found. Trinitrobenzenesulfonic Acid 144-148 nitric oxide synthase, brain Cavia porcellus 12-16 15665574-6 2004 In control, nNOS immunoreactivity was present in the mucosa, submucosa, lamina propria, and ganglion cells of the myenteric plexus, while after TNBS treatment, reduced nNOS cells were found. Trinitrobenzenesulfonic Acid 144-148 nitric oxide synthase, brain Cavia porcellus 168-172 15665574-8 2004 After administration of TNBS, iNOS immunoreactivity was increased in the mucosa and submucosa, but the number of iNOS positive ganglion cells in the myenteric plexus was not changed compared to control. Trinitrobenzenesulfonic Acid 24-28 nitric oxide synthase, inducible Cavia porcellus 30-34 15665574-8 2004 After administration of TNBS, iNOS immunoreactivity was increased in the mucosa and submucosa, but the number of iNOS positive ganglion cells in the myenteric plexus was not changed compared to control. Trinitrobenzenesulfonic Acid 24-28 nitric oxide synthase, inducible Cavia porcellus 113-117 15545995-7 2004 Moreover, PAR1 activation exacerbated and prolonged inflammation in a mouse model of IBD induced by the intracolonic administration of trinitrobenzene sulfonic acid (TNBS), while PAR1 antagonism significantly decreased the mortality and severity of colonic inflammation induced by TNBS and dextran sodium sulfate. Trinitrobenzenesulfonic Acid 135-164 coagulation factor II (thrombin) receptor Mus musculus 10-14 15502641-5 2004 In present study, the possible effects of angiotensin II-mediated apoptosis of pancreatic acinar cells were investigated in rat pancreatic fibrosis induced by trinitrobenzene sulfonic acid (TNBS) by AT1R, with special reference to the losartan administration. Trinitrobenzenesulfonic Acid 159-188 angiotensinogen Rattus norvegicus 42-56 15502641-5 2004 In present study, the possible effects of angiotensin II-mediated apoptosis of pancreatic acinar cells were investigated in rat pancreatic fibrosis induced by trinitrobenzene sulfonic acid (TNBS) by AT1R, with special reference to the losartan administration. Trinitrobenzenesulfonic Acid 190-194 angiotensinogen Rattus norvegicus 42-56 15665574-3 2004 The aim of this study was to investigate the relationship between the delay in colonic transit and the distribution of inducible NOS (iNOS) and nNOS immunoreactive cells in the myenteric plexus of trinitrobenzene sulfonic acid (TNBS)-induced colitic guinea pig. Trinitrobenzenesulfonic Acid 197-226 nitric oxide synthase, inducible Cavia porcellus 134-138 15665574-3 2004 The aim of this study was to investigate the relationship between the delay in colonic transit and the distribution of inducible NOS (iNOS) and nNOS immunoreactive cells in the myenteric plexus of trinitrobenzene sulfonic acid (TNBS)-induced colitic guinea pig. Trinitrobenzenesulfonic Acid 197-226 nitric oxide synthase, brain Cavia porcellus 144-148 15531237-11 2004 MDS and MPO scores were considerably elevated in the TNBS colons when compared with the TNBS vehicle animals. Trinitrobenzenesulfonic Acid 53-57 myeloperoxidase Rattus norvegicus 8-11 15531237-12 2004 TNBS rats treated with CPZ enemas exhibited a substantial reduction in MDS and MPO scores and demonstrated dramatically improved pathologic findings. Trinitrobenzenesulfonic Acid 0-4 myeloperoxidase Rattus norvegicus 79-82 15467203-2 2004 The aim of the present study is to clarify anti-colitic effect of HST using a model of colitis induced by intracolonic instillation of 2,4,6-trinitrobenzene sulfonic acid (TNBS) in rats, and to evaluate the pharmaceutical properties of its herbal components. Trinitrobenzenesulfonic Acid 135-170 heat shock protein family A (Hsp70) member 2 Rattus norvegicus 66-69 15467203-2 2004 The aim of the present study is to clarify anti-colitic effect of HST using a model of colitis induced by intracolonic instillation of 2,4,6-trinitrobenzene sulfonic acid (TNBS) in rats, and to evaluate the pharmaceutical properties of its herbal components. Trinitrobenzenesulfonic Acid 172-176 heat shock protein family A (Hsp70) member 2 Rattus norvegicus 66-69 15168810-0 2004 The effect of recombinant human growth hormone (rhGH) on trinitrobenzene sulfonic acid-induced colitis in rats: an experimental study. Trinitrobenzenesulfonic Acid 57-86 growth hormone 1 Homo sapiens 32-46 15307168-4 2004 DSS or TNBS led to a dramatic increase in lethality and colitis severity in IRF-1 KO compared with WT mice. Trinitrobenzenesulfonic Acid 7-11 interferon regulatory factor 1 Mus musculus 76-81 15336953-2 2004 The present study examined the role of CCL3/MIP-1alpha during trinitrobenzene sulfonic acid (TNBS)-induced colitis in the rat. Trinitrobenzenesulfonic Acid 93-97 C-C motif chemokine ligand 3 Rattus norvegicus 39-43 15336953-3 2004 Colonic CCL3/MIP-1alpha levels were elevated (>20-fold above control) within 24 h and remained elevated to day 7 of colitis induction by TNBS administration. Trinitrobenzenesulfonic Acid 140-144 C-C motif chemokine ligand 3 Rattus norvegicus 8-12 15336953-3 2004 Colonic CCL3/MIP-1alpha levels were elevated (>20-fold above control) within 24 h and remained elevated to day 7 of colitis induction by TNBS administration. Trinitrobenzenesulfonic Acid 140-144 C-C motif chemokine ligand 3 Rattus norvegicus 13-23 15240735-6 2004 Furthermore, a high level of IL-15, which inhibits activation-induced cell death to terminate inflammation, was expressed more in intestinal epithelial cells (EC) from TNBS-treated Cdelta(-/-) mice than in those from wild-type mice. Trinitrobenzenesulfonic Acid 168-172 interleukin 15 Mus musculus 29-34 15188517-6 2004 SP and CGRP were primarily expressed in the superficial laminae of the spinal cord after TNBS injection. Trinitrobenzenesulfonic Acid 89-93 calcitonin-related polypeptide alpha Rattus norvegicus 7-11 15240735-7 2004 EC from wild-type mice significantly suppressed the IFN-gamma production of IEL from TNBS-treated Cdelta(-/-) mice, whereas EC from TNBS-treated Cdelta(-/-) mice did not. Trinitrobenzenesulfonic Acid 85-89 interferon gamma Mus musculus 52-61 15241569-8 2004 Our findings also indicate that ET-A receptors but not ET-B receptors play an important role in the colonic inflammation following TNBS administration. Trinitrobenzenesulfonic Acid 131-135 endothelin receptor type A Rattus norvegicus 32-36 15016743-8 2004 Intracolonic infusion of TNBS induced a significantly higher inflammatory reaction in separated animals, as judged by enhanced MPO colonic levels, total gut permeability, and macroscopic lesions. Trinitrobenzenesulfonic Acid 25-29 myeloperoxidase Rattus norvegicus 127-130 15168810-13 2004 In conclusion, growth hormone replacement had protective effects against colonic inflammation while reducing intestinal damage on TNB-induced colitis. Trinitrobenzenesulfonic Acid 130-133 gonadotropin releasing hormone receptor Rattus norvegicus 15-29 14970176-3 2004 Mice treated with anti-mouse CEACAM1-specific monoclonal antibody (mAb) CC1 during the effector phase exhibited a reduced severity of trinitrobenzene sulfonic acid colitis in association with decreased interferon (IFN)-gamma production. Trinitrobenzenesulfonic Acid 134-163 carcinoembryonic antigen-related cell adhesion molecule 1 Mus musculus 29-36 14970176-3 2004 Mice treated with anti-mouse CEACAM1-specific monoclonal antibody (mAb) CC1 during the effector phase exhibited a reduced severity of trinitrobenzene sulfonic acid colitis in association with decreased interferon (IFN)-gamma production. Trinitrobenzenesulfonic Acid 134-163 carcinoembryonic antigen-related cell adhesion molecule 1 Mus musculus 72-75 15612245-0 2004 Effects and mechanism of the selective COX-2 inhibitor, celecoxib, on rat colitis induced by trinitrobenzene sulfonic acid. Trinitrobenzenesulfonic Acid 93-122 cytochrome c oxidase II, mitochondrial Rattus norvegicus 39-44 14738461-6 2004 IL-18 mRNA was significantly enhanced in trinitrobenzene sulphonic acid (TNBS) induced colitis, and treatment with IL-18 binding protein (IL-18BPa), which neutralizes IL-18 bioactivity, significantly reduced the severity of colitis. Trinitrobenzenesulfonic Acid 73-77 interleukin 18 Mus musculus 0-5 14738461-6 2004 IL-18 mRNA was significantly enhanced in trinitrobenzene sulphonic acid (TNBS) induced colitis, and treatment with IL-18 binding protein (IL-18BPa), which neutralizes IL-18 bioactivity, significantly reduced the severity of colitis. Trinitrobenzenesulfonic Acid 73-77 interleukin 18 Mus musculus 115-120 14738461-6 2004 IL-18 mRNA was significantly enhanced in trinitrobenzene sulphonic acid (TNBS) induced colitis, and treatment with IL-18 binding protein (IL-18BPa), which neutralizes IL-18 bioactivity, significantly reduced the severity of colitis. Trinitrobenzenesulfonic Acid 73-77 interleukin 18 Mus musculus 115-120 14684583-9 2004 TNBS increased colonic interleukin 2 (IL-2) production whereas S mansoni increased splenic IL-4 and IL-2 levels. Trinitrobenzenesulfonic Acid 0-4 interleukin 2 Rattus norvegicus 23-36 14684583-9 2004 TNBS increased colonic interleukin 2 (IL-2) production whereas S mansoni increased splenic IL-4 and IL-2 levels. Trinitrobenzenesulfonic Acid 0-4 interleukin 2 Rattus norvegicus 38-42 14688324-6 2004 of TGF-beta2-treated 2,4,6-trinitrobenzene sulfonic acid-pulsed bone marrow-derived APC (tol-APC) to experimental mice 1 day after intratracheal challenge reduced the collagen deposition in the interstitium of the lung that usually follows challenge. Trinitrobenzenesulfonic Acid 21-56 transforming growth factor, beta 2 Mus musculus 3-12 14555839-6 2004 In the delayed-type hypersensitivity (DTH) model elicited by DNFB, the number of CD8+ T cells among DNFB-2,4,6-trinitrobenzenesulfonic acid (TNBS)-peritoneal exudate cells was significantly higher in OPN-T than nontransgenic mice, while there was almost no difference in that of CD4+ T cells. Trinitrobenzenesulfonic Acid 141-145 CD4 antigen Mus musculus 279-282 14688324-6 2004 of TGF-beta2-treated 2,4,6-trinitrobenzene sulfonic acid-pulsed bone marrow-derived APC (tol-APC) to experimental mice 1 day after intratracheal challenge reduced the collagen deposition in the interstitium of the lung that usually follows challenge. Trinitrobenzenesulfonic Acid 21-56 APC, WNT signaling pathway regulator Mus musculus 84-87 14688324-6 2004 of TGF-beta2-treated 2,4,6-trinitrobenzene sulfonic acid-pulsed bone marrow-derived APC (tol-APC) to experimental mice 1 day after intratracheal challenge reduced the collagen deposition in the interstitium of the lung that usually follows challenge. Trinitrobenzenesulfonic Acid 21-56 APC, WNT signaling pathway regulator Mus musculus 93-96 14627361-0 2003 Specific CTL activity of CD8+ TCR Vbeta14+ T cell in mouse 2, 4, 6-trinitrobenzene sulfonic acid-induced colitis. Trinitrobenzenesulfonic Acid 59-96 T cell receptor alpha variable 6-3 Mus musculus 30-33 14533000-0 2003 N-3 fatty acid-rich diet prevents early response of interleukin-6 elevation in trinitrobenzene sulfonic acid-induced enteritis. Trinitrobenzenesulfonic Acid 79-108 interleukin 6 Homo sapiens 52-65 14629625-2 2003 We have recently described a novel organ-specific rat model of fibrosing cholangitis induced by intrabiliary administration of the hapten-reagent 2,4,6-trinitrobenzenesulfonic acid (TNBS) with similarities to human PSC. Trinitrobenzenesulfonic Acid 146-180 PSC Homo sapiens 215-218 14629625-2 2003 We have recently described a novel organ-specific rat model of fibrosing cholangitis induced by intrabiliary administration of the hapten-reagent 2,4,6-trinitrobenzenesulfonic acid (TNBS) with similarities to human PSC. Trinitrobenzenesulfonic Acid 182-186 PSC Homo sapiens 215-218 14724828-8 2003 RESULTS: Colons of TNBS-treated mice contained acute and chronic inflammatory infiltrates, increased collagen, fibrogenic tissue architecture, and increased expression of TNF-alpha, TGF-beta 1, IGF-1, Col1a2, MMP-1, and TIMP-1. Trinitrobenzenesulfonic Acid 19-23 tumor necrosis factor Mus musculus 171-180 14724828-8 2003 RESULTS: Colons of TNBS-treated mice contained acute and chronic inflammatory infiltrates, increased collagen, fibrogenic tissue architecture, and increased expression of TNF-alpha, TGF-beta 1, IGF-1, Col1a2, MMP-1, and TIMP-1. Trinitrobenzenesulfonic Acid 19-23 transforming growth factor, beta 1 Mus musculus 182-192 14724828-8 2003 RESULTS: Colons of TNBS-treated mice contained acute and chronic inflammatory infiltrates, increased collagen, fibrogenic tissue architecture, and increased expression of TNF-alpha, TGF-beta 1, IGF-1, Col1a2, MMP-1, and TIMP-1. Trinitrobenzenesulfonic Acid 19-23 insulin-like growth factor 1 Mus musculus 194-199 14724828-8 2003 RESULTS: Colons of TNBS-treated mice contained acute and chronic inflammatory infiltrates, increased collagen, fibrogenic tissue architecture, and increased expression of TNF-alpha, TGF-beta 1, IGF-1, Col1a2, MMP-1, and TIMP-1. Trinitrobenzenesulfonic Acid 19-23 collagen, type I, alpha 2 Mus musculus 201-207 14724828-8 2003 RESULTS: Colons of TNBS-treated mice contained acute and chronic inflammatory infiltrates, increased collagen, fibrogenic tissue architecture, and increased expression of TNF-alpha, TGF-beta 1, IGF-1, Col1a2, MMP-1, and TIMP-1. Trinitrobenzenesulfonic Acid 19-23 matrix metallopeptidase 13 Mus musculus 209-214 14724828-8 2003 RESULTS: Colons of TNBS-treated mice contained acute and chronic inflammatory infiltrates, increased collagen, fibrogenic tissue architecture, and increased expression of TNF-alpha, TGF-beta 1, IGF-1, Col1a2, MMP-1, and TIMP-1. Trinitrobenzenesulfonic Acid 19-23 tissue inhibitor of metalloproteinase 1 Mus musculus 220-226 14724828-9 2003 Colonic mesenchymal cells from TNBS-treated mice were also morphologically distinct from those of the control mice, with increased TIMP-1 expression in response to IFN-gamma treatment. Trinitrobenzenesulfonic Acid 31-35 tissue inhibitor of metalloproteinase 1 Mus musculus 131-137 14724828-9 2003 Colonic mesenchymal cells from TNBS-treated mice were also morphologically distinct from those of the control mice, with increased TIMP-1 expression in response to IFN-gamma treatment. Trinitrobenzenesulfonic Acid 31-35 interferon gamma Mus musculus 164-173 14724828-12 2003 CONCLUSIONS: Extended TNBS treatment of mice yielded chronic intestinal inflammation-associated fibrosis with extensive fibrogenic ECM changes that could be counteracted by specific blockade of NF-kappa B. Trinitrobenzenesulfonic Acid 22-26 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 194-204 14724829-0 2003 Inhibition of indoleamine 2,3-dioxygenase augments trinitrobenzene sulfonic acid colitis in mice. Trinitrobenzenesulfonic Acid 51-80 indoleamine 2,3-dioxygenase 1 Mus musculus 14-41 14724829-3 2003 We sought to determine whether IDO played a regulatory role in the T-cell helper 1 (Th1)-mediated trinitrobenzene sulfonic acid (TNBS) model of colitis. Trinitrobenzenesulfonic Acid 98-127 indoleamine 2,3-dioxygenase 1 Mus musculus 31-34 14627361-1 2003 We analyzed the functional role of CD8+ T-cell receptor (TCR) Vbeta14+ T cells, which increased specifically in the lamina propria in 2,4,6-trinitrobenzene sulfonic acid (TNBS) -induced colitis. Trinitrobenzenesulfonic Acid 134-169 T cell receptor alpha variable 6-3 Mus musculus 57-60 14627361-1 2003 We analyzed the functional role of CD8+ T-cell receptor (TCR) Vbeta14+ T cells, which increased specifically in the lamina propria in 2,4,6-trinitrobenzene sulfonic acid (TNBS) -induced colitis. Trinitrobenzenesulfonic Acid 171-175 T cell receptor alpha variable 6-3 Mus musculus 57-60 14627361-4 2003 Established T-cell clones showed specific cytotoxic activity against TNBS-conjugated self spleen cells, and this cytotoxicity was completely inhibited by anti-TCR Vbeta14 monoclonal antibody. Trinitrobenzenesulfonic Acid 69-73 T cell receptor alpha variable 6-3 Mus musculus 159-162 14527709-0 2003 Role of nerve growth factor in the trinitrobenzene sulfonic acid-induced colonic hypersensitivity. Trinitrobenzenesulfonic Acid 35-64 nerve growth factor Rattus norvegicus 8-27 14527709-5 2003 This study was designed to evaluate (1) the effect of exogenous NGF on colonic pain threshold, (2) the involvement of NGF in trinitrobenzene sulfonic acid (TNBS)-induced colonic hypersensitivity, by testing an anti-NGF antibody, and (3) finally the involvement of sensory nerves on NGF and TNBS effects using rats treated neonatally with capsaicin. Trinitrobenzenesulfonic Acid 125-154 nerve growth factor Rattus norvegicus 118-121 14527709-9 2003 Neonatal capsaicin pre-treatment inhibited NGF- and TNBS-induced decrease in colonic pain threshold: 49.4 +/- 5.3 versus 22.3 +/- 1.6 mmHg (p<0.01) for capsaicin versus vehicle in NGF-treated rats and 39.6 +/- 3.3 versus 18.0 +/- 1.0 mm Hg (p<0.001) for capsaicin versus vehicle in TNBS-treated rats. Trinitrobenzenesulfonic Acid 288-292 nerve growth factor Rattus norvegicus 43-46 14527709-5 2003 This study was designed to evaluate (1) the effect of exogenous NGF on colonic pain threshold, (2) the involvement of NGF in trinitrobenzene sulfonic acid (TNBS)-induced colonic hypersensitivity, by testing an anti-NGF antibody, and (3) finally the involvement of sensory nerves on NGF and TNBS effects using rats treated neonatally with capsaicin. Trinitrobenzenesulfonic Acid 125-154 nerve growth factor Rattus norvegicus 118-121 14527709-5 2003 This study was designed to evaluate (1) the effect of exogenous NGF on colonic pain threshold, (2) the involvement of NGF in trinitrobenzene sulfonic acid (TNBS)-induced colonic hypersensitivity, by testing an anti-NGF antibody, and (3) finally the involvement of sensory nerves on NGF and TNBS effects using rats treated neonatally with capsaicin. Trinitrobenzenesulfonic Acid 125-154 nerve growth factor Rattus norvegicus 118-121 14527709-5 2003 This study was designed to evaluate (1) the effect of exogenous NGF on colonic pain threshold, (2) the involvement of NGF in trinitrobenzene sulfonic acid (TNBS)-induced colonic hypersensitivity, by testing an anti-NGF antibody, and (3) finally the involvement of sensory nerves on NGF and TNBS effects using rats treated neonatally with capsaicin. Trinitrobenzenesulfonic Acid 156-160 nerve growth factor Rattus norvegicus 118-121 14527709-5 2003 This study was designed to evaluate (1) the effect of exogenous NGF on colonic pain threshold, (2) the involvement of NGF in trinitrobenzene sulfonic acid (TNBS)-induced colonic hypersensitivity, by testing an anti-NGF antibody, and (3) finally the involvement of sensory nerves on NGF and TNBS effects using rats treated neonatally with capsaicin. Trinitrobenzenesulfonic Acid 156-160 nerve growth factor Rattus norvegicus 118-121 14527709-5 2003 This study was designed to evaluate (1) the effect of exogenous NGF on colonic pain threshold, (2) the involvement of NGF in trinitrobenzene sulfonic acid (TNBS)-induced colonic hypersensitivity, by testing an anti-NGF antibody, and (3) finally the involvement of sensory nerves on NGF and TNBS effects using rats treated neonatally with capsaicin. Trinitrobenzenesulfonic Acid 156-160 nerve growth factor Rattus norvegicus 118-121 14527709-9 2003 Neonatal capsaicin pre-treatment inhibited NGF- and TNBS-induced decrease in colonic pain threshold: 49.4 +/- 5.3 versus 22.3 +/- 1.6 mmHg (p<0.01) for capsaicin versus vehicle in NGF-treated rats and 39.6 +/- 3.3 versus 18.0 +/- 1.0 mm Hg (p<0.001) for capsaicin versus vehicle in TNBS-treated rats. Trinitrobenzenesulfonic Acid 52-56 nerve growth factor Rattus norvegicus 183-186 12949723-7 2003 TNBS-induced increases in MPO activities in the colonic tissue were blunted significantly in glycine-fed animals. Trinitrobenzenesulfonic Acid 0-4 myeloperoxidase Rattus norvegicus 26-29 12724134-3 2003 This hypothesis was tested in the present study by examining the therapeutic effect of a novel extracellular PLA2 inhibitor (ExPLI), composed of carboxymethylcellulose-linked phosphatidylethanolamine (CMPE), on trinitrobenzenesulfonic acid-induced colitis. Trinitrobenzenesulfonic Acid 211-239 phospholipase A2 group IB Rattus norvegicus 109-113 12949723-8 2003 Further, dietary glycine largely prevented increases in IL-1beta and TNF-alpha in the colon 2 days after TNBS, and TNBS induction of CINC and MIP-2 in the colonic tissue also was abrogated by glycine. Trinitrobenzenesulfonic Acid 115-119 C-X-C motif chemokine ligand 2 Rattus norvegicus 142-147 12924779-8 2003 Therefore, we resorted to modify the amino groups of the peptidic materials with sodium 2,4,6-trinitro-benzene-1-sulfonate (TNBS) to render them more hydrophobic, so that they can be retained more strongly on the C18 or graphitized carbon cartridges. Trinitrobenzenesulfonic Acid 124-128 Bardet-Biedl syndrome 9 Homo sapiens 213-216 12941148-1 2003 The expression of allograft inflammatory factor-1 (AIF-1) in 2,4,6-trinitrobenzene sulphonic acid (TNBS)-induced colitis, a model for T helper 1 (Th1) type disease, was investigated in BALB/c mice. Trinitrobenzenesulfonic Acid 99-103 allograft inflammatory factor 1 Mus musculus 18-49 12941148-1 2003 The expression of allograft inflammatory factor-1 (AIF-1) in 2,4,6-trinitrobenzene sulphonic acid (TNBS)-induced colitis, a model for T helper 1 (Th1) type disease, was investigated in BALB/c mice. Trinitrobenzenesulfonic Acid 99-103 allograft inflammatory factor 1 Mus musculus 51-56 12941148-4 2003 When AIF-1 Tgm were administrated TNBS, the TNBS-induced colitis was ameliorated compared with that in non-transgenic littermates. Trinitrobenzenesulfonic Acid 34-38 allograft inflammatory factor 1 Mus musculus 5-10 12941148-4 2003 When AIF-1 Tgm were administrated TNBS, the TNBS-induced colitis was ameliorated compared with that in non-transgenic littermates. Trinitrobenzenesulfonic Acid 44-48 allograft inflammatory factor 1 Mus musculus 5-10 12901851-6 2003 In the control, treatment with TNBS led to a statistically significant (p < 0.05) upregulation of IFN-gamma mRNA expression in the inflammatory sites measured at post-treatment day 7. Trinitrobenzenesulfonic Acid 31-35 interferon gamma Homo sapiens 101-110 12901851-9 2003 Pretreatment with rhG-CSF drastically attenuated the degree of TNBS-induced colitis through selective downregulation of Th1-associated cytokines. Trinitrobenzenesulfonic Acid 63-67 negative elongation factor complex member C/D Homo sapiens 120-123 12730878-4 2003 The aim of the present study was to evaluate the therapeutic effects of galectin-1 on T-helper cell type 1-mediated experimental colitis induced by intrarectal administration of 2,4,6-trinitrobenzene sulfonic acid (TNBS) in mice. Trinitrobenzenesulfonic Acid 178-213 lectin, galactose binding, soluble 1 Mus musculus 72-82 12948843-5 2003 On day 3, TNBS-treated animals were killed and the severity of gut inflammation was evaluated by measuring myeloperoxidase (MPO) activity, interleukin-1beta (IL-1beta) production and by scoring macroscopic and histologic colonic damage. Trinitrobenzenesulfonic Acid 10-14 myeloperoxidase Rattus norvegicus 107-122 12948843-5 2003 On day 3, TNBS-treated animals were killed and the severity of gut inflammation was evaluated by measuring myeloperoxidase (MPO) activity, interleukin-1beta (IL-1beta) production and by scoring macroscopic and histologic colonic damage. Trinitrobenzenesulfonic Acid 10-14 myeloperoxidase Rattus norvegicus 124-127 12948843-5 2003 On day 3, TNBS-treated animals were killed and the severity of gut inflammation was evaluated by measuring myeloperoxidase (MPO) activity, interleukin-1beta (IL-1beta) production and by scoring macroscopic and histologic colonic damage. Trinitrobenzenesulfonic Acid 10-14 interleukin 1 beta Rattus norvegicus 139-156 12948843-5 2003 On day 3, TNBS-treated animals were killed and the severity of gut inflammation was evaluated by measuring myeloperoxidase (MPO) activity, interleukin-1beta (IL-1beta) production and by scoring macroscopic and histologic colonic damage. Trinitrobenzenesulfonic Acid 10-14 interleukin 1 beta Rattus norvegicus 158-166 12948843-7 2003 In the TNBS group, PG-SPI and PG-KII increased scores for the severity of colonic damage, stimulated the production of IL-1beta and increased granulocyte infiltration into the colon (MPO activity). Trinitrobenzenesulfonic Acid 7-11 interleukin 1 beta Rattus norvegicus 119-127 12948843-7 2003 In the TNBS group, PG-SPI and PG-KII increased scores for the severity of colonic damage, stimulated the production of IL-1beta and increased granulocyte infiltration into the colon (MPO activity). Trinitrobenzenesulfonic Acid 7-11 myeloperoxidase Rattus norvegicus 183-186 12730878-4 2003 The aim of the present study was to evaluate the therapeutic effects of galectin-1 on T-helper cell type 1-mediated experimental colitis induced by intrarectal administration of 2,4,6-trinitrobenzene sulfonic acid (TNBS) in mice. Trinitrobenzenesulfonic Acid 215-219 lectin, galactose binding, soluble 1 Mus musculus 72-82 12727924-2 2003 To evaluate whether MOR may also be involved in controlling gut inflammation, we first showed that subcutaneous administration of selective peripheral MOR agonists, named DALDA and DAMGO, significantly reduces inflammation in two experimental models of colitis induced by administration of 2,4,6-trinitrobenzene sulfonic acid (TNBS) or peripheral expansion of CD4(+) T cells in mice. Trinitrobenzenesulfonic Acid 290-325 opioid receptor, mu 1 Mus musculus 20-23 12727924-2 2003 To evaluate whether MOR may also be involved in controlling gut inflammation, we first showed that subcutaneous administration of selective peripheral MOR agonists, named DALDA and DAMGO, significantly reduces inflammation in two experimental models of colitis induced by administration of 2,4,6-trinitrobenzene sulfonic acid (TNBS) or peripheral expansion of CD4(+) T cells in mice. Trinitrobenzenesulfonic Acid 290-325 opioid receptor, mu 1 Mus musculus 151-154 12727924-2 2003 To evaluate whether MOR may also be involved in controlling gut inflammation, we first showed that subcutaneous administration of selective peripheral MOR agonists, named DALDA and DAMGO, significantly reduces inflammation in two experimental models of colitis induced by administration of 2,4,6-trinitrobenzene sulfonic acid (TNBS) or peripheral expansion of CD4(+) T cells in mice. Trinitrobenzenesulfonic Acid 327-331 opioid receptor, mu 1 Mus musculus 151-154 12727924-4 2003 Evidence of a genetic role for MOR in the control of gut inflammation was provided by showing that MOR-deficient mice were highly susceptible to colon inflammation, with a 50% mortality rate occurring 3 days after TNBS administration. Trinitrobenzenesulfonic Acid 214-218 opioid receptor, mu 1 Mus musculus 31-34 12727924-4 2003 Evidence of a genetic role for MOR in the control of gut inflammation was provided by showing that MOR-deficient mice were highly susceptible to colon inflammation, with a 50% mortality rate occurring 3 days after TNBS administration. Trinitrobenzenesulfonic Acid 214-218 opioid receptor, mu 1 Mus musculus 99-102 12702051-8 2003 RESULTS: Single rectal administration of TNBS developed significant colitis in IFN-R-/- mice and anti-IFN-gamma mAb-pretreated mice, as well as control wild-type mice. Trinitrobenzenesulfonic Acid 41-45 interferon gamma Mus musculus 102-111 12730857-6 2003 RESULTS: Increased activation of RhoA was found in inflamed intestinal mucosa of patients with Crohn"s disease and of rats with 2,4,6-trinitrobenzene sulfonic acid-induced colitis. Trinitrobenzenesulfonic Acid 128-163 ras homolog family member A Homo sapiens 33-37 12698869-12 2003 In the murine 2,4,6-trinitrobenzen sulfonic acid (TNBS) colitis model, an antisense oligonucleotide to NF-kappa B p65 ameliorated inflammation even after induction of colitis. Trinitrobenzenesulfonic Acid 50-54 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 103-113 12671893-3 2003 We studied the effect of VIP in trinitrobenzene sulfonic acid (TNBS)-induced colitis, which has clinical and molecular features in common with CD. Trinitrobenzenesulfonic Acid 32-61 vasoactive intestinal polypeptide Mus musculus 25-28 12671893-3 2003 We studied the effect of VIP in trinitrobenzene sulfonic acid (TNBS)-induced colitis, which has clinical and molecular features in common with CD. Trinitrobenzenesulfonic Acid 63-67 vasoactive intestinal polypeptide Mus musculus 25-28 12671893-9 2003 VIP reduced disease severity when given after disease onset and dramatically reduced disease recurrence given a second dose of TNBS. Trinitrobenzenesulfonic Acid 127-131 vasoactive intestinal polypeptide Mus musculus 0-3 12671893-10 2003 CONCLUSIONS: Our data suggest that VIP has beneficial prophylactic and therapeutic effects in TNBS-induced colitis and is a promising candidate to test for potential benefits in CD. Trinitrobenzenesulfonic Acid 94-98 vasoactive intestinal polypeptide Mus musculus 35-38 12431903-8 2003 Schistosome egg exposure diminished IFN-gamma and enhanced IL-4 production from alphaCD3-stimulated spleen and mesenteric lymph node cells of TNBS-treated mice. Trinitrobenzenesulfonic Acid 142-146 interleukin 4 Mus musculus 59-63 12431903-9 2003 Schistosome egg exposure decreased colonic IFN-gamma but increased IL-10 mRNA expression in TNBS-treated mice. Trinitrobenzenesulfonic Acid 92-96 interleukin 10 Mus musculus 67-72 12457286-0 2002 IL-10 gene therapy prevents TNBS-induced colitis. Trinitrobenzenesulfonic Acid 28-32 interleukin 10 Mus musculus 0-5 12578368-4 2003 The unfolding kinetics of the four mutant forms of barstar were monitored by measurement of the changes in the fluorescence intensity of Trp53 in the unlabeled and TNB-labeled proteins. Trinitrobenzenesulfonic Acid 164-167 tumor protein p53 Homo sapiens 137-142 12578368-7 2003 The rate of the increase in the fluorescence of Trp53 in the labeled protein, where FRET from the tryptophan to the TNB label occurs, yields the rate of decrease in FRET efficiency during unfolding. Trinitrobenzenesulfonic Acid 116-119 tumor protein p53 Homo sapiens 48-53 12853729-6 2003 The proliferative responses to TNBS of spleen T cells were partially inhibited by the addition of antimouse CD4 or CD8 antibodies to the mixed-lymphocyte culture. Trinitrobenzenesulfonic Acid 31-35 CD4 antigen Mus musculus 108-111 12853729-11 2003 Both CD4+ and CD8+ T cell subsets responded to TNBS, and the rate of CD8+ TCR V beta 14 T cells changed with histological inflammatory activity in TNBS-induced colitis. Trinitrobenzenesulfonic Acid 47-51 CD4 antigen Mus musculus 5-8 12054473-7 2002 We conclude that the signal for apoptosis induced by H(2)O(2) in the MPO-containing HL-60 cell involves the reaction of the diffusible oxidant HOCl with amines producing chloramines and a subsequent non-TNB-reactive product. Trinitrobenzenesulfonic Acid 203-206 myeloperoxidase Homo sapiens 69-72 12064794-7 2002 TNBS-treated rats showed extensive macroscopic colonic damage and a 10-fold increase in myeloperoxidase activity compared to ethanol-treated controls. Trinitrobenzenesulfonic Acid 0-4 myeloperoxidase Rattus norvegicus 88-103 12427966-0 2002 NCX-1015, a nitric-oxide derivative of prednisolone, enhances regulatory T cells in the lamina propria and protects against 2,4,6-trinitrobenzene sulfonic acid-induced colitis in mice. Trinitrobenzenesulfonic Acid 124-159 T cell leukemia, homeobox 2 Mus musculus 0-3 12427966-2 2002 In this study we show NCX-1015 protects mice against the S. A. development and induces healing of T helper cell type 1-mediated experimental colitis induced by intrarectal administration of 2,4,6-trinitrobenzene sulfonic acid (TNBS). Trinitrobenzenesulfonic Acid 190-225 T cell leukemia, homeobox 2 Mus musculus 22-25 12427966-2 2002 In this study we show NCX-1015 protects mice against the S. A. development and induces healing of T helper cell type 1-mediated experimental colitis induced by intrarectal administration of 2,4,6-trinitrobenzene sulfonic acid (TNBS). Trinitrobenzenesulfonic Acid 227-231 T cell leukemia, homeobox 2 Mus musculus 22-25 12421838-0 2002 Dietary fiber down-regulates colonic tumor necrosis factor alpha and nitric oxide production in trinitrobenzenesulfonic acid-induced colitic rats. Trinitrobenzenesulfonic Acid 96-124 tumor necrosis factor Rattus norvegicus 37-64 12370092-6 2002 RESULTS: After treated with TNBS and ethanol, the extents of CMDI, HS, OBT, and the level of MPO in model group were more higher than that in normal group. Trinitrobenzenesulfonic Acid 28-32 myeloperoxidase Rattus norvegicus 93-96 12105854-5 2002 The effects of anti-MIF antibody on chronic colitis induced by TNBS was assessed in BALB/c mice. Trinitrobenzenesulfonic Acid 63-67 macrophage migration inhibitory factor (glycosylation-inhibiting factor) Mus musculus 20-23 12044520-6 2002 In chronic cholangitis 12 weeks after TNBS Mrp2 protein and mRNA remained down-regulated by 40-50% of controls (P<0.05). Trinitrobenzenesulfonic Acid 38-42 ATP binding cassette subfamily C member 2 Homo sapiens 43-47 12059057-7 2002 The tissue content of RMCP-2 in Ws/Ws rats treated with either saline or TNBS/ethanol was only maintained at a much lower level than that in W+/W+ rats with the corresponding treatment. Trinitrobenzenesulfonic Acid 73-77 mast cell protease 2 Rattus norvegicus 22-28 12063094-4 2002 The effect of this compound was compared with that of methylprednisolone on the histological abnormalities and serum levels of tumor necrosis factor-alpha (TNF-alpha) in experimental colitis produced by 2,4,6-trinitrobenzenesulfonic acid (TNB). Trinitrobenzenesulfonic Acid 203-237 tumor necrosis factor Rattus norvegicus 127-154 12063094-4 2002 The effect of this compound was compared with that of methylprednisolone on the histological abnormalities and serum levels of tumor necrosis factor-alpha (TNF-alpha) in experimental colitis produced by 2,4,6-trinitrobenzenesulfonic acid (TNB). Trinitrobenzenesulfonic Acid 203-237 tumor necrosis factor Rattus norvegicus 156-165 11889071-3 2002 In this paper we describe the effects of a specific p38 MAPK inhibitor, SB 203580, in trinitrobenzene sulphonic acid (TNBS) induced colitis in mice. Trinitrobenzenesulfonic Acid 118-122 mitogen-activated protein kinase 14 Mus musculus 52-60 11909639-1 2002 The alkylation of amino groups of the mineralocorticoid receptor (MR) with pyridoxal 5"-phosphate or 2,4,6-trinitrobenzenesulphonate (TNBS) under controlled conditions modifies only one lysyl residue, which accounts for a 70% inhibition of steroid binding capacity. Trinitrobenzenesulfonic Acid 134-138 nuclear receptor subfamily 3 group C member 2 Homo sapiens 38-64 11884629-2 2002 Chemical modification of murine CAD with the lysine-specific reagent 2,4,6-trinitrobenzenesulphonic acid and the tyrosine-specific reagent N-acetylimidazole leads to inactivation of the nuclease, indicating that lysine and tyrosine residues are important for DNA cleavage by this enzyme. Trinitrobenzenesulfonic Acid 69-104 DNA fragmentation factor, beta subunit Mus musculus 32-35 11849839-6 2002 But the administration of Polygalae root to TNBS-induced colitis mice showed lower production of IFN-gamma and higher production of IL-4 than the TNBS-induced colitis. Trinitrobenzenesulfonic Acid 44-48 interferon gamma Mus musculus 97-106 11849839-6 2002 But the administration of Polygalae root to TNBS-induced colitis mice showed lower production of IFN-gamma and higher production of IL-4 than the TNBS-induced colitis. Trinitrobenzenesulfonic Acid 44-48 interleukin 4 Mus musculus 132-136 11909639-1 2002 The alkylation of amino groups of the mineralocorticoid receptor (MR) with pyridoxal 5"-phosphate or 2,4,6-trinitrobenzenesulphonate (TNBS) under controlled conditions modifies only one lysyl residue, which accounts for a 70% inhibition of steroid binding capacity. Trinitrobenzenesulfonic Acid 134-138 nuclear receptor subfamily 3 group C member 2 Homo sapiens 66-68 11668029-1 2001 We investigated hypothalamic neuronal corticotropin-releasing factor (CRF) gene expression changes in response to visceral inflammation induced by 2,4,6-trinitrobenzenesulfonic acid (TNB) and acute stress. Trinitrobenzenesulfonic Acid 147-181 corticotropin releasing hormone Rattus norvegicus 38-68 11884025-3 2001 The study was designed to investigate whether colitis induced by trinitrobenzene sulphonic acid (TNBS) in rats produces an increase in TACE activity and/or expression and whether its pharmacological inhibition reduces TNF-alpha levels, iNOS expression and colonic damage in this model. Trinitrobenzenesulfonic Acid 97-101 ADAM metallopeptidase domain 17 Rattus norvegicus 135-139 11884025-3 2001 The study was designed to investigate whether colitis induced by trinitrobenzene sulphonic acid (TNBS) in rats produces an increase in TACE activity and/or expression and whether its pharmacological inhibition reduces TNF-alpha levels, iNOS expression and colonic damage in this model. Trinitrobenzenesulfonic Acid 97-101 tumor necrosis factor Rattus norvegicus 218-227 11884025-3 2001 The study was designed to investigate whether colitis induced by trinitrobenzene sulphonic acid (TNBS) in rats produces an increase in TACE activity and/or expression and whether its pharmacological inhibition reduces TNF-alpha levels, iNOS expression and colonic damage in this model. Trinitrobenzenesulfonic Acid 97-101 nitric oxide synthase 2 Rattus norvegicus 236-240 11884025-7 2001 Instillation of TNBS caused an increase in TACE activity and expression and the release of TNF-alpha. Trinitrobenzenesulfonic Acid 16-20 ADAM metallopeptidase domain 17 Rattus norvegicus 43-47 11884025-7 2001 Instillation of TNBS caused an increase in TACE activity and expression and the release of TNF-alpha. Trinitrobenzenesulfonic Acid 16-20 tumor necrosis factor Rattus norvegicus 91-100 11884025-8 2001 TNBS also resulted in iNOS expression and colonic damage. Trinitrobenzenesulfonic Acid 0-4 nitric oxide synthase 2 Rattus norvegicus 22-26 11884025-9 2001 BB1101 blocked TNBS-induced increase in TACE activity, TNF-alpha release and iNOS expression. Trinitrobenzenesulfonic Acid 15-19 ADAM metallopeptidase domain 17 Rattus norvegicus 40-44 11884025-9 2001 BB1101 blocked TNBS-induced increase in TACE activity, TNF-alpha release and iNOS expression. Trinitrobenzenesulfonic Acid 15-19 tumor necrosis factor Rattus norvegicus 55-64 11884025-9 2001 BB1101 blocked TNBS-induced increase in TACE activity, TNF-alpha release and iNOS expression. Trinitrobenzenesulfonic Acid 15-19 nitric oxide synthase 2 Rattus norvegicus 77-81 11884025-11 2001 TNBS causes TNF-alpha release by an increase in TACE activity and expression and this results in the expression of iNOS and subsequent inflammation, suggesting that TACE inhibition may prove useful as a therapeutic means in IBD. Trinitrobenzenesulfonic Acid 0-4 tumor necrosis factor Rattus norvegicus 12-21 11884025-11 2001 TNBS causes TNF-alpha release by an increase in TACE activity and expression and this results in the expression of iNOS and subsequent inflammation, suggesting that TACE inhibition may prove useful as a therapeutic means in IBD. Trinitrobenzenesulfonic Acid 0-4 ADAM metallopeptidase domain 17 Rattus norvegicus 48-52 11884025-11 2001 TNBS causes TNF-alpha release by an increase in TACE activity and expression and this results in the expression of iNOS and subsequent inflammation, suggesting that TACE inhibition may prove useful as a therapeutic means in IBD. Trinitrobenzenesulfonic Acid 0-4 nitric oxide synthase 2 Rattus norvegicus 115-119 11884025-11 2001 TNBS causes TNF-alpha release by an increase in TACE activity and expression and this results in the expression of iNOS and subsequent inflammation, suggesting that TACE inhibition may prove useful as a therapeutic means in IBD. Trinitrobenzenesulfonic Acid 0-4 ADAM metallopeptidase domain 17 Rattus norvegicus 165-169 11732997-2 2001 The involvement of the lysine residue present at the active site of Ehrlich ascites carcinoma (EAC) cell glyceraldehyde-3-phosphate dehydrogenase (Gra3PDH) was investigated by using the lysine specific reagents trinitrobenzenesulfonic acid (TNBS) and pyridoxal phosphate (PP). Trinitrobenzenesulfonic Acid 211-239 glyceraldehyde-3-phosphate dehydrogenase Mus musculus 105-145 11729116-0 2001 Blockade of endogenous IL-18 ameliorates TNBS-induced colitis by decreasing local TNF-alpha production in mice. Trinitrobenzenesulfonic Acid 41-45 interleukin 18 Mus musculus 23-28 11729116-0 2001 Blockade of endogenous IL-18 ameliorates TNBS-induced colitis by decreasing local TNF-alpha production in mice. Trinitrobenzenesulfonic Acid 41-45 tumor necrosis factor Mus musculus 82-91 11729116-5 2001 METHODS: Activity of IL-18 was neutralized using recombinant human IL-18 binding protein isoform a (rhIL-18BPa) in trinitrobenzene sulfonic acid (TNBS)-induced colitis. Trinitrobenzenesulfonic Acid 115-144 interleukin 18 Homo sapiens 21-26 11729116-5 2001 METHODS: Activity of IL-18 was neutralized using recombinant human IL-18 binding protein isoform a (rhIL-18BPa) in trinitrobenzene sulfonic acid (TNBS)-induced colitis. Trinitrobenzenesulfonic Acid 115-144 interleukin 18 Homo sapiens 67-72 11729116-5 2001 METHODS: Activity of IL-18 was neutralized using recombinant human IL-18 binding protein isoform a (rhIL-18BPa) in trinitrobenzene sulfonic acid (TNBS)-induced colitis. Trinitrobenzenesulfonic Acid 146-150 interleukin 18 Homo sapiens 21-26 11729116-5 2001 METHODS: Activity of IL-18 was neutralized using recombinant human IL-18 binding protein isoform a (rhIL-18BPa) in trinitrobenzene sulfonic acid (TNBS)-induced colitis. Trinitrobenzenesulfonic Acid 146-150 interleukin 18 Homo sapiens 67-72 11936750-13 2002 PNS/TPL protected against cachexia and mortality, both usually induced by TNBS. Trinitrobenzenesulfonic Acid 74-78 BPI fold containing family A, member 5 Mus musculus 4-7 11777988-1 2002 In the present study, we define the relation between TGF-beta and IL-10 in the regulation of the Th1-mediated inflammation occurring in trinitrobenzene sulfonic acid (TNBS)-colitis. Trinitrobenzenesulfonic Acid 136-165 transforming growth factor, beta 1 Mus musculus 53-61 11777988-1 2002 In the present study, we define the relation between TGF-beta and IL-10 in the regulation of the Th1-mediated inflammation occurring in trinitrobenzene sulfonic acid (TNBS)-colitis. Trinitrobenzenesulfonic Acid 136-165 interleukin 10 Mus musculus 66-71 11777988-1 2002 In the present study, we define the relation between TGF-beta and IL-10 in the regulation of the Th1-mediated inflammation occurring in trinitrobenzene sulfonic acid (TNBS)-colitis. Trinitrobenzenesulfonic Acid 136-165 negative elongation factor complex member C/D, Th1l Mus musculus 97-100 11782017-3 2002 TNBS-treated IL-12Rbeta1(-/-) and IL-12p35(-/-) mice developed only a mild disease associated with low level IL-18 expression in IL-12p35(-/-) mice. Trinitrobenzenesulfonic Acid 0-4 interleukin 12 receptor, beta 1 Mus musculus 13-24 11782017-3 2002 TNBS-treated IL-12Rbeta1(-/-) and IL-12p35(-/-) mice developed only a mild disease associated with low level IL-18 expression in IL-12p35(-/-) mice. Trinitrobenzenesulfonic Acid 0-4 interleukin 12a Mus musculus 34-42 11782017-3 2002 TNBS-treated IL-12Rbeta1(-/-) and IL-12p35(-/-) mice developed only a mild disease associated with low level IL-18 expression in IL-12p35(-/-) mice. Trinitrobenzenesulfonic Acid 0-4 interleukin 18 Mus musculus 109-114 11782017-3 2002 TNBS-treated IL-12Rbeta1(-/-) and IL-12p35(-/-) mice developed only a mild disease associated with low level IL-18 expression in IL-12p35(-/-) mice. Trinitrobenzenesulfonic Acid 0-4 interleukin 12a Mus musculus 129-137 11782017-7 2002 These results demonstrate that IL-12p40, in contrast to IL-12p70, inhibits TNBS-induced colitis and IL-18 expression independent of IFN-gamma. Trinitrobenzenesulfonic Acid 75-79 interleukin 12b Mus musculus 31-39 11732997-2 2001 The involvement of the lysine residue present at the active site of Ehrlich ascites carcinoma (EAC) cell glyceraldehyde-3-phosphate dehydrogenase (Gra3PDH) was investigated by using the lysine specific reagents trinitrobenzenesulfonic acid (TNBS) and pyridoxal phosphate (PP). Trinitrobenzenesulfonic Acid 211-239 glyceraldehyde-3-phosphate dehydrogenase Mus musculus 147-154 11732997-2 2001 The involvement of the lysine residue present at the active site of Ehrlich ascites carcinoma (EAC) cell glyceraldehyde-3-phosphate dehydrogenase (Gra3PDH) was investigated by using the lysine specific reagents trinitrobenzenesulfonic acid (TNBS) and pyridoxal phosphate (PP). Trinitrobenzenesulfonic Acid 241-245 glyceraldehyde-3-phosphate dehydrogenase Mus musculus 105-145 11732997-2 2001 The involvement of the lysine residue present at the active site of Ehrlich ascites carcinoma (EAC) cell glyceraldehyde-3-phosphate dehydrogenase (Gra3PDH) was investigated by using the lysine specific reagents trinitrobenzenesulfonic acid (TNBS) and pyridoxal phosphate (PP). Trinitrobenzenesulfonic Acid 241-245 glyceraldehyde-3-phosphate dehydrogenase Mus musculus 147-154 11732997-3 2001 Both TNBS and PP inactivated EAC cell Gra3PDH with pseudo-first-order kinetics with the rate dependent on modifier concentration. Trinitrobenzenesulfonic Acid 5-9 glyceraldehyde-3-phosphate dehydrogenase Mus musculus 38-45 11717450-4 2001 In this study we show that PAR-2 activation prevents the development and induces healing of T helper cell type 1-mediated experimental colitis induced by intrarectal administration of 2,4,6-trinitrobenzene sulfonic acid (TNBS) in mice. Trinitrobenzenesulfonic Acid 184-219 coagulation factor II (thrombin) receptor-like 1 Mus musculus 27-32 11717450-4 2001 In this study we show that PAR-2 activation prevents the development and induces healing of T helper cell type 1-mediated experimental colitis induced by intrarectal administration of 2,4,6-trinitrobenzene sulfonic acid (TNBS) in mice. Trinitrobenzenesulfonic Acid 221-225 coagulation factor II (thrombin) receptor-like 1 Mus musculus 27-32 11717450-9 2001 Protection exerted by PAR-2 in TNBS-treated mice was reverted by injecting mice with a truncated form of calcitonin gene-related peptide and by sensory neurons ablation with the neurotoxin capsaicin. Trinitrobenzenesulfonic Acid 31-35 coagulation factor II (thrombin) receptor-like 1 Mus musculus 22-27 11668029-1 2001 We investigated hypothalamic neuronal corticotropin-releasing factor (CRF) gene expression changes in response to visceral inflammation induced by 2,4,6-trinitrobenzenesulfonic acid (TNB) and acute stress. Trinitrobenzenesulfonic Acid 183-186 corticotropin releasing hormone Rattus norvegicus 38-68 11534936-11 2001 However, L-Arg diet accelerated weight gain both pre- and post-TNBS. Trinitrobenzenesulfonic Acid 63-67 Rho guanine nucleotide exchange factor 12 Rattus norvegicus 9-14 11840838-5 2001 Colonic inflammation following TNBS induction was characterized by hemorrhagic necrosis and fibrosis of the mucosa, increased colonic wall thickness, infiltration of inflammatory cells, and increased myeloperoxidase (MPO) activity. Trinitrobenzenesulfonic Acid 31-35 myeloperoxidase Rattus norvegicus 200-215 11840838-5 2001 Colonic inflammation following TNBS induction was characterized by hemorrhagic necrosis and fibrosis of the mucosa, increased colonic wall thickness, infiltration of inflammatory cells, and increased myeloperoxidase (MPO) activity. Trinitrobenzenesulfonic Acid 31-35 myeloperoxidase Rattus norvegicus 217-220 11820457-3 2001 TNBS-induced colitis was associated with enhanced COX-2 expression in the gut and increased circulating concentrations of PGE2 metabolite (PGEM). Trinitrobenzenesulfonic Acid 0-4 prostaglandin-endoperoxide synthase 2 Rattus norvegicus 50-55 11606501-7 2001 RESULTS: The colonic mucosa of TNBS-treated mice was marked by infiltration of Mac-1-positive macrophages and up-regulation of IL-18. Trinitrobenzenesulfonic Acid 31-35 integrin alpha M Mus musculus 79-84 11606501-7 2001 RESULTS: The colonic mucosa of TNBS-treated mice was marked by infiltration of Mac-1-positive macrophages and up-regulation of IL-18. Trinitrobenzenesulfonic Acid 31-35 interleukin 18 Mus musculus 127-132 11572597-6 2001 The colonic levels of cox-2 protein, mRNA, myeloperoxidase (MPO), and prostaglandin E2 (PGE2) were increased significantly on day 1 and remained significantly elevated until day 7 post-TNBS administration, whereas cox-1 remained unaltered. Trinitrobenzenesulfonic Acid 185-189 prostaglandin-endoperoxide synthase 2 Rattus norvegicus 22-27 11509623-7 2001 This pretreatment protected IFN-gamma(-/-) mice from trinitrobenzene sulfonic acid-induced colitis; however, in normal mice this weekly treatment was less protective. Trinitrobenzenesulfonic Acid 53-82 interferon gamma Mus musculus 28-37 11447040-0 2001 Protective role of heme oxygenase-1 on trinitrobenzene sulfonic acid-induced colitis in rats. Trinitrobenzenesulfonic Acid 39-68 heme oxygenase 1 Rattus norvegicus 19-35 11447040-2 2001 The present study investigated the possible role of HO-1 in 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis in rats. Trinitrobenzenesulfonic Acid 60-95 heme oxygenase 1 Rattus norvegicus 52-56 11447040-2 2001 The present study investigated the possible role of HO-1 in 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis in rats. Trinitrobenzenesulfonic Acid 97-101 heme oxygenase 1 Rattus norvegicus 52-56 11447040-3 2001 We measured HO-1 activity in TNBS-induced colitis in rats and analyzed the severity of colitis along with altered HO activity by assessing lesion area and myeloperoxidase activity. Trinitrobenzenesulfonic Acid 29-33 heme oxygenase 1 Rattus norvegicus 12-16 11447040-4 2001 HO-1 mRNA and protein expressions were determined at different time points after TNBS induction. Trinitrobenzenesulfonic Acid 81-85 heme oxygenase 1 Rattus norvegicus 0-4 11447040-6 2001 HO activity and HO-1 gene expression increased markedly after TNBS induction. Trinitrobenzenesulfonic Acid 62-66 heme oxygenase 1 Rattus norvegicus 16-20 11510951-4 2001 The present study investigated the possible role of leptin in the pathogenesis of trinitrobenzene sulfonic acid (TNBS)-induced colitis in rats. Trinitrobenzenesulfonic Acid 82-111 leptin Rattus norvegicus 52-58 11356911-0 2001 Colon epithelial cell death in 2,4,6-trinitrobenzenesulfonic acid-induced colitis is associated with increased inducible nitric-oxide synthase expression and peroxynitrite production. Trinitrobenzenesulfonic Acid 31-65 nitric oxide synthase 2 Rattus norvegicus 111-142 11459438-6 2001 These findings indicate that the expression of iNOS accounts for most of the damage caused by TNBS and that the administration of 1400W after the onset of colitis has a beneficial action on the colonic injury. Trinitrobenzenesulfonic Acid 94-98 nitric oxide synthase 2 Rattus norvegicus 47-51 11283155-4 2001 PPARgamma(1/)- and RXRalpha(1/)- mice both displayed a significantly enhanced susceptibility to 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis compared with their wild-type littermates. Trinitrobenzenesulfonic Acid 96-131 peroxisome proliferator activated receptor gamma Mus musculus 0-9 11283155-4 2001 PPARgamma(1/)- and RXRalpha(1/)- mice both displayed a significantly enhanced susceptibility to 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis compared with their wild-type littermates. Trinitrobenzenesulfonic Acid 96-131 retinoid X receptor alpha Mus musculus 19-30 11283155-4 2001 PPARgamma(1/)- and RXRalpha(1/)- mice both displayed a significantly enhanced susceptibility to 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis compared with their wild-type littermates. Trinitrobenzenesulfonic Acid 133-137 peroxisome proliferator activated receptor gamma Mus musculus 0-9 11283155-4 2001 PPARgamma(1/)- and RXRalpha(1/)- mice both displayed a significantly enhanced susceptibility to 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis compared with their wild-type littermates. Trinitrobenzenesulfonic Acid 133-137 retinoid X receptor alpha Mus musculus 19-30 11283155-6 2001 TNBS-induced colitis was significantly reduced by the administration of both PPARgamma and RXR agonists. Trinitrobenzenesulfonic Acid 0-4 peroxisome proliferator activated receptor gamma Mus musculus 77-86 11379790-6 2001 By contrast, upregulation of brain ICAM-1 in colitic animals was only observed in the CD45RBhigh transfer (3-fold) and the TNBS-induced (1.5-fold models). Trinitrobenzenesulfonic Acid 123-127 intercellular adhesion molecule 1 Rattus norvegicus 35-41 11167873-11 2001 CONCLUSION: The systemic response to TNBS-induced colitis appears to be at least partially dependent on TNF. Trinitrobenzenesulfonic Acid 37-41 tumor necrosis factor Rattus norvegicus 104-107 11207312-1 2001 Trinitrobenzene sulfonic acid (TNBS)-induced colitis is an IL-12-driven, Th1 T cell-mediated colitis that resembles human Crohn"s disease. Trinitrobenzenesulfonic Acid 0-29 negative elongation factor complex member C/D Homo sapiens 73-76 11207312-1 2001 Trinitrobenzene sulfonic acid (TNBS)-induced colitis is an IL-12-driven, Th1 T cell-mediated colitis that resembles human Crohn"s disease. Trinitrobenzenesulfonic Acid 31-35 negative elongation factor complex member C/D Homo sapiens 73-76 11123336-8 2001 Administration on days 7 through 14 after trinitrobenzene sulfonic acid administration of a CCR1/CCR5 receptor antagonist, Met-RANTES, resulted in a significant reduction of both macroscopic and microscopic colonic damage, as well as reducing the recruitment into the colon of monocytes, mast cells, and neutrophils. Trinitrobenzenesulfonic Acid 42-71 C-C motif chemokine receptor 1 Rattus norvegicus 92-96 11137876-4 2001 Results indicated that pretreatment with cyclooxygenase-2 inhibitors not only protected against 2,4,6-trinitrobenzenesulfonic acid-induced inflammatory bowel disease, but also attenuated the potentiating effect of cigarette-smoke exposure on colonic damage. Trinitrobenzenesulfonic Acid 96-130 prostaglandin-endoperoxide synthase 2 Rattus norvegicus 41-57 11137876-6 2001 The present study suggests that the highly induced cyclooxygenase-2 expression not only plays a pathogenic role in 2,4,6-trinitrobenzenesulfonic acid-induced inflammatory bowel disease, but also contributes to the adverse action of cigarette-smoke exposure on this disorder. Trinitrobenzenesulfonic Acid 115-149 prostaglandin-endoperoxide synthase 2 Rattus norvegicus 51-67 11173915-10 2001 These results suggest that neutrophil-endothelial cell interactions via P-selectin and ICAM-1 play an important role in the development of TNB-induced colitis in rats. Trinitrobenzenesulfonic Acid 139-142 selectin P Rattus norvegicus 72-82 11173915-10 2001 These results suggest that neutrophil-endothelial cell interactions via P-selectin and ICAM-1 play an important role in the development of TNB-induced colitis in rats. Trinitrobenzenesulfonic Acid 139-142 intercellular adhesion molecule 1 Rattus norvegicus 87-93 11268945-6 2001 Exposure to the trinitrobenzene sulfonic acid enema inhibited the increase in body weight of rats, and markedly increased the colonic damage scores, wet weight, thiobarbituric acid-reactive substances and myeloperoxidase activity. Trinitrobenzenesulfonic Acid 16-45 myeloperoxidase Rattus norvegicus 205-220 11268945-8 2001 The increases in the colonic damage scores, wet weight, thiobarbituric acid-reactive substances and myeloperoxidase activity in trinitrobenzene sulfonic acid-colitis were significantly inhibited by aminoguanidine treatment, although they tended to be aggravated by NG-nitro-L-arginine treatment. Trinitrobenzenesulfonic Acid 128-157 myeloperoxidase Rattus norvegicus 100-115 11136818-4 2001 In hFc epsilon RI transgenic mice, 2,4,6-tri-nitrobenzenesulfonic acid (TNBS)-induced colitis was also more pronounced, whereas Fc epsilon RI-deficient animals were protected from colitis, demonstrating that Fc epsilon RI can affect the onset of intestinal inflammation. Trinitrobenzenesulfonic Acid 35-70 Fc epsilon receptor Ia Homo sapiens 3-17 11136818-4 2001 In hFc epsilon RI transgenic mice, 2,4,6-tri-nitrobenzenesulfonic acid (TNBS)-induced colitis was also more pronounced, whereas Fc epsilon RI-deficient animals were protected from colitis, demonstrating that Fc epsilon RI can affect the onset of intestinal inflammation. Trinitrobenzenesulfonic Acid 35-70 Fc receptor, IgE, high affinity I, alpha polypeptide Mus musculus 4-17 11136818-4 2001 In hFc epsilon RI transgenic mice, 2,4,6-tri-nitrobenzenesulfonic acid (TNBS)-induced colitis was also more pronounced, whereas Fc epsilon RI-deficient animals were protected from colitis, demonstrating that Fc epsilon RI can affect the onset of intestinal inflammation. Trinitrobenzenesulfonic Acid 72-76 Fc epsilon receptor Ia Homo sapiens 3-17 11136818-4 2001 In hFc epsilon RI transgenic mice, 2,4,6-tri-nitrobenzenesulfonic acid (TNBS)-induced colitis was also more pronounced, whereas Fc epsilon RI-deficient animals were protected from colitis, demonstrating that Fc epsilon RI can affect the onset of intestinal inflammation. Trinitrobenzenesulfonic Acid 72-76 Fc receptor, IgE, high affinity I, alpha polypeptide Mus musculus 4-17 11123336-8 2001 Administration on days 7 through 14 after trinitrobenzene sulfonic acid administration of a CCR1/CCR5 receptor antagonist, Met-RANTES, resulted in a significant reduction of both macroscopic and microscopic colonic damage, as well as reducing the recruitment into the colon of monocytes, mast cells, and neutrophils. Trinitrobenzenesulfonic Acid 42-71 C-C motif chemokine receptor 5 Rattus norvegicus 97-101 11123336-8 2001 Administration on days 7 through 14 after trinitrobenzene sulfonic acid administration of a CCR1/CCR5 receptor antagonist, Met-RANTES, resulted in a significant reduction of both macroscopic and microscopic colonic damage, as well as reducing the recruitment into the colon of monocytes, mast cells, and neutrophils. Trinitrobenzenesulfonic Acid 42-71 C-C motif chemokine ligand 5 Rattus norvegicus 127-133 11131446-10 2000 Anti-neutrophil cytoplasmic antibodies with specificity against myeloperoxidase, catalase and actin were found between 1 and 12 weeks after TNBS injection. Trinitrobenzenesulfonic Acid 140-144 myeloperoxidase Rattus norvegicus 64-79 11040184-3 2000 The aim of this study was to determine whether IL-16 production is increased in inflammatory bowel disease and whether IL-16 participates in trinitrobenzene sulfonic acid (TNBS)-induced colitis in mice. Trinitrobenzenesulfonic Acid 141-170 interleukin 16 Mus musculus 119-124 11113077-9 2000 Treatment of animals with neutralizing anti-IL-6 antibody reduced the TNBS-induced growth and activation of the adrenal cortices. Trinitrobenzenesulfonic Acid 70-74 interleukin 6 Mus musculus 44-48 11040184-3 2000 The aim of this study was to determine whether IL-16 production is increased in inflammatory bowel disease and whether IL-16 participates in trinitrobenzene sulfonic acid (TNBS)-induced colitis in mice. Trinitrobenzenesulfonic Acid 172-176 interleukin 16 Mus musculus 119-124 11040184-8 2000 Anti-IL-16 mAb treatment significantly reduced TNBS-induced weight loss (P< 0.001), mucosal ulceration (P<0.05), myeloperoxidase activity (P< 0.001), and TNBS-mediated increases in mucosal levels of IL-1beta (P<0.05) and tumor necrosis factor alpha (P<0.01). Trinitrobenzenesulfonic Acid 47-51 interleukin 16 Mus musculus 5-10 11040184-8 2000 Anti-IL-16 mAb treatment significantly reduced TNBS-induced weight loss (P< 0.001), mucosal ulceration (P<0.05), myeloperoxidase activity (P< 0.001), and TNBS-mediated increases in mucosal levels of IL-1beta (P<0.05) and tumor necrosis factor alpha (P<0.01). Trinitrobenzenesulfonic Acid 47-51 interleukin 1 beta Mus musculus 208-216 11040184-8 2000 Anti-IL-16 mAb treatment significantly reduced TNBS-induced weight loss (P< 0.001), mucosal ulceration (P<0.05), myeloperoxidase activity (P< 0.001), and TNBS-mediated increases in mucosal levels of IL-1beta (P<0.05) and tumor necrosis factor alpha (P<0.01). Trinitrobenzenesulfonic Acid 47-51 tumor necrosis factor Mus musculus 233-260 11040184-9 2000 CONCLUSIONS: Anti-IL-16 mAb reduced colonic injury and inflammation induced by TNBS in mice. Trinitrobenzenesulfonic Acid 79-83 interleukin 16 Mus musculus 18-23 10945850-0 2000 Dose-dependent effects of recombinant human interleukin-11 on contractile properties in rabbit 2,4,6-trinitrobenzene sulfonic acid colitis. Trinitrobenzenesulfonic Acid 95-130 interleukin 11 Homo sapiens 44-58 11011247-3 2000 AIM: To evaluate the anti-inflammatory functions of PPARgamma agonist during a trinitrobenzene sulfonic acid (TNBS)-induced colitis in mice. Trinitrobenzenesulfonic Acid 79-108 peroxisome proliferator activated receptor gamma Mus musculus 52-61 11011247-3 2000 AIM: To evaluate the anti-inflammatory functions of PPARgamma agonist during a trinitrobenzene sulfonic acid (TNBS)-induced colitis in mice. Trinitrobenzenesulfonic Acid 110-114 peroxisome proliferator activated receptor gamma Mus musculus 52-61 11011247-7 2000 RESULTS: TNBS induced severe macroscopic and histologic lesions, with high mucosal MPO, IL-1B and TNFalpha mRNA concentrations. Trinitrobenzenesulfonic Acid 9-13 myeloperoxidase Mus musculus 83-86 11011247-7 2000 RESULTS: TNBS induced severe macroscopic and histologic lesions, with high mucosal MPO, IL-1B and TNFalpha mRNA concentrations. Trinitrobenzenesulfonic Acid 9-13 interleukin 1 beta Mus musculus 88-93 11011247-7 2000 RESULTS: TNBS induced severe macroscopic and histologic lesions, with high mucosal MPO, IL-1B and TNFalpha mRNA concentrations. Trinitrobenzenesulfonic Acid 9-13 tumor necrosis factor Mus musculus 98-106 11011247-9 2000 CONCLUSION: PPARgamma agonist decreases the intensity of TNBS induced colitis through normalization of IL-1B and TNFalpha expression. Trinitrobenzenesulfonic Acid 57-61 peroxisome proliferator activated receptor gamma Mus musculus 12-21 11011247-9 2000 CONCLUSION: PPARgamma agonist decreases the intensity of TNBS induced colitis through normalization of IL-1B and TNFalpha expression. Trinitrobenzenesulfonic Acid 57-61 interleukin 1 beta Mus musculus 103-108 11011247-9 2000 CONCLUSION: PPARgamma agonist decreases the intensity of TNBS induced colitis through normalization of IL-1B and TNFalpha expression. Trinitrobenzenesulfonic Acid 57-61 tumor necrosis factor Mus musculus 113-121 10880525-0 2000 Treatment of experimental (Trinitrobenzene sulfonic acid) colitis by intranasal administration of transforming growth factor (TGF)-beta1 plasmid: TGF-beta1-mediated suppression of T helper cell type 1 response occurs by interleukin (IL)-10 induction and IL-12 receptor beta2 chain downregulation. Trinitrobenzenesulfonic Acid 27-56 transforming growth factor beta 1 Homo sapiens 98-136 11022836-7 2000 The platelet count and the fibrinogen level were higher in the TNB-S group than in the healthy control group and the AT-III level was slightly lower in the TNB-S group than in the healthy control group and lower still in the TNB-H group. Trinitrobenzenesulfonic Acid 156-161 serpin family C member 1 Rattus norvegicus 117-123 10880525-0 2000 Treatment of experimental (Trinitrobenzene sulfonic acid) colitis by intranasal administration of transforming growth factor (TGF)-beta1 plasmid: TGF-beta1-mediated suppression of T helper cell type 1 response occurs by interleukin (IL)-10 induction and IL-12 receptor beta2 chain downregulation. Trinitrobenzenesulfonic Acid 27-56 transforming growth factor beta 1 Homo sapiens 146-155 10880525-0 2000 Treatment of experimental (Trinitrobenzene sulfonic acid) colitis by intranasal administration of transforming growth factor (TGF)-beta1 plasmid: TGF-beta1-mediated suppression of T helper cell type 1 response occurs by interleukin (IL)-10 induction and IL-12 receptor beta2 chain downregulation. Trinitrobenzenesulfonic Acid 27-56 interleukin 10 Homo sapiens 220-239 10880525-1 2000 In this study, we show that a single intranasal dose of a plasmid encoding active transforming growth factor beta1 (pCMV-TGF-beta1) prevents the development of T helper cell type 1 (Th1)-mediated experimental colitis induced by the haptenating reagent, 2,4, 6-trinitrobenzene sulfonic acid (TNBS). Trinitrobenzenesulfonic Acid 253-289 transforming growth factor beta 1 Homo sapiens 82-114 10880525-1 2000 In this study, we show that a single intranasal dose of a plasmid encoding active transforming growth factor beta1 (pCMV-TGF-beta1) prevents the development of T helper cell type 1 (Th1)-mediated experimental colitis induced by the haptenating reagent, 2,4, 6-trinitrobenzene sulfonic acid (TNBS). Trinitrobenzenesulfonic Acid 253-289 transforming growth factor beta 1 Homo sapiens 121-130 10880525-1 2000 In this study, we show that a single intranasal dose of a plasmid encoding active transforming growth factor beta1 (pCMV-TGF-beta1) prevents the development of T helper cell type 1 (Th1)-mediated experimental colitis induced by the haptenating reagent, 2,4, 6-trinitrobenzene sulfonic acid (TNBS). Trinitrobenzenesulfonic Acid 291-295 transforming growth factor beta 1 Homo sapiens 82-114 10880525-1 2000 In this study, we show that a single intranasal dose of a plasmid encoding active transforming growth factor beta1 (pCMV-TGF-beta1) prevents the development of T helper cell type 1 (Th1)-mediated experimental colitis induced by the haptenating reagent, 2,4, 6-trinitrobenzene sulfonic acid (TNBS). Trinitrobenzenesulfonic Acid 291-295 transforming growth factor beta 1 Homo sapiens 121-130 10877837-1 2000 The receptor responsible for CGRP-induced ion transport and permeability was examined in tissues from animals treated 7 days previously with trinitrobenzenesulfonic acid to induce colitis or in controls. Trinitrobenzenesulfonic Acid 141-169 calcitonin-related polypeptide alpha Rattus norvegicus 29-33 10827154-8 2000 Treatment with trinitrobenzene sulfonic acid induced significant cholestasis and caused translocation of immunostaining for 7H6, but not that for ZO-1, to the cytoplasm and diminished immunostaining for mrp2 on the canaliculus membrane. Trinitrobenzenesulfonic Acid 15-44 tight junction protein 1 Rattus norvegicus 146-150 10959551-6 2000 METHODS: Inflammation in the TNBS model was assessed by measuring the tissue myeloperoxidase activity, leukotriene B4 concentration, inducible nitric oxide protein expression, the ex-vivo production of tumour necrosis factor alpha (TNFalpha), macroscopic damage score, plasma corticosterone levels and by a qualitative histological evolution. Trinitrobenzenesulfonic Acid 29-33 myeloperoxidase Homo sapiens 77-92 10959551-6 2000 METHODS: Inflammation in the TNBS model was assessed by measuring the tissue myeloperoxidase activity, leukotriene B4 concentration, inducible nitric oxide protein expression, the ex-vivo production of tumour necrosis factor alpha (TNFalpha), macroscopic damage score, plasma corticosterone levels and by a qualitative histological evolution. Trinitrobenzenesulfonic Acid 29-33 tumor necrosis factor Homo sapiens 232-240 10827154-8 2000 Treatment with trinitrobenzene sulfonic acid induced significant cholestasis and caused translocation of immunostaining for 7H6, but not that for ZO-1, to the cytoplasm and diminished immunostaining for mrp2 on the canaliculus membrane. Trinitrobenzenesulfonic Acid 15-44 ATP binding cassette subfamily B member 4 Rattus norvegicus 203-207 10839497-2 2000 Treatment of male Swiss Albino rats with ethanol (50%) and trinitrobenzenesulfonic acid (TNBS) (30 mg/kg) produced colitis as evidenced by histopathologic damage and inflammatory alterations, lipid peroxidation [increased malondialdehyde (MDA) levels], and enhanced neutrophil infiltration [increased myeloperoxidase (MPO) activity] without marked change in glutathione status. Trinitrobenzenesulfonic Acid 59-87 myeloperoxidase Rattus norvegicus 301-316 10820397-5 2000 Moreover, IL-18 and IL-12 p40 RNA levels were comparably up-regulated after TNBS treatment in IFN-gammaR1(- / -) wild-type mice. Trinitrobenzenesulfonic Acid 76-80 interleukin 18 Mus musculus 10-15 10820397-5 2000 Moreover, IL-18 and IL-12 p40 RNA levels were comparably up-regulated after TNBS treatment in IFN-gammaR1(- / -) wild-type mice. Trinitrobenzenesulfonic Acid 76-80 interleukin 12b Mus musculus 26-29 10820397-5 2000 Moreover, IL-18 and IL-12 p40 RNA levels were comparably up-regulated after TNBS treatment in IFN-gammaR1(- / -) wild-type mice. Trinitrobenzenesulfonic Acid 76-80 interferon gamma receptor 1 Mus musculus 94-112 10830784-7 2000 Interestingly, GSH levels in TNBS+ethanol-treated rats recovered by 1-2 weeks, an effect that was accounted for by an increase of gamma-glutamylcysteine synthetase (gamma-GCS) activity due to an induction of gamma-GCS-heavy subunit chain mRNA. Trinitrobenzenesulfonic Acid 29-33 glutamate-cysteine ligase, catalytic subunit Rattus norvegicus 130-163 10830784-7 2000 Interestingly, GSH levels in TNBS+ethanol-treated rats recovered by 1-2 weeks, an effect that was accounted for by an increase of gamma-glutamylcysteine synthetase (gamma-GCS) activity due to an induction of gamma-GCS-heavy subunit chain mRNA. Trinitrobenzenesulfonic Acid 29-33 glutamate-cysteine ligase, catalytic subunit Rattus norvegicus 165-174 10830784-7 2000 Interestingly, GSH levels in TNBS+ethanol-treated rats recovered by 1-2 weeks, an effect that was accounted for by an increase of gamma-glutamylcysteine synthetase (gamma-GCS) activity due to an induction of gamma-GCS-heavy subunit chain mRNA. Trinitrobenzenesulfonic Acid 29-33 glutamate-cysteine ligase, catalytic subunit Rattus norvegicus 208-217 10839497-2 2000 Treatment of male Swiss Albino rats with ethanol (50%) and trinitrobenzenesulfonic acid (TNBS) (30 mg/kg) produced colitis as evidenced by histopathologic damage and inflammatory alterations, lipid peroxidation [increased malondialdehyde (MDA) levels], and enhanced neutrophil infiltration [increased myeloperoxidase (MPO) activity] without marked change in glutathione status. Trinitrobenzenesulfonic Acid 59-87 myeloperoxidase Rattus norvegicus 318-321 10839497-2 2000 Treatment of male Swiss Albino rats with ethanol (50%) and trinitrobenzenesulfonic acid (TNBS) (30 mg/kg) produced colitis as evidenced by histopathologic damage and inflammatory alterations, lipid peroxidation [increased malondialdehyde (MDA) levels], and enhanced neutrophil infiltration [increased myeloperoxidase (MPO) activity] without marked change in glutathione status. Trinitrobenzenesulfonic Acid 89-93 myeloperoxidase Rattus norvegicus 301-316 10839497-2 2000 Treatment of male Swiss Albino rats with ethanol (50%) and trinitrobenzenesulfonic acid (TNBS) (30 mg/kg) produced colitis as evidenced by histopathologic damage and inflammatory alterations, lipid peroxidation [increased malondialdehyde (MDA) levels], and enhanced neutrophil infiltration [increased myeloperoxidase (MPO) activity] without marked change in glutathione status. Trinitrobenzenesulfonic Acid 89-93 myeloperoxidase Rattus norvegicus 318-321 10640290-8 2000 However, CCK receptor antagonists no longer enhance morphine antinociception after instillation of intracolonic TNBS, suggesting that visceral inflammation may lead to a reduction in spinal CCK release. Trinitrobenzenesulfonic Acid 112-116 cholecystokinin Rattus norvegicus 9-12 10727461-5 2000 The expression of Th2 cytokines (IL-4, IL-5) in TNCB-challenged skin tissues and the supernatants from T cells stimulated by 2,4,6-trinitrobenzene sulfonate-modified spleen cells, as well as the immunoglobulin (Ig)E and IgG1 response after challenge, were also profoundly reduced in STAT6(-/)- mice, whereas the expression of interferon gamma was the same in STAT6(-/)- and wt mice after challenge. Trinitrobenzenesulfonic Acid 125-156 heart and neural crest derivatives expressed 2 Mus musculus 18-21 10500069-0 1999 Protection of trinitrobenzene sulfonic acid-induced colitis by an interleukin 2-IgG2b fusion protein in mice. Trinitrobenzenesulfonic Acid 14-43 interleukin 2 Mus musculus 66-79 10686438-5 2000 METHODS: EPO was carbamylated by incubation with cyanate at 37 degrees C. The extent of carbamylation was monitored using trinitrobenzenesulfonic acid. Trinitrobenzenesulfonic Acid 122-150 erythropoietin Homo sapiens 9-12 10572418-5 1999 3)therapy with antisense oligonucleotide against ICAM-1 in Crohn"s disease, and against p65 subunit of NF-kappa B in TNBS induced colitis in mice. Trinitrobenzenesulfonic Acid 117-121 RELA proto-oncogene, NF-kB subunit Homo sapiens 88-113 10562585-9 1999 A four- to fivefold increase in iNOS mRNA was observed in wild type mice at 72 hours and seven days post-TNBS and was absent in iNOS deficient mice. Trinitrobenzenesulfonic Acid 105-109 nitric oxide synthase 2, inducible Mus musculus 32-36 10500069-0 1999 Protection of trinitrobenzene sulfonic acid-induced colitis by an interleukin 2-IgG2b fusion protein in mice. Trinitrobenzenesulfonic Acid 14-43 immunoglobulin heavy constant gamma 2B Mus musculus 80-85 10500069-7 1999 The protective role of IL-10 was demonstrated by the finding that neutralization of IL-10 in vivo using IL-10-specific antibodies inhibited the IL-2-IgG2b effects in TNBS-induced colitis. Trinitrobenzenesulfonic Acid 166-170 interleukin 10 Mus musculus 23-28 10500069-7 1999 The protective role of IL-10 was demonstrated by the finding that neutralization of IL-10 in vivo using IL-10-specific antibodies inhibited the IL-2-IgG2b effects in TNBS-induced colitis. Trinitrobenzenesulfonic Acid 166-170 interleukin 10 Mus musculus 84-89 10500069-7 1999 The protective role of IL-10 was demonstrated by the finding that neutralization of IL-10 in vivo using IL-10-specific antibodies inhibited the IL-2-IgG2b effects in TNBS-induced colitis. Trinitrobenzenesulfonic Acid 166-170 interleukin 10 Mus musculus 84-89 10500069-7 1999 The protective role of IL-10 was demonstrated by the finding that neutralization of IL-10 in vivo using IL-10-specific antibodies inhibited the IL-2-IgG2b effects in TNBS-induced colitis. Trinitrobenzenesulfonic Acid 166-170 interleukin 2 Mus musculus 144-148 10500069-7 1999 The protective role of IL-10 was demonstrated by the finding that neutralization of IL-10 in vivo using IL-10-specific antibodies inhibited the IL-2-IgG2b effects in TNBS-induced colitis. Trinitrobenzenesulfonic Acid 166-170 immunoglobulin heavy constant gamma 2B Mus musculus 149-154 10489933-1 1999 Immunoblotting and immunohistochemical analysis were performed to identify the cells expressing and secreting annexin 1 during experimental rat colitis induced by trinitrobenzene sulfonic acid. Trinitrobenzenesulfonic Acid 163-192 annexin A1 Rattus norvegicus 110-119 10403731-3 1999 METHODS: Trinitrobenzene sulphonic acid (TNBS) was instilled per rectum to induce a lethal colitis in iNOS deficient mice and in wild type controls. Trinitrobenzenesulfonic Acid 41-45 nitric oxide synthase 2, inducible Mus musculus 102-106 10403731-5 1999 RESULTS: TNBS administration induced a high mortality and weight loss associated with a severe colonic mucosal erosion and ulceration, increased myeloperoxidase activity, increased concentrations of malondialdehyde, and an intense staining for nitrotyrosine and ICAM-1 in wild type mice. Trinitrobenzenesulfonic Acid 9-13 myeloperoxidase Mus musculus 145-160 10403731-5 1999 RESULTS: TNBS administration induced a high mortality and weight loss associated with a severe colonic mucosal erosion and ulceration, increased myeloperoxidase activity, increased concentrations of malondialdehyde, and an intense staining for nitrotyrosine and ICAM-1 in wild type mice. Trinitrobenzenesulfonic Acid 9-13 intercellular adhesion molecule 1 Mus musculus 262-268 10403731-6 1999 Genetic ablation of iNOS gene conferred to mice a significant resistance to TNBS induced lethality and colonic damage, and notably reduced nitrotyrosine formation and concentrations of malondialdehyde; it did not, however, affect neutrophil infiltration and intestinal ICAM-1 expression in the injured tissue. Trinitrobenzenesulfonic Acid 76-80 nitric oxide synthase 2, inducible Mus musculus 20-24 10492128-5 1999 Colitis induced by intrarectal administration of trinitrobenzenesulfonic acid was monitored by measuring the myeloperoxidase activity and histology. Trinitrobenzenesulfonic Acid 49-77 myeloperoxidase Homo sapiens 109-124 10489933-3 1999 Likewise, annexin 1 secretion was induced in inflamed colons at one, three, six, and nine days after trinitrobenzene sulfonic acid treatment but was not detected in colons from controls and rats at 12 days. Trinitrobenzenesulfonic Acid 101-130 annexin A1 Rattus norvegicus 10-19 10209035-2 1999 Intracolonic administration of TNBS to either normal (IFN-gamma+/+) or Th1-deficient IFN-gamma knockout (IFN-gamma-/-) BALB/c mice resulted in significant colitis. Trinitrobenzenesulfonic Acid 31-35 interferon gamma Mus musculus 54-63 10209035-2 1999 Intracolonic administration of TNBS to either normal (IFN-gamma+/+) or Th1-deficient IFN-gamma knockout (IFN-gamma-/-) BALB/c mice resulted in significant colitis. Trinitrobenzenesulfonic Acid 31-35 negative elongation factor complex member C/D, Th1l Mus musculus 71-74 10209035-2 1999 Intracolonic administration of TNBS to either normal (IFN-gamma+/+) or Th1-deficient IFN-gamma knockout (IFN-gamma-/-) BALB/c mice resulted in significant colitis. Trinitrobenzenesulfonic Acid 31-35 interferon gamma Mus musculus 85-94 10209035-2 1999 Intracolonic administration of TNBS to either normal (IFN-gamma+/+) or Th1-deficient IFN-gamma knockout (IFN-gamma-/-) BALB/c mice resulted in significant colitis. Trinitrobenzenesulfonic Acid 31-35 interferon gamma Mus musculus 85-94 10070033-6 1999 Both PKC activity and mucosal injury increased significantly within 4 h of TNBS treatment. Trinitrobenzenesulfonic Acid 75-79 protein kinase C, gamma Rattus norvegicus 5-8 10092309-12 1999 CONCLUSIONS: Induction of colitis in rats by TNBS is followed by up-regulation of endothelial VCAM-1. Trinitrobenzenesulfonic Acid 45-49 vascular cell adhesion molecule 1 Rattus norvegicus 94-100 10198347-2 1999 Intracolonic administration of 2,4,6-trinitrobenzenesulfonic acid (TNB) induced colitis of similar severity in both strains as assessed on day 7 by macroscopic scoring, histological evaluation, tissue myeloperoxidase (MPO) activity, and decrease in food intake and body weight. Trinitrobenzenesulfonic Acid 31-65 myeloperoxidase Rattus norvegicus 201-216 10070033-8 1999 In contrast, neutrophil infiltration as assessed by myeloperoxidase activity only increased 12 h after TNBS treatment, became maximal 1 day after TNBS administration, and declined thereafter. Trinitrobenzenesulfonic Acid 103-107 myeloperoxidase Rattus norvegicus 52-67 10070033-8 1999 In contrast, neutrophil infiltration as assessed by myeloperoxidase activity only increased 12 h after TNBS treatment, became maximal 1 day after TNBS administration, and declined thereafter. Trinitrobenzenesulfonic Acid 146-150 myeloperoxidase Rattus norvegicus 52-67 10070033-9 1999 PKCbeta, -delta, and -epsilon were increased in response to TNBS, whereas PKCalpha protein content was decreased. Trinitrobenzenesulfonic Acid 60-64 protein kinase C, beta Rattus norvegicus 0-29 10070033-10 1999 The PKC antagonists staurosporine and GF-109203X (25 ng/kg iv) reduced TNBS-induced changes in mucosal PKC activity and the degree of mucosal damage. Trinitrobenzenesulfonic Acid 71-75 protein kinase C, gamma Rattus norvegicus 4-7 10070033-14 1999 The PKC-mediated response to TNBS does not appear to involve neutrophil infiltration. Trinitrobenzenesulfonic Acid 29-33 protein kinase C, gamma Rattus norvegicus 4-7 9922946-5 1998 The examinations using mice and guinea pigs showed that mouse PLN responses to TNBS, penicillin G and cephalothin correlated with the allergenicity responses obtained in the GP-PCA reaction to three compounds. Trinitrobenzenesulfonic Acid 79-83 phospholamban Mus musculus 62-65 10327390-3 1999 In this study we have evaluated three highly selective COX-2 inhibitors, NS-398, SC-58125 and PD-138387, on the trinitro-benzene sulfonic acid (TNBS) model of colitis in rats. Trinitrobenzenesulfonic Acid 112-142 cytochrome c oxidase II, mitochondrial Rattus norvegicus 55-60 9933118-2 1999 Here we assessed the therapeutic effect of a synthetic mimetic of CD4 designed to mimic both the sequence and conformation of the complementarity-determining region 3 of murine CD4 V1 domain (rD-mPGPtide) in a mouse colitis model using immunization with 2,4,6-trinitrobenzene sulfonic acid (TNB). Trinitrobenzenesulfonic Acid 254-289 CD4 antigen Mus musculus 66-69 9933118-2 1999 Here we assessed the therapeutic effect of a synthetic mimetic of CD4 designed to mimic both the sequence and conformation of the complementarity-determining region 3 of murine CD4 V1 domain (rD-mPGPtide) in a mouse colitis model using immunization with 2,4,6-trinitrobenzene sulfonic acid (TNB). Trinitrobenzenesulfonic Acid 291-294 CD4 antigen Mus musculus 66-69 9824605-4 1998 METHODS: Plasma leptin was measured at different time points in rats with trinitrobenzene sulphonic acid (TNBS) induced colitis, indomethacin induced ileitis, or endotoxic shock caused by lipopolysaccharide (LPS). Trinitrobenzenesulfonic Acid 106-110 leptin Rattus norvegicus 16-22 9864264-3 1998 We tested the efficacy and safety of anti-TNFalpha therapy in experimental colitis induced by trinitrobenzenesulfonic acid. Trinitrobenzenesulfonic Acid 94-122 tumor necrosis factor Rattus norvegicus 42-50 9808369-6 1998 In TNBS treated groups, inflammation was enhanced by capsaicin pretreatment, as determined by an increased gut permeability, MPO activity, and histological damage score. Trinitrobenzenesulfonic Acid 3-7 myeloperoxidase Rattus norvegicus 125-128 9722668-7 1998 We used the fluorescent probes 4-fluoro-7-sulfamoylbezofurazan, 2-(4"-maleimidylanilino)naphthalene-6-sulfonic acid, and trinitrobenzene-sulfonate, which bind to SH1, SH2, and RLR, respectively, to examine differences in local conformations within myosin.ADP.phosphate analogue (BeFn, Vi, AlF4-, and ScFn) complexes. Trinitrobenzenesulfonic Acid 121-146 myosin heavy chain 14 Homo sapiens 248-254 9785600-3 1998 Moreover, plaunotol, at a dose of 600 mg/kg/day, significantly depressed the myeloperoxidase activity of the lesioned area induced by TNB of the rat colon. Trinitrobenzenesulfonic Acid 134-137 myeloperoxidase Rattus norvegicus 77-92 9686562-5 1998 TNBS plus anti-CD44v7-treated mice developed early signs of inflammation, with infiltration of leukocytes in the lamina propria and increased IFN-gamma production. Trinitrobenzenesulfonic Acid 0-4 interferon gamma Mus musculus 142-151 9697106-6 1998 VIP immunoreactivity was abundantly distributed in the colonic wall and underwent an immediate reduction in the mucosa after TNBS treatment. Trinitrobenzenesulfonic Acid 125-129 vasoactive intestinal peptide Rattus norvegicus 0-3 9683549-6 1998 Interestingly, intraperitoneal administration of anti-CD4 mAbs could suppress severe inflammation in the model with decrease of anti-TNB Ab titer. Trinitrobenzenesulfonic Acid 133-136 Cd4 molecule Rattus norvegicus 54-57 9812022-9 1998 Myeloperoxidase activity was increased, whereas glutathione peroxidase activity was significantly decreased in the colon inflamed by HAc or TNBS as compared to the controls. Trinitrobenzenesulfonic Acid 140-144 myeloperoxidase Rattus norvegicus 0-15 9649183-0 1998 CD4+ T cells from 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis rodents migrate to the recipient"s colon upon transfer; down-regulation by CD8+ T cells. Trinitrobenzenesulfonic Acid 18-53 Cd4 molecule Rattus norvegicus 0-3 9649183-0 1998 CD4+ T cells from 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis rodents migrate to the recipient"s colon upon transfer; down-regulation by CD8+ T cells. Trinitrobenzenesulfonic Acid 55-59 Cd4 molecule Rattus norvegicus 0-3 9649183-9 1998 The results show that CD4+ T cells from donor rats with TNBS/ethanol-induced colitis migrate in particular to the colon upon transfer to naive recipients, and that this process is down-regulated by CD8+ T cells. Trinitrobenzenesulfonic Acid 56-60 CD4 molecule Homo sapiens 22-25 9580638-3 1998 The objective of this study was to examine the expression of the NHE-1 isoform during colitis induced by acetic acid or trinitrobenzenesulfonic acid in Sprague-Dawley male rats. Trinitrobenzenesulfonic Acid 120-148 solute carrier family 9 member A1 Rattus norvegicus 65-70 9458791-9 1998 These drugs also significantly reduced TNBS-induced MPO accumulation and release of rat mast cell protease II. Trinitrobenzenesulfonic Acid 39-43 myeloperoxidase Rattus norvegicus 52-55 9458791-9 1998 These drugs also significantly reduced TNBS-induced MPO accumulation and release of rat mast cell protease II. Trinitrobenzenesulfonic Acid 39-43 mast cell protease 2 Rattus norvegicus 88-109 9384236-2 1997 Intracolonic instillation of TNBS (30 mg in 0.25 ml of 50% ethanol) led to macroscopic injury, an increase of mucosal myeloperoxidase activity and the expression of the Ca2+-independent inducible NO synthase over 8 days. Trinitrobenzenesulfonic Acid 29-33 myeloperoxidase Rattus norvegicus 118-133 9440646-2 1997 Recently an increase in the inducible form of nitric oxide synthase (iNOS) has been found in the rat trinitrobenzene sulfonic acid model of experimental colitis, and inhibition of nitric oxide synthase activity resulted in an amelioration of tissue injury. Trinitrobenzenesulfonic Acid 101-130 nitric oxide synthase 2 Rattus norvegicus 69-73 9384236-2 1997 Intracolonic instillation of TNBS (30 mg in 0.25 ml of 50% ethanol) led to macroscopic injury, an increase of mucosal myeloperoxidase activity and the expression of the Ca2+-independent inducible NO synthase over 8 days. Trinitrobenzenesulfonic Acid 29-33 nitric oxide synthase 2 Rattus norvegicus 186-207 9384236-5 1997 In contrast, when L-NAME was administered 6 h after TNBS instillation, at time of expression of inducible NO synthase, the macroscopic lesions were reduced, as well as the enhanced inducible NO synthase activity, determined, over 72 h. Delayed (6 h after TNBS) administration of L-NAME also attenuated the colonic myeloperoxidase activity provoked by TNBS, after 24 h. This activity was not affected by pretreatment (2 days before TNBS) with L-NAME. Trinitrobenzenesulfonic Acid 52-56 nitric oxide synthase 2 Rattus norvegicus 96-117 9384236-5 1997 In contrast, when L-NAME was administered 6 h after TNBS instillation, at time of expression of inducible NO synthase, the macroscopic lesions were reduced, as well as the enhanced inducible NO synthase activity, determined, over 72 h. Delayed (6 h after TNBS) administration of L-NAME also attenuated the colonic myeloperoxidase activity provoked by TNBS, after 24 h. This activity was not affected by pretreatment (2 days before TNBS) with L-NAME. Trinitrobenzenesulfonic Acid 255-259 nitric oxide synthase 2 Rattus norvegicus 96-117 9384236-5 1997 In contrast, when L-NAME was administered 6 h after TNBS instillation, at time of expression of inducible NO synthase, the macroscopic lesions were reduced, as well as the enhanced inducible NO synthase activity, determined, over 72 h. Delayed (6 h after TNBS) administration of L-NAME also attenuated the colonic myeloperoxidase activity provoked by TNBS, after 24 h. This activity was not affected by pretreatment (2 days before TNBS) with L-NAME. Trinitrobenzenesulfonic Acid 255-259 nitric oxide synthase 2 Rattus norvegicus 96-117 9384236-5 1997 In contrast, when L-NAME was administered 6 h after TNBS instillation, at time of expression of inducible NO synthase, the macroscopic lesions were reduced, as well as the enhanced inducible NO synthase activity, determined, over 72 h. Delayed (6 h after TNBS) administration of L-NAME also attenuated the colonic myeloperoxidase activity provoked by TNBS, after 24 h. This activity was not affected by pretreatment (2 days before TNBS) with L-NAME. Trinitrobenzenesulfonic Acid 255-259 nitric oxide synthase 2 Rattus norvegicus 96-117 8852756-1 1996 Lysine and arginine residues of pig kidney diamine oxidase (DAO) were modified with 2,4,6-trinitrobenzenesulphonic acid (TNBS), 2,3-butanedione and phenylglyoxal, respectively, using different concentrations and time periods. Trinitrobenzenesulfonic Acid 84-119 amine oxidase copper containing 1 Sus scrofa 43-58 9326394-2 1997 To address this issue, a novel CD45+/major histocompatibility complex class I+ (H-2k)/II-/CD80+ dendritic cell line, termed 80/1, which is capable of stimulating naive, allogeneic CD8+ but not CD4+ T cells in vitro, was derivatized with trinitrobenzenesulfonic acid and co-cultured for 4 d with syngeneic, naive CD8+ T cells. Trinitrobenzenesulfonic Acid 237-265 CD4 antigen Mus musculus 31-34 8942729-7 1996 RESULTS: Six weeks after administration of TNBS, stress caused a significant increase in myeloperoxidase activity in TNBS-treated rats but not in stressed controls; plasma corticosterone responses were similar. Trinitrobenzenesulfonic Acid 43-47 myeloperoxidase Rattus norvegicus 89-104 8942729-7 1996 RESULTS: Six weeks after administration of TNBS, stress caused a significant increase in myeloperoxidase activity in TNBS-treated rats but not in stressed controls; plasma corticosterone responses were similar. Trinitrobenzenesulfonic Acid 117-121 myeloperoxidase Rattus norvegicus 89-104 8769290-0 1996 Protection by recombinant human interleukin-11 against experimental TNB-induced colitis in rats. Trinitrobenzenesulfonic Acid 68-71 interleukin 11 Homo sapiens 32-46 8769290-1 1996 The potential effect of recombinant human interleukin-11 (rhIL-11) on trinitrobenzene sulfonic acid (TNB)-induced colitis was investigated in rats. Trinitrobenzenesulfonic Acid 70-99 interleukin 11 Homo sapiens 42-56 8769290-4 1996 TNB administration also significantly enhanced the colonic mucosal myeloperoxidase (MPO) levels, which paralleled the severity of colitis. Trinitrobenzenesulfonic Acid 0-3 myeloperoxidase Homo sapiens 67-82 8769290-4 1996 TNB administration also significantly enhanced the colonic mucosal myeloperoxidase (MPO) levels, which paralleled the severity of colitis. Trinitrobenzenesulfonic Acid 0-3 myeloperoxidase Homo sapiens 84-87 8707089-7 1996 RESULTS: In the untreated and the saline enema treated TNBS groups, diarrhoea and extensive colonic damage were seen, associated with increased tissue MPO activities and absent butyrate stimulated Na+ absorption. Trinitrobenzenesulfonic Acid 55-59 myeloperoxidase Rattus norvegicus 151-154 8804580-1 1996 Rat kidney gamma-glutamylcysteine synthetase (gamma GCS) was inactivated by reaction with trinitrobenzene sulfonate (TNBS), and the reaction followed pseudo-first-order kinetics. Trinitrobenzenesulfonic Acid 90-115 glutamate-cysteine ligase, catalytic subunit Rattus norvegicus 11-44 8804580-1 1996 Rat kidney gamma-glutamylcysteine synthetase (gamma GCS) was inactivated by reaction with trinitrobenzene sulfonate (TNBS), and the reaction followed pseudo-first-order kinetics. Trinitrobenzenesulfonic Acid 90-115 glutamate-cysteine ligase, catalytic subunit Rattus norvegicus 46-55 9391247-11 1997 CONCLUSION: Prophylactic glutamine supplementation modulates the inflammatory activities of IL-8 and TNF-alpha in TNBS induced colitis. Trinitrobenzenesulfonic Acid 114-118 tumor necrosis factor Rattus norvegicus 101-110 9277547-7 1997 The colons of all TNBS-injected animals (controls, adrenalectomized, dexamethasone treated, hypophysectomized) overexpressed and secreted lipocortin 1. Trinitrobenzenesulfonic Acid 18-22 annexin A1 Rattus norvegicus 138-150 9288117-5 1997 On day 0 all mice were immunized with 100 micrograms trinitrobenzene sulfonic acid (TNP) haptenated ovalbumin (TNP-OVA) in complete Freund"s adjuvant. Trinitrobenzenesulfonic Acid 53-82 serine (or cysteine) peptidase inhibitor, clade B, member 1, pseudogene Mus musculus 100-109 9247586-2 1997 Here, we analyze the functional role of TNF-alpha in a mouse model of chronic intestinal inflammation induced by the hapten reagent 2,4,6,-trinitrobenzene sulfonic acid (TNBS) that mimics some characteristics of Crohn"s disease in humans. Trinitrobenzenesulfonic Acid 132-168 tumor necrosis factor Mus musculus 40-49 9247586-2 1997 Here, we analyze the functional role of TNF-alpha in a mouse model of chronic intestinal inflammation induced by the hapten reagent 2,4,6,-trinitrobenzene sulfonic acid (TNBS) that mimics some characteristics of Crohn"s disease in humans. Trinitrobenzenesulfonic Acid 170-174 tumor necrosis factor Mus musculus 40-49 9247586-6 1997 The predominant role of TNF-alpha in the mouse TNBS-induced colitis model was further underlined by the finding that striking colonic inflammation and lethal pancolitis was induced in TNF-alpha-transgenic mice upon TNBS treatment. Trinitrobenzenesulfonic Acid 47-51 tumor necrosis factor Mus musculus 24-33 9247586-6 1997 The predominant role of TNF-alpha in the mouse TNBS-induced colitis model was further underlined by the finding that striking colonic inflammation and lethal pancolitis was induced in TNF-alpha-transgenic mice upon TNBS treatment. Trinitrobenzenesulfonic Acid 47-51 tumor necrosis factor Mus musculus 184-193 9247586-6 1997 The predominant role of TNF-alpha in the mouse TNBS-induced colitis model was further underlined by the finding that striking colonic inflammation and lethal pancolitis was induced in TNF-alpha-transgenic mice upon TNBS treatment. Trinitrobenzenesulfonic Acid 215-219 tumor necrosis factor Mus musculus 24-33 9247586-6 1997 The predominant role of TNF-alpha in the mouse TNBS-induced colitis model was further underlined by the finding that striking colonic inflammation and lethal pancolitis was induced in TNF-alpha-transgenic mice upon TNBS treatment. Trinitrobenzenesulfonic Acid 215-219 tumor necrosis factor Mus musculus 184-193 8757344-7 1996 Oral administration of TNBS before induction of colitis markedly decreased mucosal anti-TNP responses and completely inhibited anti-TNP IgG2a and IgG2b responses. Trinitrobenzenesulfonic Acid 23-27 immunoglobulin heavy variable V1-9 Mus musculus 136-141 8757344-7 1996 Oral administration of TNBS before induction of colitis markedly decreased mucosal anti-TNP responses and completely inhibited anti-TNP IgG2a and IgG2b responses. Trinitrobenzenesulfonic Acid 23-27 immunoglobulin heavy constant gamma 2B Mus musculus 146-151 8676081-6 1996 Finally, and most importantly, the suppressive effect of orally administered HCP was abrogated by the concomitant systemic administration of anti-TGF-beta or rIL-12 suggesting a reciprocal relationship between IL-12 and TGF-beta on tolerance induction in TNBS-induced colitis. Trinitrobenzenesulfonic Acid 255-259 transforming growth factor, beta 1 Mus musculus 146-154 8612996-3 1996 METHODS: KGF was administered before or after induction of colitis with 2,4,6-trinitrobenzenesulfonic acid/ethanol. Trinitrobenzenesulfonic Acid 72-106 fibroblast growth factor 7 Rattus norvegicus 9-12 8627184-2 1996 We therefore investigated the in vivo relevance of this interaction in an experimental model for a Th1-mediated disease, the hapten reagent (2,4,6-trinitrobenzene sulfonic acid [TNBS])-induced colitis. Trinitrobenzenesulfonic Acid 178-182 negative elongation factor complex member C/D Homo sapiens 99-102 8627184-6 1996 In addition, the injection of recombinant IL-12 p70 heterodimer into TNBS + anti-gp39-treated mice reversed the effect of anti-gp39 and resulted in severe disease activity. Trinitrobenzenesulfonic Acid 69-73 CD40 ligand Mus musculus 127-131 8852756-1 1996 Lysine and arginine residues of pig kidney diamine oxidase (DAO) were modified with 2,4,6-trinitrobenzenesulphonic acid (TNBS), 2,3-butanedione and phenylglyoxal, respectively, using different concentrations and time periods. Trinitrobenzenesulfonic Acid 84-119 amine oxidase copper containing 1 Sus scrofa 60-63 8852756-1 1996 Lysine and arginine residues of pig kidney diamine oxidase (DAO) were modified with 2,4,6-trinitrobenzenesulphonic acid (TNBS), 2,3-butanedione and phenylglyoxal, respectively, using different concentrations and time periods. Trinitrobenzenesulfonic Acid 121-125 amine oxidase copper containing 1 Sus scrofa 43-58 8852756-1 1996 Lysine and arginine residues of pig kidney diamine oxidase (DAO) were modified with 2,4,6-trinitrobenzenesulphonic acid (TNBS), 2,3-butanedione and phenylglyoxal, respectively, using different concentrations and time periods. Trinitrobenzenesulfonic Acid 121-125 amine oxidase copper containing 1 Sus scrofa 60-63 8535797-7 1995 There were increases in IL-6 and alpha 2M concentrations in TNBS-E-treated animals but no significant change in TNF concentrations. Trinitrobenzenesulfonic Acid 60-64 interleukin 6 Homo sapiens 24-28 8535797-7 1995 There were increases in IL-6 and alpha 2M concentrations in TNBS-E-treated animals but no significant change in TNF concentrations. Trinitrobenzenesulfonic Acid 60-64 alpha-2-macroglobulin Homo sapiens 33-41 8563896-8 1995 After treatment with anti-CD4 Abs, the anti-TNB Ab titer, the number of CD45RC(high)CD4+ cells, and interferon-gamma mRNA expression were significantly decreased in the mucosa of the model. Trinitrobenzenesulfonic Acid 44-47 CD4 molecule Homo sapiens 26-29 16843944-7 1995 There was a significant increase in CMS, colon weight, splenic weight, IL6 and alpha(2)M in TNBS/E animals compared to controls (P< 0.01). Trinitrobenzenesulfonic Acid 92-96 alpha-2-macroglobulin Rattus norvegicus 79-88 7595199-3 1995 The colon of TNBS-treated mice on day 7 was marked by infiltration of CD4+ T cells; furthermore, in situ polymerase chain reaction studies revealed high levels of interferon (IFN)-gamma mRNA in diseased colons. Trinitrobenzenesulfonic Acid 13-17 interferon gamma Mus musculus 163-185 7595199-4 1995 Isolated lamina propria (LP) CD4+ T cells from TNBS-treated mice stimulated with anti-CD3 and anti-CD28 antibodies exhibited a Th1 pattern of cytokine secretion: a 20-50-fold increase in IL-2 and IFN-gamma levels and a 5-fold decrease in IL-4 levels as compared with those of stimulated LP CD4+ T cells from control BALB/c mice. Trinitrobenzenesulfonic Acid 47-51 CD28 antigen Mus musculus 99-103 7595199-4 1995 Isolated lamina propria (LP) CD4+ T cells from TNBS-treated mice stimulated with anti-CD3 and anti-CD28 antibodies exhibited a Th1 pattern of cytokine secretion: a 20-50-fold increase in IL-2 and IFN-gamma levels and a 5-fold decrease in IL-4 levels as compared with those of stimulated LP CD4+ T cells from control BALB/c mice. Trinitrobenzenesulfonic Acid 47-51 interleukin 2 Mus musculus 187-191 7595199-4 1995 Isolated lamina propria (LP) CD4+ T cells from TNBS-treated mice stimulated with anti-CD3 and anti-CD28 antibodies exhibited a Th1 pattern of cytokine secretion: a 20-50-fold increase in IL-2 and IFN-gamma levels and a 5-fold decrease in IL-4 levels as compared with those of stimulated LP CD4+ T cells from control BALB/c mice. Trinitrobenzenesulfonic Acid 47-51 interferon gamma Mus musculus 196-205 7595199-4 1995 Isolated lamina propria (LP) CD4+ T cells from TNBS-treated mice stimulated with anti-CD3 and anti-CD28 antibodies exhibited a Th1 pattern of cytokine secretion: a 20-50-fold increase in IL-2 and IFN-gamma levels and a 5-fold decrease in IL-4 levels as compared with those of stimulated LP CD4+ T cells from control BALB/c mice. Trinitrobenzenesulfonic Acid 47-51 interleukin 4 Mus musculus 238-242 7595199-7 1995 In summary, the data demonstrate the pivotal role of IL-12 and IFN-gamma in a TNBS-induced murine model of chronic intestinal inflammation. Trinitrobenzenesulfonic Acid 78-82 interferon gamma Mus musculus 63-72 7556213-6 1995 Annexin 1 expression in colons increased after trinitrobenzenesulfonic acid treatment and was maximal between days 1 to 9, during the cellular stage of the inflammation that corresponded to maximal myeloperoxidase activity. Trinitrobenzenesulfonic Acid 47-75 annexin A1 Rattus norvegicus 0-9 7556213-6 1995 Annexin 1 expression in colons increased after trinitrobenzenesulfonic acid treatment and was maximal between days 1 to 9, during the cellular stage of the inflammation that corresponded to maximal myeloperoxidase activity. Trinitrobenzenesulfonic Acid 47-75 myeloperoxidase Rattus norvegicus 198-213 7556213-7 1995 From 12 h to 9 days after trinitrobenzenesulfonic acid/ethanol treatment, annexin 1 was specifically secreted. Trinitrobenzenesulfonic Acid 26-54 annexin A1 Rattus norvegicus 74-83 7627705-12 1995 TFPI activity was almost totally abolished (< 1.4%) when the TNBS reactivities of acetylated LDL, malondialdehyde-modified LDL, and 4-hydroxynonenal-modified LDL were 31%, 21%, and 43% that of native LDL, respectively. Trinitrobenzenesulfonic Acid 64-68 tissue factor pathway inhibitor Homo sapiens 0-4 7641075-1 1995 The inactivation of bovine liver high-Km aldehyde reductase (ALR) by heat (47 degrees C), 0.3 mM 2,4,6-trinitrobenzene sulfonate (TNBS) and 0.03 mM pyridoxal 5"-phosphate (PAL-P) followed pseudo-first-order kinetic as a function of incubation-time and concentration of TNBS. Trinitrobenzenesulfonic Acid 97-128 aldo-keto reductase family 1 member B1 Bos taurus 41-59 7557576-10 1995 Seven days after TNB treatment lesion area was reduced by 55%, colonic weight by 37%, and myeloperoxidase and NOS activity by 59% and 42%, respectively. Trinitrobenzenesulfonic Acid 17-20 myeloperoxidase Rattus norvegicus 90-105 7641075-1 1995 The inactivation of bovine liver high-Km aldehyde reductase (ALR) by heat (47 degrees C), 0.3 mM 2,4,6-trinitrobenzene sulfonate (TNBS) and 0.03 mM pyridoxal 5"-phosphate (PAL-P) followed pseudo-first-order kinetic as a function of incubation-time and concentration of TNBS. Trinitrobenzenesulfonic Acid 97-128 aldo-keto reductase family 1 member B1 Bos taurus 61-64 7641075-1 1995 The inactivation of bovine liver high-Km aldehyde reductase (ALR) by heat (47 degrees C), 0.3 mM 2,4,6-trinitrobenzene sulfonate (TNBS) and 0.03 mM pyridoxal 5"-phosphate (PAL-P) followed pseudo-first-order kinetic as a function of incubation-time and concentration of TNBS. Trinitrobenzenesulfonic Acid 130-134 aldo-keto reductase family 1 member B1 Bos taurus 61-64 7641075-1 1995 The inactivation of bovine liver high-Km aldehyde reductase (ALR) by heat (47 degrees C), 0.3 mM 2,4,6-trinitrobenzene sulfonate (TNBS) and 0.03 mM pyridoxal 5"-phosphate (PAL-P) followed pseudo-first-order kinetic as a function of incubation-time and concentration of TNBS. Trinitrobenzenesulfonic Acid 269-273 aldo-keto reductase family 1 member B1 Bos taurus 61-64 8031794-4 1994 A single equivalent of DTNB suffices to inactivate IA-cPLA2, giving a TNB-labeled enzyme, with the loss of activity correlating with release of an equivalent of 5-thio-2-nitrobenzoate. Trinitrobenzenesulfonic Acid 24-27 phospholipase A2 group IVA Homo sapiens 54-59 7600140-10 1995 CONCLUSIONS: Direct intramuscular transforming growth factor-beta 1 gene delivery effectively ameliorates trinitrobenzene sulfonic acid-induced colitis, suggesting that gene therapy with immunosuppressive cytokines may be a novel approach for the treatment of inflammatory bowel disease. Trinitrobenzenesulfonic Acid 106-135 transforming growth factor, beta 1 Rattus norvegicus 34-67 7733288-6 1995 The indexes of inflammation, tissue myeloperoxidase, and synthetic capacities for prostaglandin E2 and leukotriene B4 were all significantly elevated from 1 day to 2 wk post-TNBS. Trinitrobenzenesulfonic Acid 174-178 myeloperoxidase Rattus norvegicus 36-51 7733288-6 1995 The indexes of inflammation, tissue myeloperoxidase, and synthetic capacities for prostaglandin E2 and leukotriene B4 were all significantly elevated from 1 day to 2 wk post-TNBS. Trinitrobenzenesulfonic Acid 174-178 dihydrolipoamide S-succinyltransferase Rattus norvegicus 96-117 7945563-8 1994 The stimulatory effect of insulin was confirmed by measurements of other indices of LDL oxidation, i.e. absorbance at 234 nm, trinitrobenzene sulfonic acid reactivity and electrophoretic mobility. Trinitrobenzenesulfonic Acid 126-155 insulin Homo sapiens 26-33 8020654-10 1994 CONCLUSIONS: Systemic EGF administration reduces mucosal damage and inflammation in a trinitrobenzenesulfonic acid/ethanol model of colitis in rats through a mechanism involving mucosal protection. Trinitrobenzenesulfonic Acid 86-114 epidermal growth factor like 1 Rattus norvegicus 22-25 8190118-0 1994 2,4,6-Trinitrobenzenesulfonic acid modification of the carboxyl-terminal region (C-domain) of calreticulin. Trinitrobenzenesulfonic Acid 0-34 calreticulin Homo sapiens 94-106 8131687-5 1994 Inflammation was scored subjectively and by tissue weight and myeloperoxidase content; each index was increased dose-dependently by trinitrobenzene sulfonic acid doses of 0.3-10 mg. Six milligrams of trinitrobenzene sulfonic acid induced reproducible inflammation for up to four weeks. Trinitrobenzenesulfonic Acid 200-229 myeloperoxidase Mus musculus 62-77 8190118-3 1994 Inclusion of Ca2+ and/or Mg2+ decreased both the amount of TNBS bound to calreticulin and the apparent affinity constant of the slower reaction. Trinitrobenzenesulfonic Acid 59-63 calreticulin Homo sapiens 73-85 8190118-5 1994 Analysis of TNBS binding to the carboxyl-terminal (C-domain) and aminoterminal (N-domain) of calreticulin revealed that the C-domain and N-domain are responsible for the slow and fast component of the TNBS binding, respectively. Trinitrobenzenesulfonic Acid 12-16 calreticulin Homo sapiens 93-105 8190118-5 1994 Analysis of TNBS binding to the carboxyl-terminal (C-domain) and aminoterminal (N-domain) of calreticulin revealed that the C-domain and N-domain are responsible for the slow and fast component of the TNBS binding, respectively. Trinitrobenzenesulfonic Acid 201-205 calreticulin Homo sapiens 93-105 8190118-1 1994 The role of the primary amino groups of lysine sidechains in Ca2+ binding to calreticulin was evaluated by chemical modification of the amino group with 2,4,6-trinitrobenzenesulfonic acid (TNBS). Trinitrobenzenesulfonic Acid 153-187 calreticulin Homo sapiens 77-89 8190118-7 1994 TNBS modification of calreticulin significantly decreased Ca2+ binding to the low affinity/high capacity Ca2+ binding site(s) which are localized to the C-domain but had no effect on the high affinity/low capacity Ca2+ binding localized to the N domain. Trinitrobenzenesulfonic Acid 0-4 calreticulin Homo sapiens 21-33 8190118-1 1994 The role of the primary amino groups of lysine sidechains in Ca2+ binding to calreticulin was evaluated by chemical modification of the amino group with 2,4,6-trinitrobenzenesulfonic acid (TNBS). Trinitrobenzenesulfonic Acid 189-193 calreticulin Homo sapiens 77-89 8190118-2 1994 TNBS binding to calreticulin could be described by two steps: (i) a fast reaction, with low affinity, and (ii) a slow reaction with a relatively high affinity. Trinitrobenzenesulfonic Acid 0-4 calreticulin Homo sapiens 16-28 8228339-4 1993 Using this approach, it has been determined that UVB radiation, intradermally injected tumor necrosis factor-alpha, and epicutaneously applied cis-urocanic acid can impair contact hypersensitivity induction by transepidermally delivered trinitrobenzene sulfonic acid, and that animals that fail to become sensitized proceed to acquire hapten-specific unresponsiveness. Trinitrobenzenesulfonic Acid 237-266 tumor necrosis factor Mus musculus 87-114 8373816-1 1993 Lysine residues of porcine pancreatic alpha-amylase (PPA) were modified with trinitrobenzenesulfonate (TNBS). Trinitrobenzenesulfonic Acid 77-101 amylase alpha 2A Homo sapiens 27-51 8391716-4 1993 Four days after TNB instillation the growth hormone-treated rats had lower macroscopic and microscopic damage scores and less infiltration of neutrophils, measured as myeloperoxidase activity (MPO), than controls. Trinitrobenzenesulfonic Acid 16-19 gonadotropin releasing hormone receptor Rattus norvegicus 37-51 7690187-6 1993 TNBS administration caused an increase in ileal MPO activity that peaked at day 7 and increased mucosal leak of protein. Trinitrobenzenesulfonic Acid 0-4 myeloperoxidase Cavia porcellus 48-51 7690187-7 1993 Misoprostol attenuated the granulocyte infiltration (MPO) response to TNBS but exacerbated the mucosal leak of protein. Trinitrobenzenesulfonic Acid 70-74 myeloperoxidase Cavia porcellus 53-56 7678028-11 1993 Similar to IL-2-LAK, the IL-4-LAK subsets appeared to display a bias as to their susceptible target cells with the NK1.1-CD8 alpha+beta+ subset being most potent against trinitrophenyl-modified autologous lymphoblasts (2,4,6-trinitrobenzene sulfonic acid (TNBS)-self). Trinitrobenzenesulfonic Acid 219-254 killer cell lectin-like receptor subfamily B member 1C Mus musculus 115-120 8385121-1 1993 A molecule of myosin subfragment 1 (S1) from skeletal muscle has one reactive lysine residue (RLR) that is rapidly and stoichiometrically modified by trinitrobenzene sulfonate (TNBS). Trinitrobenzenesulfonic Acid 150-175 myosin heavy chain 14 Homo sapiens 14-20 8450204-16 1993 administration of TNBSA may, in part, be due to a PG-dependent suppressor factor that inhibits the responsiveness of target cells to IL-2. Trinitrobenzenesulfonic Acid 18-23 interleukin 2 Mus musculus 133-137 7763539-6 1993 Furthermore SP-MAF1 had a capacity to suppress the TNBS-induced DTH reaction. Trinitrobenzenesulfonic Acid 51-55 MFP1 attachment factor 1 Glycine max 15-19 7678028-11 1993 Similar to IL-2-LAK, the IL-4-LAK subsets appeared to display a bias as to their susceptible target cells with the NK1.1-CD8 alpha+beta+ subset being most potent against trinitrophenyl-modified autologous lymphoblasts (2,4,6-trinitrobenzene sulfonic acid (TNBS)-self). Trinitrobenzenesulfonic Acid 256-260 killer cell lectin-like receptor subfamily B member 1C Mus musculus 115-120 1368335-0 1992 Colorimetric measurement of angiotensin I-converting enzyme inhibitory activity with trinitrobenzene sulfonate. Trinitrobenzenesulfonic Acid 85-110 angiotensin I converting enzyme Homo sapiens 28-59 7678645-7 1993 TNBS administration resulted in an increase in tissue thickness, myeloperoxidase and lavage protein and nitrite levels over sham controls. Trinitrobenzenesulfonic Acid 0-4 myeloperoxidase Cavia porcellus 65-80 2171436-1 1990 2-Methyl-2-nitrosopropane (tNB)-radical adducts from incubation mixtures of fatty acids and soybean lipoxygenase in borate buffer (pH 9.0) were measured by electron paramagnetic resonance (EPR). Trinitrobenzenesulfonic Acid 27-30 linoleate 9S-lipoxygenase-4 Glycine max 100-112 1648528-10 1991 Using purified preparations of two flavoproteins found in the rat colon, it was shown that the addition of TNBS (1 mmol/L) to purified NADH dehydrogenase or glutathione reductase increased the rate of superoxide formation by these enzymes from normally undetectable levels to 1.6 nmol/min and 1.2 nmol/min, respectively. Trinitrobenzenesulfonic Acid 107-111 glutathione-disulfide reductase Rattus norvegicus 157-178 2019613-3 1991 It was evident in the experiment using 2,4,6-trinitrobenzene sulfonate that PVS elicited the activity of antithrombin III by interacting with amino groups of the protein as does heparin. Trinitrobenzenesulfonic Acid 39-70 serpin family C member 1 Homo sapiens 105-121 2171436-4 1990 EPR spectra of tNB-radical adducts formed in mixtures of either linoleic acid, arachidonic acid, or 15-hydroperoxyeicosatetraenoic acid with lipoxygenase exhibited hyperfine structure characteristic of tNB/.CH2CH2-R with hyperfine coupling constants: aN = 17.1 G; aH beta = 11.2 G (2H); and aH gamma = 0.6 G (2H). Trinitrobenzenesulfonic Acid 15-18 linoleate 9S-lipoxygenase-4 Glycine max 141-153 2171436-4 1990 EPR spectra of tNB-radical adducts formed in mixtures of either linoleic acid, arachidonic acid, or 15-hydroperoxyeicosatetraenoic acid with lipoxygenase exhibited hyperfine structure characteristic of tNB/.CH2CH2-R with hyperfine coupling constants: aN = 17.1 G; aH beta = 11.2 G (2H); and aH gamma = 0.6 G (2H). Trinitrobenzenesulfonic Acid 202-205 linoleate 9S-lipoxygenase-4 Glycine max 141-153 33942299-4 2021 The aberrant upregulation of iASPP in IBD was subsequently confirmed, based on online datasets, clinical sample examinations, and 2,4,6-trinitrobenzene sulfonic acid (TNBS)- and dextran sulfate sodium (DSS)-induced colitis mice models. Trinitrobenzenesulfonic Acid 130-165 protein phosphatase 1, regulatory subunit 13 like Mus musculus 29-34 2104892-12 1990 YAC-1 was lysed exclusively by the NK1.1+ B220+ Ly-24+ subset, 2,4,6-trinitrobenzene sulfonic acid-self was lysed exclusively by the CD8+ B220+ Ly-24+ subset whereas CL27A was lysed by both subsets. Trinitrobenzenesulfonic Acid 63-98 CD8a molecule Homo sapiens 133-136 2104892-12 1990 YAC-1 was lysed exclusively by the NK1.1+ B220+ Ly-24+ subset, 2,4,6-trinitrobenzene sulfonic acid-self was lysed exclusively by the CD8+ B220+ Ly-24+ subset whereas CL27A was lysed by both subsets. Trinitrobenzenesulfonic Acid 63-98 protein tyrosine phosphatase, receptor type, C Mus musculus 138-142 33942299-6 2021 In both types of colitis mice models, iASPP overexpression improved, whereas iASPP knockdown aggravated TNBS or DSS stimulation-caused colon shortness, bodyweight loss, and mice colon oxidative stress and inflammation. Trinitrobenzenesulfonic Acid 104-108 protein phosphatase 1, regulatory subunit 13 like Mus musculus 77-82 2386793-7 1990 Several parameters of the apo B-100 structure were investigated: molecular size (by SDS-PAGE) and TNBS-reactive amino groups (chemical determination by trinitrobenzene sulfonic acid). Trinitrobenzenesulfonic Acid 98-102 apolipoprotein B Homo sapiens 26-35 2386793-7 1990 Several parameters of the apo B-100 structure were investigated: molecular size (by SDS-PAGE) and TNBS-reactive amino groups (chemical determination by trinitrobenzene sulfonic acid). Trinitrobenzenesulfonic Acid 152-181 apolipoprotein B Homo sapiens 26-35 2302740-2 1990 To further pursue this question, responsiveness toward TNP and an anti-TNP monoclonal antibody (Sp6) carrying a recurrent idiotype was evaluated in prenatally trinitrobenzenesulfonic acid (TNBS)-treated mice. Trinitrobenzenesulfonic Acid 189-193 trans-acting transcription factor 6 Mus musculus 96-99 33942299-4 2021 The aberrant upregulation of iASPP in IBD was subsequently confirmed, based on online datasets, clinical sample examinations, and 2,4,6-trinitrobenzene sulfonic acid (TNBS)- and dextran sulfate sodium (DSS)-induced colitis mice models. Trinitrobenzenesulfonic Acid 167-171 protein phosphatase 1, regulatory subunit 13 like Mus musculus 29-34 33803551-8 2021 Notably, the protective effect of TauCl on oxidative stress and inflammation in the colon of TNBS-treated mice was associated with elevated activation of Nrf2 and upregulation of its target genes encoding heme oxygenase-1, NAD(P)H:quinone oxidoreductase, glutamate cysteine ligase catalytic subunit, and glutathione S-transferase. Trinitrobenzenesulfonic Acid 93-97 nuclear factor, erythroid derived 2, like 2 Mus musculus 154-158 33769664-5 2021 The overexpression of miR-155 significantly aggravated TNBS-induced CD-associated intestinal fibrosis. Trinitrobenzenesulfonic Acid 55-59 microRNA 155 Homo sapiens 22-29 33803551-8 2021 Notably, the protective effect of TauCl on oxidative stress and inflammation in the colon of TNBS-treated mice was associated with elevated activation of Nrf2 and upregulation of its target genes encoding heme oxygenase-1, NAD(P)H:quinone oxidoreductase, glutamate cysteine ligase catalytic subunit, and glutathione S-transferase. Trinitrobenzenesulfonic Acid 93-97 heme oxygenase 1 Mus musculus 205-221 33803551-8 2021 Notably, the protective effect of TauCl on oxidative stress and inflammation in the colon of TNBS-treated mice was associated with elevated activation of Nrf2 and upregulation of its target genes encoding heme oxygenase-1, NAD(P)H:quinone oxidoreductase, glutamate cysteine ligase catalytic subunit, and glutathione S-transferase. Trinitrobenzenesulfonic Acid 93-97 crystallin, zeta Mus musculus 231-253 33803551-8 2021 Notably, the protective effect of TauCl on oxidative stress and inflammation in the colon of TNBS-treated mice was associated with elevated activation of Nrf2 and upregulation of its target genes encoding heme oxygenase-1, NAD(P)H:quinone oxidoreductase, glutamate cysteine ligase catalytic subunit, and glutathione S-transferase. Trinitrobenzenesulfonic Acid 93-97 glutamate-cysteine ligase, catalytic subunit Mus musculus 255-298 33803551-8 2021 Notably, the protective effect of TauCl on oxidative stress and inflammation in the colon of TNBS-treated mice was associated with elevated activation of Nrf2 and upregulation of its target genes encoding heme oxygenase-1, NAD(P)H:quinone oxidoreductase, glutamate cysteine ligase catalytic subunit, and glutathione S-transferase. Trinitrobenzenesulfonic Acid 93-97 hematopoietic prostaglandin D synthase Mus musculus 304-329 33776781-7 2021 Similarly, in the DSS- and TNBS-induced mouse colitis models, ghrelin could also protect intestinal tissues from apoptosis in DSS- and TNBS-induced colitis depending on GHS-R1a. Trinitrobenzenesulfonic Acid 27-31 ghrelin Mus musculus 62-69 34744725-5 2021 Proteomics analysis based upon TNBS-induced UC model rats revealed that Amine oxidase copper-containing 1 (AOC1) was a potential target of LD4-PDT. Trinitrobenzenesulfonic Acid 31-35 amine oxidase, copper containing 1 Rattus norvegicus 72-105 34507168-4 2022 UV-vis diffuse reflectance spectroscopy analysis revealed a red shift in the absorption spectra of the SnS2@N-TNB and SnS2@N-TNB/g-C3N4 samples. Trinitrobenzenesulfonic Acid 125-128 sodium voltage-gated channel alpha subunit 11 Homo sapiens 118-122 34904630-10 2021 Moreover, CK2 blockade alleviated TNBS-induced colitis in mice. Trinitrobenzenesulfonic Acid 34-38 casein kinase 2, alpha prime polypeptide Mus musculus 10-13 34904630-13 2021 Sirtuin 1 upregulation ameliorated TNBS-induced colitis, whereas SIRT1 blockade aggravated TNBS-induced colitis in mice. Trinitrobenzenesulfonic Acid 35-39 sirtuin 1 Mus musculus 0-9 34904630-13 2021 Sirtuin 1 upregulation ameliorated TNBS-induced colitis, whereas SIRT1 blockade aggravated TNBS-induced colitis in mice. Trinitrobenzenesulfonic Acid 91-95 sirtuin 1 Mus musculus 65-70 34880646-10 2021 The outcome of this TNBS induced experimental colitis model verified that the expression of PTGS2 and mir-429 was consistent with results of previous bioinformatics analysis. Trinitrobenzenesulfonic Acid 20-24 prostaglandin-endoperoxide synthase 2 Homo sapiens 92-97 34880646-10 2021 The outcome of this TNBS induced experimental colitis model verified that the expression of PTGS2 and mir-429 was consistent with results of previous bioinformatics analysis. Trinitrobenzenesulfonic Acid 20-24 microRNA 429 Homo sapiens 102-109 34925530-8 2021 In conclusion, SSP effectively treated chronic colitis induced by TNBS, which may have been achieved by inhibiting PI3K/Akt signal to suppress activation of the Rho/ROCK signaling pathway to finally maintain the integrity of the intestinal mucosal barrier. Trinitrobenzenesulfonic Acid 66-70 AKT serine/threonine kinase 1 Rattus norvegicus 120-123 34925530-8 2021 In conclusion, SSP effectively treated chronic colitis induced by TNBS, which may have been achieved by inhibiting PI3K/Akt signal to suppress activation of the Rho/ROCK signaling pathway to finally maintain the integrity of the intestinal mucosal barrier. Trinitrobenzenesulfonic Acid 66-70 Rho-associated coiled-coil containing protein kinase 1 Rattus norvegicus 165-169 34862575-3 2021 Acetylcholinesterase (AChE) could catalyze the hydrolysis of acetylthiocholine (ATCh) to produce thiocholine which was further reacted with Ehrman"s reagent and decomposed to form a yellow product 2-nitro-5-thiobenate anion (TNB). Trinitrobenzenesulfonic Acid 225-228 acetylcholinesterase (Cartwright blood group) Homo sapiens 0-20 34862575-3 2021 Acetylcholinesterase (AChE) could catalyze the hydrolysis of acetylthiocholine (ATCh) to produce thiocholine which was further reacted with Ehrman"s reagent and decomposed to form a yellow product 2-nitro-5-thiobenate anion (TNB). Trinitrobenzenesulfonic Acid 225-228 acetylcholinesterase (Cartwright blood group) Homo sapiens 22-26 34862575-4 2021 Due to the obvious overlap between the excitation spectrum of Ti3C2 MQDs and the absorption spectrum of TNB, AChE catalyzed the hydrolysis of substrate DTNB/ATCh to form TNB, which can effectively quench the fluorescence of Ti3C2 MQDs through the inner filter effect (IFE). Trinitrobenzenesulfonic Acid 104-107 acetylcholinesterase (Cartwright blood group) Homo sapiens 109-113 34862575-4 2021 Due to the obvious overlap between the excitation spectrum of Ti3C2 MQDs and the absorption spectrum of TNB, AChE catalyzed the hydrolysis of substrate DTNB/ATCh to form TNB, which can effectively quench the fluorescence of Ti3C2 MQDs through the inner filter effect (IFE). Trinitrobenzenesulfonic Acid 104-107 dystrobrevin beta Homo sapiens 152-156 34862575-4 2021 Due to the obvious overlap between the excitation spectrum of Ti3C2 MQDs and the absorption spectrum of TNB, AChE catalyzed the hydrolysis of substrate DTNB/ATCh to form TNB, which can effectively quench the fluorescence of Ti3C2 MQDs through the inner filter effect (IFE). Trinitrobenzenesulfonic Acid 170-173 acetylcholinesterase (Cartwright blood group) Homo sapiens 109-113 34862575-4 2021 Due to the obvious overlap between the excitation spectrum of Ti3C2 MQDs and the absorption spectrum of TNB, AChE catalyzed the hydrolysis of substrate DTNB/ATCh to form TNB, which can effectively quench the fluorescence of Ti3C2 MQDs through the inner filter effect (IFE). Trinitrobenzenesulfonic Acid 170-173 dystrobrevin beta Homo sapiens 152-156 34884536-9 2021 Furthermore, the expression of members of NETs formation: peptidyl arginine deiminase 4 (PAD4), citrullinated histone H3 (citH3), myeloperoxidase (MPO) and inflammatory regulators, such as nuclear transcription factor-kappa B (NF-kappaB) and high-mobility group box 1 (HMGB1) were reduced in H2S treated group compared to TNBS. Trinitrobenzenesulfonic Acid 322-326 peptidyl arginine deiminase 4 Rattus norvegicus 58-87 34884536-9 2021 Furthermore, the expression of members of NETs formation: peptidyl arginine deiminase 4 (PAD4), citrullinated histone H3 (citH3), myeloperoxidase (MPO) and inflammatory regulators, such as nuclear transcription factor-kappa B (NF-kappaB) and high-mobility group box 1 (HMGB1) were reduced in H2S treated group compared to TNBS. Trinitrobenzenesulfonic Acid 322-326 peptidyl arginine deiminase 4 Rattus norvegicus 89-93 34884536-9 2021 Furthermore, the expression of members of NETs formation: peptidyl arginine deiminase 4 (PAD4), citrullinated histone H3 (citH3), myeloperoxidase (MPO) and inflammatory regulators, such as nuclear transcription factor-kappa B (NF-kappaB) and high-mobility group box 1 (HMGB1) were reduced in H2S treated group compared to TNBS. Trinitrobenzenesulfonic Acid 322-326 myeloperoxidase Rattus norvegicus 130-145 34884536-9 2021 Furthermore, the expression of members of NETs formation: peptidyl arginine deiminase 4 (PAD4), citrullinated histone H3 (citH3), myeloperoxidase (MPO) and inflammatory regulators, such as nuclear transcription factor-kappa B (NF-kappaB) and high-mobility group box 1 (HMGB1) were reduced in H2S treated group compared to TNBS. Trinitrobenzenesulfonic Acid 322-326 myeloperoxidase Rattus norvegicus 147-150 34884536-9 2021 Furthermore, the expression of members of NETs formation: peptidyl arginine deiminase 4 (PAD4), citrullinated histone H3 (citH3), myeloperoxidase (MPO) and inflammatory regulators, such as nuclear transcription factor-kappa B (NF-kappaB) and high-mobility group box 1 (HMGB1) were reduced in H2S treated group compared to TNBS. Trinitrobenzenesulfonic Acid 322-326 high mobility group box 1 Rattus norvegicus 242-267 34884536-9 2021 Furthermore, the expression of members of NETs formation: peptidyl arginine deiminase 4 (PAD4), citrullinated histone H3 (citH3), myeloperoxidase (MPO) and inflammatory regulators, such as nuclear transcription factor-kappa B (NF-kappaB) and high-mobility group box 1 (HMGB1) were reduced in H2S treated group compared to TNBS. Trinitrobenzenesulfonic Acid 322-326 high mobility group box 1 Rattus norvegicus 269-274 34829924-10 2021 hAAT-MSC therapy also suppressed TRPV1 expression in DRG and reduced pancreatic mast cell density induced by TNBS. Trinitrobenzenesulfonic Acid 109-113 transient receptor potential cation channel, subfamily V, member 1 Mus musculus 33-38 34857989-10 2021 Increased colonic damage and myeloperoxidase activity after 2,4,6-trinitrobenzene sulfonic acid treatment were suppressed in yacon-containing diet-received mice. Trinitrobenzenesulfonic Acid 60-95 myeloperoxidase Mus musculus 29-44 34744725-5 2021 Proteomics analysis based upon TNBS-induced UC model rats revealed that Amine oxidase copper-containing 1 (AOC1) was a potential target of LD4-PDT. Trinitrobenzenesulfonic Acid 31-35 amine oxidase, copper containing 1 Rattus norvegicus 107-111 34631698-3 2021 Here we report that conditional ablation of SIRT1, a class III lysine deacetylase, in intestinal epithelial cells exacerbated 2, 4, 6-trinitro-benzene sulfonic acid (TNBS) induced intestinal fibrosis in mice. Trinitrobenzenesulfonic Acid 166-170 sirtuin 1 Mus musculus 44-49 34707499-0 2021 Tnfaip6 Secreted by Bone Marrow-Derived Mesenchymal Stem Cells Attenuates TNBS-Induced Colitis by Modulating Follicular Helper T Cells and Follicular Regulatory T Cells Balance in Mice. Trinitrobenzenesulfonic Acid 74-78 tumor necrosis factor alpha induced protein 6 Mus musculus 0-7 34539182-5 2021 Methods: We established a TNBS-induced IBS mouse model, in which KAR was administrated, and mucosal cytokine expression was measured by qRT-PCR. Trinitrobenzenesulfonic Acid 26-30 KAR Homo sapiens 65-68 34539182-11 2021 Using macrophage-depleted mice, we found that chimera mice with AhR-/- macrophages were more susceptible to TNBS-induced IBS and the therapeutic effect of KAR on IBS was significantly impaired in mice with AhR-/- macrophages. Trinitrobenzenesulfonic Acid 108-112 aryl-hydrocarbon receptor Mus musculus 64-67 34231472-3 2021 The purpose of this study was to examine whether miR-7a-5p regulates 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced inflammatory responses via the JNK pathway. Trinitrobenzenesulfonic Acid 69-104 mitogen-activated protein kinase 8 Mus musculus 151-154 34399822-0 2021 Traditional herbal formula Wu-Mei-Wan alleviates TNBS-induced colitis in mice by inhibiting necroptosis through increasing RIPK3 O-GlcNAcylation. Trinitrobenzenesulfonic Acid 49-53 receptor-interacting serine-threonine kinase 3 Mus musculus 123-128 34399822-16 2021 CONCLUSION: Our work demonstrated that WMW can alleviate TNBS-induced colitis in mice by inhibiting necroptosis through increasing RIPK3 O-GlcNAcylation. Trinitrobenzenesulfonic Acid 57-61 receptor-interacting serine-threonine kinase 3 Mus musculus 131-136 34444876-6 2021 Administration of FFAR4 agonist GSK137647 attenuated both TNBS-induced and DSS-induced colitis in mice, as indicated by macroscopic parameters and myeloperoxidase activity. Trinitrobenzenesulfonic Acid 58-62 free fatty acid receptor 4 Mus musculus 18-23 34156157-7 2021 The protein expression levels of formyl peptide receptor 1 (FPR1) and nuclear respiratory factor 2 (Nrf2) were upregulated in the colonic tissues of TNBS-treated mice. Trinitrobenzenesulfonic Acid 149-153 formyl peptide receptor 1 Mus musculus 33-58 34156157-7 2021 The protein expression levels of formyl peptide receptor 1 (FPR1) and nuclear respiratory factor 2 (Nrf2) were upregulated in the colonic tissues of TNBS-treated mice. Trinitrobenzenesulfonic Acid 149-153 formyl peptide receptor 1 Mus musculus 60-64 34144987-5 2021 Mice lacking Gal1 exhibited exacerbated colitis and augmented mucosal CD8+ T cell activation in response to 2,4,6-trinitrobenzenesulfonic acid; this phenotype was partially ameliorated by treatment with recombinant Gal1. Trinitrobenzenesulfonic Acid 108-142 lectin, galactose binding, soluble 1 Mus musculus 13-17 34144987-5 2021 Mice lacking Gal1 exhibited exacerbated colitis and augmented mucosal CD8+ T cell activation in response to 2,4,6-trinitrobenzenesulfonic acid; this phenotype was partially ameliorated by treatment with recombinant Gal1. Trinitrobenzenesulfonic Acid 108-142 lectin, galactose binding, soluble 1 Mus musculus 215-219 34088740-6 2021 TNB-585 pairs a tumor-targeting anti-PSMA arm together with a unique, low-affinity anti-CD3 arm in bispecific format. Trinitrobenzenesulfonic Acid 0-3 folate hydrolase 1 Homo sapiens 37-41 34088740-7 2021 We tested TNB-585 in T cell-redirected cytotoxicity assays against PSMA+ tumor cells in both two-dimensional (2D) cultures and three-dimensional (3D) spheroids as well as against patient-derived prostate tumor cells. Trinitrobenzenesulfonic Acid 10-13 folate hydrolase 1 Homo sapiens 67-71 34132111-0 2021 Leptin resistant Zucker rats with trinitrobenzene sulfonic acid colitis present a reduced inflammatory response but enhanced epithelial damage. Trinitrobenzenesulfonic Acid 34-63 leptin Rattus norvegicus 0-6 34156157-7 2021 The protein expression levels of formyl peptide receptor 1 (FPR1) and nuclear respiratory factor 2 (Nrf2) were upregulated in the colonic tissues of TNBS-treated mice. Trinitrobenzenesulfonic Acid 149-153 nuclear factor, erythroid derived 2, like 2 Mus musculus 70-98 34156157-7 2021 The protein expression levels of formyl peptide receptor 1 (FPR1) and nuclear respiratory factor 2 (Nrf2) were upregulated in the colonic tissues of TNBS-treated mice. Trinitrobenzenesulfonic Acid 149-153 nuclear factor, erythroid derived 2, like 2 Mus musculus 100-104 34063607-2 2021 In this article, we aimed to explore which mediators and cells were involved in Ang II-mediated colonic contraction in the TNBS-induced rat model of colitis. Trinitrobenzenesulfonic Acid 123-127 angiotensinogen Rattus norvegicus 80-86 34063607-5 2021 Ang II caused AT1 receptor-mediated colonic contraction that was markedly decreased along the colons of TNBS-induced rats, consistent with reduced AT1 mRNA expression. Trinitrobenzenesulfonic Acid 104-108 angiotensinogen Rattus norvegicus 0-6 34231472-3 2021 The purpose of this study was to examine whether miR-7a-5p regulates 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced inflammatory responses via the JNK pathway. Trinitrobenzenesulfonic Acid 106-110 mitogen-activated protein kinase 8 Mus musculus 151-154 34231472-9 2021 RESULTS: miR-7a-5p and p-JNK expression were higher in the intestinal tissue of the TNBS group as compared to NC. Trinitrobenzenesulfonic Acid 84-88 mitogen-activated protein kinase 8 Mus musculus 25-28 35443853-4 2022 The results showed that the expression of colonic mucosal PYY and PYY receptors Y1, Y2, Y4 were significantly increased in mice with TNBS-induced colitis. Trinitrobenzenesulfonic Acid 133-137 peptide YY Mus musculus 66-69 35603939-9 2022 Mice with TNBS induced colitis had increased expression of Grp78 and Gro-alpha in colonic epithelia. Trinitrobenzenesulfonic Acid 10-14 heat shock protein 5 Mus musculus 59-64 35603939-9 2022 Mice with TNBS induced colitis had increased expression of Grp78 and Gro-alpha in colonic epithelia. Trinitrobenzenesulfonic Acid 10-14 C-X-C motif chemokine ligand 1 Homo sapiens 69-78 35571126-5 2022 SBP could effectively strengthen epithelial barrier integrity in TNBS-induced colitis by increasing the secretion of mucin and tight junction and inhibiting apoptosis. Trinitrobenzenesulfonic Acid 65-69 solute carrier family 13 member 2 Rattus norvegicus 117-122 35561427-7 2022 Moreover, lower doses of SDH showed the similar or better efficacy than cyclosporine A (CsA) and mesalazine in DSS- or TNBS-induced colitis animals. Trinitrobenzenesulfonic Acid 119-123 serine dehydratase Homo sapiens 25-28 35553628-8 2022 To verify these in vitro findings, we created mice overexpressing IRF4 in DCs and showed that these mice were resistant to trinitrobenzene sulfonic acid-induced colitis as compared with wild-type mice; these effects were accompanied by reduced expression levels of cIAP1 and cIAP2. Trinitrobenzenesulfonic Acid 123-152 interferon regulatory factor 4 Mus musculus 66-70 35563130-3 2022 METHODS: Experimental colitis was induced by the rectal administration of multiple doses of TNBS in female CD-1 mice. Trinitrobenzenesulfonic Acid 92-96 CD1 antigen complex Mus musculus 107-111 35530951-0 2022 miR-21 antagonist alleviates colitis and angiogenesis via the PTEN/PI3K/AKT pathway in colitis mice induced by TNBS. Trinitrobenzenesulfonic Acid 111-115 microRNA 21a Mus musculus 0-6 35530951-0 2022 miR-21 antagonist alleviates colitis and angiogenesis via the PTEN/PI3K/AKT pathway in colitis mice induced by TNBS. Trinitrobenzenesulfonic Acid 111-115 phosphatase and tensin homolog Mus musculus 62-66 35530951-0 2022 miR-21 antagonist alleviates colitis and angiogenesis via the PTEN/PI3K/AKT pathway in colitis mice induced by TNBS. Trinitrobenzenesulfonic Acid 111-115 thymoma viral proto-oncogene 1 Mus musculus 72-75 35530951-13 2022 In addition, agomir-21 obviously inhibited the expression of PTEN and activated the PI3K/AKT/VEGF pathway in mice induced by TNBS, while antagomir-21 effectively antagonized this effect. Trinitrobenzenesulfonic Acid 125-129 phosphatase and tensin homolog Mus musculus 61-65 35530951-13 2022 In addition, agomir-21 obviously inhibited the expression of PTEN and activated the PI3K/AKT/VEGF pathway in mice induced by TNBS, while antagomir-21 effectively antagonized this effect. Trinitrobenzenesulfonic Acid 125-129 thymoma viral proto-oncogene 1 Mus musculus 89-92 35530951-13 2022 In addition, agomir-21 obviously inhibited the expression of PTEN and activated the PI3K/AKT/VEGF pathway in mice induced by TNBS, while antagomir-21 effectively antagonized this effect. Trinitrobenzenesulfonic Acid 125-129 vascular endothelial growth factor A Mus musculus 93-97 35530951-14 2022 Conclusions: miR-21 can promote the progression of colitis in mice induced by TNBS and aggravate the disordered angiogenesis by regulating the PTEN/PI3K/AKT axis. Trinitrobenzenesulfonic Acid 78-82 microRNA 21a Mus musculus 13-19 35443853-4 2022 The results showed that the expression of colonic mucosal PYY and PYY receptors Y1, Y2, Y4 were significantly increased in mice with TNBS-induced colitis. Trinitrobenzenesulfonic Acid 133-137 transporter 2, ATP-binding cassette, sub-family B (MDR/TAP) Mus musculus 80-90 35239781-8 2022 The TNBS-induced colitis rats showed significant increases in disease activity scores, serum TNF-alpha, IL-2, and IL-6 levels, and colonic myeloperoxidase and malonaldehyde content. Trinitrobenzenesulfonic Acid 4-8 tumor necrosis factor Rattus norvegicus 93-102 35343079-6 2022 Importantly, conditional knockout of Gpr65 in CD4+ T cells ameliorated trinitrobenzene sulfonic acid (TNBS)-induced acute murine colitis and a chronic colitis in Rag1-/- mice reconstituted with CD45RBhigh CD4+ T cells in vivo, characterised by attenuated Th1 and Th17 cell immune response in colon mucosa and decreased infiltration of CD4+ T cells, neutrophils and macrophages. Trinitrobenzenesulfonic Acid 71-100 G-protein coupled receptor 65 Mus musculus 37-42 35343079-6 2022 Importantly, conditional knockout of Gpr65 in CD4+ T cells ameliorated trinitrobenzene sulfonic acid (TNBS)-induced acute murine colitis and a chronic colitis in Rag1-/- mice reconstituted with CD45RBhigh CD4+ T cells in vivo, characterised by attenuated Th1 and Th17 cell immune response in colon mucosa and decreased infiltration of CD4+ T cells, neutrophils and macrophages. Trinitrobenzenesulfonic Acid 102-106 G-protein coupled receptor 65 Mus musculus 37-42 35545319-12 2022 RESULTS: Compared with the control, the disease activity index, colonic myeloperoxidase activity, and histopathological score were all significantly increased at the 3rd, 5th, and 7th days post TNBS (all P<0.01), the serum aspartate aminotransferase level and hepatic histopathologic score were also obviously elevated at the 7th day post TNBS (all P<0.05). Trinitrobenzenesulfonic Acid 194-198 glutamic-oxaloacetic transaminase 2 Rattus norvegicus 223-249 35545319-14 2022 Moreover, compared with the control, hepatic GSH content and the activity of GSH-Px and GR were all significantly decreased at the 3rd and 5th days post TNBS (P<0.05 or P<0.01), and the protein expressions of GCL, GSH-Px, and GR were all obviously down-regulated at the 3rd, 5th, and 7th days post TNBS (P<0.05 or P<0.01). Trinitrobenzenesulfonic Acid 153-157 glutathione-disulfide reductase Rattus norvegicus 88-90 35545319-14 2022 Moreover, compared with the control, hepatic GSH content and the activity of GSH-Px and GR were all significantly decreased at the 3rd and 5th days post TNBS (P<0.05 or P<0.01), and the protein expressions of GCL, GSH-Px, and GR were all obviously down-regulated at the 3rd, 5th, and 7th days post TNBS (P<0.05 or P<0.01). Trinitrobenzenesulfonic Acid 298-302 glutathione-disulfide reductase Rattus norvegicus 88-90 35239781-8 2022 The TNBS-induced colitis rats showed significant increases in disease activity scores, serum TNF-alpha, IL-2, and IL-6 levels, and colonic myeloperoxidase and malonaldehyde content. Trinitrobenzenesulfonic Acid 4-8 interleukin 2 Rattus norvegicus 104-108 35239781-8 2022 The TNBS-induced colitis rats showed significant increases in disease activity scores, serum TNF-alpha, IL-2, and IL-6 levels, and colonic myeloperoxidase and malonaldehyde content. Trinitrobenzenesulfonic Acid 4-8 interleukin 6 Rattus norvegicus 114-118 35092511-8 2022 Specifically, in bladder cancer and melanoma, the high 12-chemokine TLS signature score was found to potentially reflect an expanded cancer-immunity status characterized by high TNB and an immune-inflamed feature. Trinitrobenzenesulfonic Acid 178-181 FUS RNA binding protein Homo sapiens 68-71 35124427-7 2022 FINDINGS: Upregulated expression of SOX9 in the disease-affected intestine mucosa was identified in both patients with CD and mice challenged with trinitrobenzene sulfonic acid (TNBS). Trinitrobenzenesulfonic Acid 147-176 SRY-box transcription factor 9 Homo sapiens 36-40 3182816-5 1988 The triglyceride content of LDL was found to be reciprocally related to the number of free lysine amino groups of LDL apolipoprotein B (apoB) which could be labeled with trinitrobenzenesulfonic acid. Trinitrobenzenesulfonic Acid 170-198 apolipoprotein B Homo sapiens 118-134 35496825-6 2022 We observed that the AB strain presented increased mortality, higher neutrophilic intestinal infiltration, decreased goblet cell numbers and decreased IL-10 expression when exposed to TNBS, compared to the TU strain. Trinitrobenzenesulfonic Acid 184-188 interleukin 10 Danio rerio 151-156 35290143-4 2022 Moreover, TLR9/Myd88/NF-kappaB signal pathway is a part of the most important pathways for regulating the immune response.Methods: We explored the influence of OMT with different dosages on UC by establishing a 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis model. Trinitrobenzenesulfonic Acid 211-246 toll-like receptor 9 Rattus norvegicus 10-14 35290143-4 2022 Moreover, TLR9/Myd88/NF-kappaB signal pathway is a part of the most important pathways for regulating the immune response.Methods: We explored the influence of OMT with different dosages on UC by establishing a 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis model. Trinitrobenzenesulfonic Acid 211-246 MYD88, innate immune signal transduction adaptor Rattus norvegicus 15-20 35290143-4 2022 Moreover, TLR9/Myd88/NF-kappaB signal pathway is a part of the most important pathways for regulating the immune response.Methods: We explored the influence of OMT with different dosages on UC by establishing a 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis model. Trinitrobenzenesulfonic Acid 248-252 toll-like receptor 9 Rattus norvegicus 10-14 34232309-4 2022 METHODS: OTUD5 expression was evaluated in mucosal samples of patients with Crohn"s disease (CD), patients with ulcerative colitis (UC) and controls, as well as in mice with trinitrobenzene-sulfonic acid (TNBS)-induced colitis by real-time PCR, Western blotting, immunohistochemistry and immunofluorescence. Trinitrobenzenesulfonic Acid 205-209 OTU deubiquitinase 5 Homo sapiens 9-14 3182816-5 1988 The triglyceride content of LDL was found to be reciprocally related to the number of free lysine amino groups of LDL apolipoprotein B (apoB) which could be labeled with trinitrobenzenesulfonic acid. Trinitrobenzenesulfonic Acid 170-198 apolipoprotein B Homo sapiens 136-140 2979005-8 1988 The partial sequence of this peptide showed that it corresponds to the same peptide isolated from rabbit muscle pyruvate kinase labeled with dialdehyde-ADP and with trinitrobenzenesulfonate. Trinitrobenzenesulfonic Acid 165-189 pyruvate kinase PKLR Oryctolagus cuniculus 112-127 2847506-2 1988 The colonic damage produced by TNB was accompanied, after 12-36 hours, by a marked increase in MPO, which was directly correlated to leukocyte infiltration, assessed histologically. Trinitrobenzenesulfonic Acid 31-34 myeloperoxidase Rattus norvegicus 95-98 2847506-4 1988 However, a further increase in MPO-cellular infiltration, between 36-72 hours after TNB, was accompanied by a reduction in 12- and 15-HETE formation. Trinitrobenzenesulfonic Acid 84-87 myeloperoxidase Rattus norvegicus 31-34 2843563-1 1988 Myosin was reacted with 2,4,6-trinitrobenzene sulphonate (TNBS) in the presence or absence of Mg-pyrophosphate. Trinitrobenzenesulfonic Acid 58-62 myosin heavy chain 14 Homo sapiens 0-6 3126367-0 1988 Inactivation of rat testicular NADPH-cytochrome P-450 reductase by 2,4,6-trinitrobenzenesulfonate. Trinitrobenzenesulfonic Acid 67-97 cytochrome p450 oxidoreductase Rattus norvegicus 31-63 3126367-1 1988 Rat testicular NADPH-cytochrome P-450 reductase was inactivated by treatment with 2,4,6-trinitrobenzene sulfonate (TNBS) or with 2",3"-dialdehyde derivatives of 5"-ATP and NADP+. Trinitrobenzenesulfonic Acid 82-113 cytochrome p450 oxidoreductase Rattus norvegicus 15-47 3126367-1 1988 Rat testicular NADPH-cytochrome P-450 reductase was inactivated by treatment with 2,4,6-trinitrobenzene sulfonate (TNBS) or with 2",3"-dialdehyde derivatives of 5"-ATP and NADP+. Trinitrobenzenesulfonic Acid 115-119 cytochrome p450 oxidoreductase Rattus norvegicus 15-47 3126367-4 1988 Cytochrome c and DCPIP prevented NADPH-cytochrome P-450 reductase from inactivation by TNBS, but NADP(H) protected to a lesser extent. Trinitrobenzenesulfonic Acid 87-91 cytochrome p450 oxidoreductase Rattus norvegicus 33-65 3126367-7 1988 By differential and sequential modification by 5,5"-dithio-bis(2-nitrobenzoic acid), TNBS and dithiothreitol, the residues of lysine and cysteine were identified in the active site of NADPH-cytochrome P-450 reductase. Trinitrobenzenesulfonic Acid 85-89 cytochrome p450 oxidoreductase Rattus norvegicus 184-216 3003077-0 1986 Reduction of 2,4,6-trinitrobenzenesulfonate by glutathione reductase and the effect of NADP+ on the electron transfer. Trinitrobenzenesulfonic Acid 13-43 glutathione-disulfide reductase Homo sapiens 47-68 3121595-8 1987 We have performed chemical modification of antithrombin III with trinitrobenzene sulfonic acid in order to determine the location of these lysine residues. Trinitrobenzenesulfonic Acid 65-94 serpin family C member 1 Homo sapiens 43-59 3121595-9 1987 When antithrombin III was treated with 100 M excess of trinitrobenzene sulfonic acid for 10 min, about 3.2 mol of amino group per mol of antithrombin III were modified. Trinitrobenzenesulfonic Acid 55-84 serpin family C member 1 Homo sapiens 5-21 3121595-9 1987 When antithrombin III was treated with 100 M excess of trinitrobenzene sulfonic acid for 10 min, about 3.2 mol of amino group per mol of antithrombin III were modified. Trinitrobenzenesulfonic Acid 55-84 serpin family C member 1 Homo sapiens 137-153 3121595-13 1987 When antithrombin III was pretreated with heparin, followed by trinitrobenzene sulfonic acid modification, the extent of modification at Lys114 and Lys125 decreased from 75% and 94% to 20% and 40%, respectively, whereas the modification at Lys287 remained nearly quantitative (greater than 95%). Trinitrobenzenesulfonic Acid 63-92 serpin family C member 1 Homo sapiens 5-21 3578755-2 1987 It is based on the observation that the product of ornithine decarboxylase, putrescine, reacts with 2,4,6-trinitrobenzenesulfonic acid to give a colored product soluble in 1-pentanol whereas ornithine does not. Trinitrobenzenesulfonic Acid 100-134 ornithine decarboxylase 1 Homo sapiens 51-74 3095926-8 1986 Amino group analysis of aspirin-treated antithrombin III using trinitrobenzenesulfonic acid revealed that one to two primary amino groups are lost relative to the untreated antithrombin III. Trinitrobenzenesulfonic Acid 63-91 serpin family C member 1 Homo sapiens 40-56 3007131-2 1986 Chemical modification of rat hepatic NADPH-cytochrome P-450 reductase by sodium 2,4,6-trinitrobenzenesulfonate (TNBS) resulted in a time-dependent loss of the reducing activity for cytochrome c. The inactivation exhibited pseudo-first-order kinetics with a reaction order approximately one, and a second-order constant of 4.8 min-1 X M-1. Trinitrobenzenesulfonic Acid 112-116 cytochrome p450 oxidoreductase Rattus norvegicus 37-69 3007131-4 1986 Almost complete protection of the NADPH-cytochrome P-450 reductase from inactivation by TNBS was achieved by NADP(H), while partial protection was obtained with a high concentration of NADH. Trinitrobenzenesulfonic Acid 88-92 cytochrome p450 oxidoreductase Rattus norvegicus 34-66 3236071-0 1988 Modification and inactivation of rhodanese by 2,4,6-trinitrobenzenesulphonic acid. Trinitrobenzenesulfonic Acid 46-81 thiosulfate sulfurtransferase Bos taurus 33-42 3236071-1 1988 Bovine liver rhodanese (thiosulphate sulphurtransferase, EC 2.8.1.1) is modified by 2,4,6-trinitrobenzenesulphonic acid, by the use of modifying agent concentrations in large excess over enzyme protein concentration. Trinitrobenzenesulfonic Acid 84-119 thiosulfate sulfurtransferase Bos taurus 13-22 3236071-5 1988 Rhodanese primary amino groups modification by 2,4,6-trinitrobenzenesulphonic acid is described by a summation of exponential functions of reaction time at pH values of 8.00 or higher, while at lower pH values it is described by a single exponential function of reaction time. Trinitrobenzenesulfonic Acid 47-82 thiosulfate sulfurtransferase Bos taurus 0-9 3236071-9 1988 It is accordingly concluded that, when concentrations of 2,4,6-trinitrobenzenesulphonic acid in excess of protein concentration are used, all rhodanese modifiable amino groups are essential for enzyme activity. Trinitrobenzenesulfonic Acid 57-92 thiosulfate sulfurtransferase Bos taurus 142-151 2879870-6 1987 It was found that depletion of Thy 1- or Lyt 2-bearing precursor cells abolished the ability of spleen cells to generate LAK against TNBS-self, but had no effect on the generation of LAK against tumor cells. Trinitrobenzenesulfonic Acid 133-137 thymus cell antigen 1, theta Mus musculus 31-36 2879870-6 1987 It was found that depletion of Thy 1- or Lyt 2-bearing precursor cells abolished the ability of spleen cells to generate LAK against TNBS-self, but had no effect on the generation of LAK against tumor cells. Trinitrobenzenesulfonic Acid 133-137 CD8 antigen, alpha chain Mus musculus 41-46 2879870-11 1987 The precursors generating LAK against TNBS-self were Thy-1+, Lyt-2+, AGM1+ in both fractions. Trinitrobenzenesulfonic Acid 38-42 CD8 antigen, alpha chain Mus musculus 61-66 3003077-1 1986 Glutathione reductase has been found to catalyze an NAD(P)H-dependent electron transfer to 2,4,6-trinitrobenzenesulfonate (TNBS). Trinitrobenzenesulfonic Acid 91-121 glutathione-disulfide reductase Homo sapiens 0-21 3003077-1 1986 Glutathione reductase has been found to catalyze an NAD(P)H-dependent electron transfer to 2,4,6-trinitrobenzenesulfonate (TNBS). Trinitrobenzenesulfonic Acid 123-127 glutathione-disulfide reductase Homo sapiens 0-21 3003077-5 1986 In the absence of oxygen (or cytochrome c), TNBS limits the reaction and accepts a total of four electrons. Trinitrobenzenesulfonic Acid 44-48 cytochrome c, somatic Homo sapiens 29-41 2863142-3 1985 Modification by 2-hydroxy-5-nitrobenzyl bromide, N-bromosuccinimide, diethylpyrocarbonate and trinitrobenzenesulfonic acid caused a parallel inactivation of both pseudocholinesterase and aryl acylamidase activities that could be prevented by butyrylcholine iodide. Trinitrobenzenesulfonic Acid 94-122 butyrylcholinesterase Homo sapiens 162-182 6197193-8 1983 In addition, Lyt 2-depleted spleen and LN cells from sc primed BALB/c mice could restore the ability of tolerant spleen cells from 2,4,6-trinitrobenzenesulfonic acid (TNBS)-injected BALB/c mice to generate TNP-specific CTLs. Trinitrobenzenesulfonic Acid 131-165 CD8 antigen, alpha chain Mus musculus 13-18 3917936-0 1985 The effect of 2,4,6-trinitrobenzenesulfonate on mercuric reductase, glutathione reductase and lipoamide dehydrogenase. Trinitrobenzenesulfonic Acid 14-44 glutathione-disulfide reductase Homo sapiens 68-89 3917936-0 1985 The effect of 2,4,6-trinitrobenzenesulfonate on mercuric reductase, glutathione reductase and lipoamide dehydrogenase. Trinitrobenzenesulfonic Acid 14-44 dihydrolipoamide dehydrogenase Homo sapiens 94-117 3917936-1 1985 Among the three closely related enzymes, lipoamide dehydrogenase, mercuric reductase, and glutathione reductase only the latter is inhibited by 2,4,6-trinitrobenzenesulfonate (TNBS). Trinitrobenzenesulfonic Acid 144-174 dihydrolipoamide dehydrogenase Homo sapiens 41-64 3917936-1 1985 Among the three closely related enzymes, lipoamide dehydrogenase, mercuric reductase, and glutathione reductase only the latter is inhibited by 2,4,6-trinitrobenzenesulfonate (TNBS). Trinitrobenzenesulfonic Acid 144-174 glutathione-disulfide reductase Homo sapiens 90-111 3917936-1 1985 Among the three closely related enzymes, lipoamide dehydrogenase, mercuric reductase, and glutathione reductase only the latter is inhibited by 2,4,6-trinitrobenzenesulfonate (TNBS). Trinitrobenzenesulfonic Acid 176-180 dihydrolipoamide dehydrogenase Homo sapiens 41-64 3917936-1 1985 Among the three closely related enzymes, lipoamide dehydrogenase, mercuric reductase, and glutathione reductase only the latter is inhibited by 2,4,6-trinitrobenzenesulfonate (TNBS). Trinitrobenzenesulfonic Acid 176-180 glutathione-disulfide reductase Homo sapiens 90-111 3917936-3 1985 In the case of glutathione reductase and mercuric reductase this TNBS-dependent activity displays substrate inhibition by excess of NADPH and is strongly stimulated by NADP+. Trinitrobenzenesulfonic Acid 65-69 glutathione-disulfide reductase Homo sapiens 15-36 6201586-1 1984 Several anti-H-2Kk but not anti-H-2Dd monoclonal antibodies (mAb) exhibited enhanced binding to B10.A murine spleen cells after modification of the cells with trinitrobenzene sulfonate (TNBS). Trinitrobenzenesulfonic Acid 159-184 histocompatibility 2, K1, K region Mus musculus 13-18 6197193-8 1983 In addition, Lyt 2-depleted spleen and LN cells from sc primed BALB/c mice could restore the ability of tolerant spleen cells from 2,4,6-trinitrobenzenesulfonic acid (TNBS)-injected BALB/c mice to generate TNP-specific CTLs. Trinitrobenzenesulfonic Acid 167-171 CD8 antigen, alpha chain Mus musculus 13-18 6165798-3 1981 Intravenous injection of 0.01 mM 2,4,6-trinitrobenzene sulfonic acid-derivatized syngeneic lymphoid cells generates a Thy-1-positive, antigen-specific suppressor cell for contact sensitivity which requires an I-J allogeneic effect to become fully activated. Trinitrobenzenesulfonic Acid 33-68 Thy-1 cell surface antigen Homo sapiens 118-123 6832378-2 1983 The amino group reactive reagent 2,4,6-trinitrobenzenesulfonate (TNBS), however, inhibited specifically the direct interactions of EF-2 with guanine nucleotides, but not the binding of GuoPP(CH2)P to the EF-2-ribosome complex. Trinitrobenzenesulfonic Acid 33-63 eukaryotic translation elongation factor 2 Rattus norvegicus 131-135 6832378-2 1983 The amino group reactive reagent 2,4,6-trinitrobenzenesulfonate (TNBS), however, inhibited specifically the direct interactions of EF-2 with guanine nucleotides, but not the binding of GuoPP(CH2)P to the EF-2-ribosome complex. Trinitrobenzenesulfonic Acid 65-69 eukaryotic translation elongation factor 2 Rattus norvegicus 131-135 6832378-2 1983 The amino group reactive reagent 2,4,6-trinitrobenzenesulfonate (TNBS), however, inhibited specifically the direct interactions of EF-2 with guanine nucleotides, but not the binding of GuoPP(CH2)P to the EF-2-ribosome complex. Trinitrobenzenesulfonic Acid 65-69 eukaryotic translation elongation factor 2 Rattus norvegicus 204-208 6832378-3 1983 The different sensitivities of EF-2 to MalNEt and to TNBS suggested that the binding sites involved in the binary vs. ternary complex might correspond to different conformational states or might even be distinct physical entities. Trinitrobenzenesulfonic Acid 53-57 eukaryotic translation elongation factor 2 Rattus norvegicus 31-35 6864486-0 1983 Kinetics of the rapid modification of human serum albumin with trinitrobenzenesulfonate and localization of its site. Trinitrobenzenesulfonic Acid 63-87 albumin Homo sapiens 50-57 6864486-1 1983 The rapid reaction of human serum albumin with trinitrobenzenesulfonate (I) and the location of the reactive site were investigated to characterize the chemical modification of albumin by I. Trinitrobenzenesulfonic Acid 47-71 albumin Homo sapiens 34-41 6864486-1 1983 The rapid reaction of human serum albumin with trinitrobenzenesulfonate (I) and the location of the reactive site were investigated to characterize the chemical modification of albumin by I. Trinitrobenzenesulfonic Acid 47-71 albumin Homo sapiens 177-184 6814322-0 1982 Selective expansion of H-2 restricted cytotoxic T lymphocytes to TNP-self by injection of trinitrobenzene sulfonate. Trinitrobenzenesulfonic Acid 90-115 relaxin 2 Homo sapiens 23-26 6111344-6 1981 Conversely, 2,4,6-trinitrobenzenesulfonic acid was a potent inactivator of ecto-5"-nucleotidase but had no effect on ecto-ATPase. Trinitrobenzenesulfonic Acid 12-46 5' nucleotidase, ecto Rattus norvegicus 75-95 6304549-1 1983 Treatment of the C6 glioblastoma cell with trinitrobenzenesulfonic acid (TNBS) resulted in the selective inactivation of ecto-5"-nucleotidase under conditions which maintained cell viability. Trinitrobenzenesulfonic Acid 43-71 5'-nucleotidase ecto Homo sapiens 121-141 87418-0 1979 Cell types required for H-2-restricted cytotoxic responses generated by trinitrobenzene sulfonate-modified syngeneic cells or trinitrophenyl-conjugated proteins. Trinitrobenzenesulfonic Acid 72-97 histocompatibility-2, MHC Mus musculus 24-27 7350231-0 1980 H-2 linked genetic control of priming for secondary cytotoxic responses to autologous cells modified with low concentrations of trinitrobenzene sulfonate. Trinitrobenzenesulfonic Acid 128-153 relaxin 2 Homo sapiens 0-3 218922-0 1979 Differential modification of specific lysine residues in the two kinds of subfragment-1 of myosin with 2, 4, 6-trinitrobenzenesulfonate. Trinitrobenzenesulfonic Acid 104-136 myosin heavy chain 14 Homo sapiens 91-97 159905-5 1979 About 0.5 mol of TNBS per mol of myosin head was incorporated rapidly, irrespective of the presence of PP1 (2mM), into both types of myosin studied. Trinitrobenzenesulfonic Acid 17-21 myosin, heavy chain 15 Gallus gallus 33-39 159905-5 1979 About 0.5 mol of TNBS per mol of myosin head was incorporated rapidly, irrespective of the presence of PP1 (2mM), into both types of myosin studied. Trinitrobenzenesulfonic Acid 17-21 myosin, heavy chain 15 Gallus gallus 133-139 159905-9 1979 The rapid incorporation of TNBS into cardiac muscle myosin was accompanied by a rapid decrease in the size of the initial P1 burst, and it was completely lost after modification for 20 min. Trinitrobenzenesulfonic Acid 27-31 myosin, heavy chain 15 Gallus gallus 52-58 66272-2 1977 H-2 antigens on cells treated with trinitrobenzene sulfonic acid are derivatized. Trinitrobenzenesulfonic Acid 35-64 relaxin 2 Homo sapiens 0-3 421899-0 1979 Inhibition of glutathione reductase by interaction of 2, 4, 6-trinitrobenzenesulfonate with the active-site dithiol. Trinitrobenzenesulfonic Acid 54-86 glutathione-disulfide reductase Homo sapiens 14-35 310316-2 1978 Chemical modifications of human plasma alpha1-antitrypsin with reagents which modify lysyl residues (citraconic anhydride, acetic anhydride, formaldehyde and 2,4,6-trinitrobenzenesulfonic acid) and arginyl residued (1,2-cyclohexanedione) were examined with regard to their effect upon the elastase inhibitory capacity of the glycoprotein. Trinitrobenzenesulfonic Acid 158-192 serpin family A member 1 Homo sapiens 39-57 744387-0 1978 Inactivation of cathepsin D by 2,4,6-trinitrobenzenesulphonic acid [proceedings]. Trinitrobenzenesulfonic Acid 31-66 cathepsin D Homo sapiens 16-27 690447-4 1978 Cells treated with high concentrations of TNBS had their cell membrane H-2 molecules derivatized and functioned antigenically as inhibitors in a cold target TNP-CML competition assay. Trinitrobenzenesulfonic Acid 42-46 relaxin 2 Homo sapiens 71-74 690447-7 1978 When cells were treated with 3H-TNBS, it was observed that TNP couples to cell membrane H-2, Ia and Ig molecules, and an estimate of the number of TNP molecules bound per cell at varying concentrations of TNBS was determined. Trinitrobenzenesulfonic Acid 32-36 relaxin 2 Homo sapiens 88-91 132437-2 1976 Use of 2, 4, 6-trinitrobenzenesulfonate to show functional movements of the ATPase molecule. Trinitrobenzenesulfonic Acid 7-39 dynein axonemal heavy chain 8 Homo sapiens 76-82 132437-7 1976 SR vesicles were allowed to react with 0.5 mM 2,4,6-trinitrobenzenesulfonate (TBS) at pH 8.0 and 0 degrees, keeping the ATPase in one of the enzymatic states listed above. Trinitrobenzenesulfonic Acid 78-81 dynein axonemal heavy chain 8 Homo sapiens 120-126 132437-10 1976 In all the enzymatic states of ATPase tested, the amount of TBS bound with SR protein increased exponentially with time, and reached a maximum level 10 min after starting the reaction. Trinitrobenzenesulfonic Acid 60-63 dynein axonemal heavy chain 8 Homo sapiens 31-37 132437-10 1976 In all the enzymatic states of ATPase tested, the amount of TBS bound with SR protein increased exponentially with time, and reached a maximum level 10 min after starting the reaction. Trinitrobenzenesulfonic Acid 60-63 RNA binding protein with serine rich domain 1 Homo sapiens 75-85 132437-13 1976 The SR ATPase activity and the amount of EP formed decreased only slightly, even when the amount of TBS bound to SR protein reached the maximum level. Trinitrobenzenesulfonic Acid 100-103 RNA binding protein with serine rich domain 1 Homo sapiens 113-123 132437-15 1976 The maximum amount of TBS bound to SR protein varied on changing the enzymatic state of SR ATPase. Trinitrobenzenesulfonic Acid 22-25 RNA binding protein with serine rich domain 1 Homo sapiens 35-45 132437-15 1976 The maximum amount of TBS bound to SR protein varied on changing the enzymatic state of SR ATPase. Trinitrobenzenesulfonic Acid 22-25 dynein axonemal heavy chain 8 Homo sapiens 91-97 132437-16 1976 Namely, about 2,3,1,3, or 4, and 3 moles of TNP were incorporated per mole of SR ATPase, when SR was allowed to react with TBS in the enzymatic states MgE, MgECa, MgEATP" CaECa, and CaECap, respectively. Trinitrobenzenesulfonic Acid 123-126 dynein axonemal heavy chain 8 Homo sapiens 81-87 132437-18 1976 When the enzymatic state was changed from MgE to MgECa 10 min after starting the reaction with TBS, about 4 moles of TBS was bound per mole of ATPase within 10 min, while the maximum levels of TBS bound in states MgE and MgECa were about 2 and 3 moles per mole of ATPase, respectively, as mentioned above. Trinitrobenzenesulfonic Acid 95-98 dynein axonemal heavy chain 8 Homo sapiens 143-149 132437-18 1976 When the enzymatic state was changed from MgE to MgECa 10 min after starting the reaction with TBS, about 4 moles of TBS was bound per mole of ATPase within 10 min, while the maximum levels of TBS bound in states MgE and MgECa were about 2 and 3 moles per mole of ATPase, respectively, as mentioned above. Trinitrobenzenesulfonic Acid 117-120 dynein axonemal heavy chain 8 Homo sapiens 143-149 132437-18 1976 When the enzymatic state was changed from MgE to MgECa 10 min after starting the reaction with TBS, about 4 moles of TBS was bound per mole of ATPase within 10 min, while the maximum levels of TBS bound in states MgE and MgECa were about 2 and 3 moles per mole of ATPase, respectively, as mentioned above. Trinitrobenzenesulfonic Acid 117-120 dynein axonemal heavy chain 8 Homo sapiens 264-270 134478-5 1976 Blocking of amino groups of myosin by TNBS had no effect on its activating capacity, but decreased its influence on thermostability of creatine kinase. Trinitrobenzenesulfonic Acid 38-42 myosin heavy chain 14 Homo sapiens 28-34 132437-18 1976 When the enzymatic state was changed from MgE to MgECa 10 min after starting the reaction with TBS, about 4 moles of TBS was bound per mole of ATPase within 10 min, while the maximum levels of TBS bound in states MgE and MgECa were about 2 and 3 moles per mole of ATPase, respectively, as mentioned above. Trinitrobenzenesulfonic Acid 117-120 dynein axonemal heavy chain 8 Homo sapiens 143-149 132437-18 1976 When the enzymatic state was changed from MgE to MgECa 10 min after starting the reaction with TBS, about 4 moles of TBS was bound per mole of ATPase within 10 min, while the maximum levels of TBS bound in states MgE and MgECa were about 2 and 3 moles per mole of ATPase, respectively, as mentioned above. Trinitrobenzenesulfonic Acid 117-120 dynein axonemal heavy chain 8 Homo sapiens 264-270 132437-19 1976 7; When the enzymatic state was changed from MgE to MfEATP 10 min after starting the reaction with TBS, about 3 moles of TBS was bound per mole of ATPase within 10 min, while the maximum levels of TBS bound in states MgE and MgEATP were about 2 and 1 moles per mole of ATPase, respectively, as mentioned above. Trinitrobenzenesulfonic Acid 99-102 dynein axonemal heavy chain 8 Homo sapiens 147-153 132437-19 1976 7; When the enzymatic state was changed from MgE to MfEATP 10 min after starting the reaction with TBS, about 3 moles of TBS was bound per mole of ATPase within 10 min, while the maximum levels of TBS bound in states MgE and MgEATP were about 2 and 1 moles per mole of ATPase, respectively, as mentioned above. Trinitrobenzenesulfonic Acid 99-102 dynein axonemal heavy chain 8 Homo sapiens 269-275 132437-19 1976 7; When the enzymatic state was changed from MgE to MfEATP 10 min after starting the reaction with TBS, about 3 moles of TBS was bound per mole of ATPase within 10 min, while the maximum levels of TBS bound in states MgE and MgEATP were about 2 and 1 moles per mole of ATPase, respectively, as mentioned above. Trinitrobenzenesulfonic Acid 121-124 dynein axonemal heavy chain 8 Homo sapiens 147-153 132437-19 1976 7; When the enzymatic state was changed from MgE to MfEATP 10 min after starting the reaction with TBS, about 3 moles of TBS was bound per mole of ATPase within 10 min, while the maximum levels of TBS bound in states MgE and MgEATP were about 2 and 1 moles per mole of ATPase, respectively, as mentioned above. Trinitrobenzenesulfonic Acid 121-124 dynein axonemal heavy chain 8 Homo sapiens 269-275 132437-19 1976 7; When the enzymatic state was changed from MgE to MfEATP 10 min after starting the reaction with TBS, about 3 moles of TBS was bound per mole of ATPase within 10 min, while the maximum levels of TBS bound in states MgE and MgEATP were about 2 and 1 moles per mole of ATPase, respectively, as mentioned above. Trinitrobenzenesulfonic Acid 121-124 dynein axonemal heavy chain 8 Homo sapiens 147-153 132437-19 1976 7; When the enzymatic state was changed from MgE to MfEATP 10 min after starting the reaction with TBS, about 3 moles of TBS was bound per mole of ATPase within 10 min, while the maximum levels of TBS bound in states MgE and MgEATP were about 2 and 1 moles per mole of ATPase, respectively, as mentioned above. Trinitrobenzenesulfonic Acid 121-124 dynein axonemal heavy chain 8 Homo sapiens 269-275 132437-21 1976 When the enzymatic state was changed from CaECa to CaECap 10 min after starting the reaction with TBS, about 4 moles of TBS was bound per mole of ATPase, while the maximum levels of TBS bound in states CaECa and CaECap were about 3 or 4 moles per mole of ATPase, respectively. Trinitrobenzenesulfonic Acid 98-101 dynein axonemal heavy chain 8 Homo sapiens 146-152 132437-21 1976 When the enzymatic state was changed from CaECa to CaECap 10 min after starting the reaction with TBS, about 4 moles of TBS was bound per mole of ATPase, while the maximum levels of TBS bound in states CaECa and CaECap were about 3 or 4 moles per mole of ATPase, respectively. Trinitrobenzenesulfonic Acid 120-123 dynein axonemal heavy chain 8 Homo sapiens 146-152 132437-21 1976 When the enzymatic state was changed from CaECa to CaECap 10 min after starting the reaction with TBS, about 4 moles of TBS was bound per mole of ATPase, while the maximum levels of TBS bound in states CaECa and CaECap were about 3 or 4 moles per mole of ATPase, respectively. Trinitrobenzenesulfonic Acid 120-123 dynein axonemal heavy chain 8 Homo sapiens 255-261 132437-21 1976 When the enzymatic state was changed from CaECa to CaECap 10 min after starting the reaction with TBS, about 4 moles of TBS was bound per mole of ATPase, while the maximum levels of TBS bound in states CaECa and CaECap were about 3 or 4 moles per mole of ATPase, respectively. Trinitrobenzenesulfonic Acid 120-123 dynein axonemal heavy chain 8 Homo sapiens 146-152 132437-21 1976 When the enzymatic state was changed from CaECa to CaECap 10 min after starting the reaction with TBS, about 4 moles of TBS was bound per mole of ATPase, while the maximum levels of TBS bound in states CaECa and CaECap were about 3 or 4 moles per mole of ATPase, respectively. Trinitrobenzenesulfonic Acid 120-123 dynein axonemal heavy chain 8 Homo sapiens 255-261 1175611-10 1975 Chlorothricin decreases the rate of inactivation observed when rat liver pyruvate carboxylase is incubated with trinitrobenzenesulfonate and when chicken liver pyruvate carboxylase is incubated at 2 degrees C. The maximal decrease in inactivation observed in the presence of saturating concentrations of antibiotic is 50% for cold inactivation of the chicken liver enzyme and 60% for inactivation of the enzyme from rat liver by trinitrobenzenesulfonate. Trinitrobenzenesulfonic Acid 112-136 pyruvate carboxylase Rattus norvegicus 73-93 5011008-0 1972 Reaction of human serum albumin and human erythrocytes with tritiated 2,4,6-trinitrobenzenesulfonic acid and tritiated picryl chloride. Trinitrobenzenesulfonic Acid 70-104 albumin Homo sapiens 24-31 1140888-1 1975 Human serum albumin has been modified with 2,4,6-trinitrobenzenesulphonic acid and picryl chloride in low ratios of reagents/albumin. Trinitrobenzenesulfonic Acid 43-78 albumin Homo sapiens 6-19 5114914-0 1971 The use of trinitrobenzenesulfonic acid in studies on the binding of fatty acid anions to bovine serum albumin. Trinitrobenzenesulfonic Acid 11-39 albumin Homo sapiens 97-110 34059101-10 2021 The expression of multiple inflammatory factors, including il1beta, clcx8a, mmp and tnfalpha, were increased in TNBS-treated fish, which were variously inhibited by the compounds, with aesculin showing the most potent effects. Trinitrobenzenesulfonic Acid 112-116 tumor necrosis factor a (TNF superfamily, member 2) Danio rerio 84-92 5667253-10 1968 The reactions of insulin, chymotrypsinogen and ribonuclease with 2,4,6-trinitrobenzenesulphonic acid were analysed in terms of three exponential rate curves, each referring to one or more amino groups of the proteins. Trinitrobenzenesulfonic Acid 65-100 insulin Homo sapiens 17-24 33676036-5 2021 One of these proteins, subsequently named Na-AIP-1, was effective at suppressing disease when administered prophylactically in the acute TNBS-induced model of colitis. Trinitrobenzenesulfonic Acid 137-141 membrane associated guanylate kinase, WW and PDZ domain containing 2 Mus musculus 45-50 34042286-12 2021 Our data reveal a novel mechanism that a decreased miR-128-3p level in TNBS-induced colitis could inhibit production of inflammatory factors, which activates NF-kappaB signaling by targeting TRAF6. Trinitrobenzenesulfonic Acid 71-75 TNF receptor associated factor 6 Rattus norvegicus 191-196 33201214-10 2021 Intracolonic administration of the thrombin inhibitor Dabigatran, as well as inhibition of protease-activated receptor-1, prevented trinitrobenzene sulfonic acid-induced colitis in rodent models. Trinitrobenzenesulfonic Acid 132-161 coagulation factor II Mus musculus 35-43 33667522-2 2021 The present study aimed to investigate the potential of linagliptin, a potent/selective DPP-4 inhibitor with marked anti-inflammatory actions, to attenuate trinitrobenzene sulfonic acid (TNBS)-evoked colitis in rats; an experimental model of IBD, and the implicated molecular mechanisms. Trinitrobenzenesulfonic Acid 187-191 dipeptidylpeptidase 4 Rattus norvegicus 88-93 34042266-0 2021 Eriodictyol attenuates TNBS-induced ulcerative colitis through repressing TLR4/NF-kB signaling pathway in rats. Trinitrobenzenesulfonic Acid 23-27 toll-like receptor 4 Rattus norvegicus 74-78 34042266-0 2021 Eriodictyol attenuates TNBS-induced ulcerative colitis through repressing TLR4/NF-kB signaling pathway in rats. Trinitrobenzenesulfonic Acid 23-27 RELA proto-oncogene, NF-kB subunit Rattus norvegicus 79-84 34042266-13 2021 Moreover, EDT regulated TNBS-induced TLR4/NF-kappaB pathway activation, therefore inhibiting the progression of UC. Trinitrobenzenesulfonic Acid 24-28 toll-like receptor 4 Rattus norvegicus 37-41 34042286-0 2021 MiR-128-3p alleviates TNBS-induced colitis through inactivating TRAF6/NF-kappaB signaling pathway in rats. Trinitrobenzenesulfonic Acid 22-26 TNF receptor associated factor 6 Rattus norvegicus 64-69 34051231-7 2021 Acan1 and Nak1 displayed anticolitic properties via significantly reducing weight loss and colon atrophy, oedema, ulceration, and necrosis in 2,4,6-trinitrobenzene sulfonic acid exposed mice. Trinitrobenzenesulfonic Acid 142-177 nuclear receptor subfamily 4 group A member 1 Homo sapiens 10-14 33201214-10 2021 Intracolonic administration of the thrombin inhibitor Dabigatran, as well as inhibition of protease-activated receptor-1, prevented trinitrobenzene sulfonic acid-induced colitis in rodent models. Trinitrobenzenesulfonic Acid 132-161 coagulation factor II thrombin receptor Homo sapiens 91-120 33759562-5 2021 HIF-1alpha inhibitors treatments ameliorated 2,4,6-trinitrobenzenesulfonic acid (TNBS)- or dextran sulfate sodium (DSS)-induced colitis in animal models. Trinitrobenzenesulfonic Acid 45-79 hypoxia inducible factor 1 subunit alpha Homo sapiens 0-10 33759562-5 2021 HIF-1alpha inhibitors treatments ameliorated 2,4,6-trinitrobenzenesulfonic acid (TNBS)- or dextran sulfate sodium (DSS)-induced colitis in animal models. Trinitrobenzenesulfonic Acid 81-85 hypoxia inducible factor 1 subunit alpha Homo sapiens 0-10 33245673-10 2021 Article Highlights No single model of colitis can predict clinical efficacy in UC, however some, like the mdr1a-/- and the chronic TNBS models have proven insightful in dissecting mechanism-of-action of potential therapeutic targets such as IL13, IL12/IL23 and IL-17. Trinitrobenzenesulfonic Acid 131-135 interleukin 13 Homo sapiens 241-245 33506998-11 2021 The vast majority of TNB and PVNB were non-MYCN amplified (100% and 86%, respectively) and carried better prognosis (OS 86% and 83%, respectively). Trinitrobenzenesulfonic Acid 21-24 MYCN proto-oncogene, bHLH transcription factor Homo sapiens 43-47 33461587-0 2021 Anemoside B4 ameliorates TNBS-induced colitis through S100A9/MAPK/NF-kappaB signaling pathway. Trinitrobenzenesulfonic Acid 25-29 nuclear factor kappa B subunit 1 Homo sapiens 66-75 33880135-7 2021 The number of EphB1- and p-EphB1-immunopositive cells, the average optical (AO) value of EphB1, and its phosphorylated form in the spinal dorsal horn were significantly increased in the TNBS group than in the control group, but they were obviously reduced by intrathecal administration of EphB2-Fc. Trinitrobenzenesulfonic Acid 186-190 Eph receptor B1 Rattus norvegicus 27-32 33880135-7 2021 The number of EphB1- and p-EphB1-immunopositive cells, the average optical (AO) value of EphB1, and its phosphorylated form in the spinal dorsal horn were significantly increased in the TNBS group than in the control group, but they were obviously reduced by intrathecal administration of EphB2-Fc. Trinitrobenzenesulfonic Acid 186-190 Eph receptor B1 Rattus norvegicus 27-32 33880135-7 2021 The number of EphB1- and p-EphB1-immunopositive cells, the average optical (AO) value of EphB1, and its phosphorylated form in the spinal dorsal horn were significantly increased in the TNBS group than in the control group, but they were obviously reduced by intrathecal administration of EphB2-Fc. Trinitrobenzenesulfonic Acid 186-190 Eph receptor B2 Rattus norvegicus 289-294 33125572-0 2021 Oridonin Attenuates TNBS-induced Post-inflammatory Irritable Bowel Syndrome via PXR/NF-kappaB Signaling. Trinitrobenzenesulfonic Acid 20-24 nuclear receptor subfamily 1 group I member 2 Homo sapiens 80-83 33125572-0 2021 Oridonin Attenuates TNBS-induced Post-inflammatory Irritable Bowel Syndrome via PXR/NF-kappaB Signaling. Trinitrobenzenesulfonic Acid 20-24 nuclear factor kappa B subunit 1 Homo sapiens 84-93 33711031-8 2021 Chemogenetic inhibition of primary afferent pathway that was governed by Nav1.8-expressing cells attenuated TNBS-induced up-regulations of AICP, DeltaP/Deltat, and colonic pain behavior in response to CRD. Trinitrobenzenesulfonic Acid 108-112 sodium channel, voltage-gated, type X, alpha Mus musculus 73-79 32996043-10 2021 ASE 100 mg/kg significantly reduced TNBS-induced expression of the TLR4, COX-2 and NF-kappaB p65. Trinitrobenzenesulfonic Acid 36-40 toll-like receptor 4 Rattus norvegicus 67-71 32996043-10 2021 ASE 100 mg/kg significantly reduced TNBS-induced expression of the TLR4, COX-2 and NF-kappaB p65. Trinitrobenzenesulfonic Acid 36-40 cytochrome c oxidase II, mitochondrial Rattus norvegicus 73-78 32996043-10 2021 ASE 100 mg/kg significantly reduced TNBS-induced expression of the TLR4, COX-2 and NF-kappaB p65. Trinitrobenzenesulfonic Acid 36-40 synaptotagmin 1 Rattus norvegicus 93-96 33461587-0 2021 Anemoside B4 ameliorates TNBS-induced colitis through S100A9/MAPK/NF-kappaB signaling pathway. Trinitrobenzenesulfonic Acid 25-29 S100 calcium binding protein A9 Rattus norvegicus 54-60 33522063-0 2021 Cinnamaldehyde and hesperetin attenuate TNBS-induced ulcerative colitis in rats through modulation of the JAk2/STAT3/SOCS3 pathway. Trinitrobenzenesulfonic Acid 40-44 Janus kinase 2 Rattus norvegicus 106-110 33522063-0 2021 Cinnamaldehyde and hesperetin attenuate TNBS-induced ulcerative colitis in rats through modulation of the JAk2/STAT3/SOCS3 pathway. Trinitrobenzenesulfonic Acid 40-44 signal transducer and activator of transcription 3 Rattus norvegicus 111-116 33522063-0 2021 Cinnamaldehyde and hesperetin attenuate TNBS-induced ulcerative colitis in rats through modulation of the JAk2/STAT3/SOCS3 pathway. Trinitrobenzenesulfonic Acid 40-44 suppressor of cytokine signaling 3 Rattus norvegicus 117-122 33522063-8 2021 In conclusion, cinnamaldehyde and hesperetin counteracted TNBS-induced ulcerative colitis through antioxidant, anti-inflammatory properties as well as modulation of the JAk2/STAT3/SOCS3 pathway. Trinitrobenzenesulfonic Acid 58-62 Janus kinase 2 Rattus norvegicus 169-173 33522063-8 2021 In conclusion, cinnamaldehyde and hesperetin counteracted TNBS-induced ulcerative colitis through antioxidant, anti-inflammatory properties as well as modulation of the JAk2/STAT3/SOCS3 pathway. Trinitrobenzenesulfonic Acid 58-62 signal transducer and activator of transcription 3 Rattus norvegicus 174-179 33522063-8 2021 In conclusion, cinnamaldehyde and hesperetin counteracted TNBS-induced ulcerative colitis through antioxidant, anti-inflammatory properties as well as modulation of the JAk2/STAT3/SOCS3 pathway. Trinitrobenzenesulfonic Acid 58-62 suppressor of cytokine signaling 3 Rattus norvegicus 180-185 33880135-6 2021 The spinal expressions of EphB1, p-EphB1, ephrinB2, and p-ephrinB2 were significantly increased in the TNBS group compared with the control group, but visceral hyperalgesia and elevation of spinal EphB1 and p-EphB1 expressions were evidently alleviated by intrathecal administration of EphB2-Fc in the TNBS + EphB2-Fc group. Trinitrobenzenesulfonic Acid 103-107 Eph receptor B1 Rattus norvegicus 26-31 33880135-6 2021 The spinal expressions of EphB1, p-EphB1, ephrinB2, and p-ephrinB2 were significantly increased in the TNBS group compared with the control group, but visceral hyperalgesia and elevation of spinal EphB1 and p-EphB1 expressions were evidently alleviated by intrathecal administration of EphB2-Fc in the TNBS + EphB2-Fc group. Trinitrobenzenesulfonic Acid 103-107 Eph receptor B1 Rattus norvegicus 35-40 33880135-6 2021 The spinal expressions of EphB1, p-EphB1, ephrinB2, and p-ephrinB2 were significantly increased in the TNBS group compared with the control group, but visceral hyperalgesia and elevation of spinal EphB1 and p-EphB1 expressions were evidently alleviated by intrathecal administration of EphB2-Fc in the TNBS + EphB2-Fc group. Trinitrobenzenesulfonic Acid 103-107 ephrin B2 Rattus norvegicus 42-50 33880135-6 2021 The spinal expressions of EphB1, p-EphB1, ephrinB2, and p-ephrinB2 were significantly increased in the TNBS group compared with the control group, but visceral hyperalgesia and elevation of spinal EphB1 and p-EphB1 expressions were evidently alleviated by intrathecal administration of EphB2-Fc in the TNBS + EphB2-Fc group. Trinitrobenzenesulfonic Acid 103-107 ephrin B2 Rattus norvegicus 58-66 33880135-6 2021 The spinal expressions of EphB1, p-EphB1, ephrinB2, and p-ephrinB2 were significantly increased in the TNBS group compared with the control group, but visceral hyperalgesia and elevation of spinal EphB1 and p-EphB1 expressions were evidently alleviated by intrathecal administration of EphB2-Fc in the TNBS + EphB2-Fc group. Trinitrobenzenesulfonic Acid 103-107 Eph receptor B1 Rattus norvegicus 35-40 33880135-6 2021 The spinal expressions of EphB1, p-EphB1, ephrinB2, and p-ephrinB2 were significantly increased in the TNBS group compared with the control group, but visceral hyperalgesia and elevation of spinal EphB1 and p-EphB1 expressions were evidently alleviated by intrathecal administration of EphB2-Fc in the TNBS + EphB2-Fc group. Trinitrobenzenesulfonic Acid 103-107 Eph receptor B1 Rattus norvegicus 35-40 33880135-6 2021 The spinal expressions of EphB1, p-EphB1, ephrinB2, and p-ephrinB2 were significantly increased in the TNBS group compared with the control group, but visceral hyperalgesia and elevation of spinal EphB1 and p-EphB1 expressions were evidently alleviated by intrathecal administration of EphB2-Fc in the TNBS + EphB2-Fc group. Trinitrobenzenesulfonic Acid 103-107 Eph receptor B2 Rattus norvegicus 286-291 33880135-6 2021 The spinal expressions of EphB1, p-EphB1, ephrinB2, and p-ephrinB2 were significantly increased in the TNBS group compared with the control group, but visceral hyperalgesia and elevation of spinal EphB1 and p-EphB1 expressions were evidently alleviated by intrathecal administration of EphB2-Fc in the TNBS + EphB2-Fc group. Trinitrobenzenesulfonic Acid 103-107 Eph receptor B2 Rattus norvegicus 309-314 33880135-7 2021 The number of EphB1- and p-EphB1-immunopositive cells, the average optical (AO) value of EphB1, and its phosphorylated form in the spinal dorsal horn were significantly increased in the TNBS group than in the control group, but they were obviously reduced by intrathecal administration of EphB2-Fc. Trinitrobenzenesulfonic Acid 186-190 Eph receptor B1 Rattus norvegicus 14-19 33533318-0 2021 Optical clearing reveals TNBS-induced morphological changes of VGLUT2-positive nerve fibers in mouse colorectum. Trinitrobenzenesulfonic Acid 25-29 solute carrier family 17 (sodium-dependent inorganic phosphate cotransporter), member 6 Mus musculus 63-69 33533318-7 2021 Intracolonic TNBS treatment significantly reduced the number of VGLUT2-positive nerve fibers in submucosal, myenteric plexus, and mucosal layers at day 7 post TNBS, which mostly recovered by day 28. Trinitrobenzenesulfonic Acid 13-17 solute carrier family 17 (sodium-dependent inorganic phosphate cotransporter), member 6 Mus musculus 64-70 33533318-10 2021 Altogether, the present morphological study reveals profound changes in the distribution of VGLUT2-positive fibers in mouse colorectum undergoing TNBS-induced colitis, and draw attention to curvy fibers in the submucosa with potential roles in visceral nociception. Trinitrobenzenesulfonic Acid 146-150 solute carrier family 17 (sodium-dependent inorganic phosphate cotransporter), member 6 Mus musculus 92-98 33647259-9 2021 MPO and MDA were reduced by up to 61.69% and 92.45%, respectively, compared to TNBS-treated rats alone. Trinitrobenzenesulfonic Acid 79-83 myeloperoxidase Rattus norvegicus 0-3 33717161-6 2021 Here, we show that treatment with LD IL-2 reduced 2,4,6-trinitrobenzensulfonic acid (TNBS) colitis severity in NOD.PrkdcscidIl2rg-/- (NSG) mice reconstituted with human CD34+ hematopoietic stem cells. Trinitrobenzenesulfonic Acid 85-89 interleukin 2 Mus musculus 37-41 33461587-20 2021 CONCLUSIONS: Our results demonstrate that anemoside B4 prevents TNBS-induced colitis by inhibiting the NF-kappaB signaling pathway through deactivating S100A9, suggesting that anemoside B4 is a promising therapeutic candidate for colitis. Trinitrobenzenesulfonic Acid 64-68 nuclear factor kappa B subunit 1 Homo sapiens 103-112 33461587-20 2021 CONCLUSIONS: Our results demonstrate that anemoside B4 prevents TNBS-induced colitis by inhibiting the NF-kappaB signaling pathway through deactivating S100A9, suggesting that anemoside B4 is a promising therapeutic candidate for colitis. Trinitrobenzenesulfonic Acid 64-68 S100 calcium binding protein A9 Homo sapiens 152-158 33100902-11 2020 Moreover, the expression of Ang II, ACE2, Ang (1-7), IL-17A, and IL-10 in the TNBS group increased compared to that in the control group. Trinitrobenzenesulfonic Acid 78-82 angiotensin I converting enzyme (peptidyl-dipeptidase A) 2 Mus musculus 36-40 32473073-0 2020 Invasive Lactococcus lactis producing mycobacterial Hsp65 ameliorates intestinal inflammation in acute TNBS-induced colitis in mice by increasing the levels of the cytokine IL-10 and secretory IgA. Trinitrobenzenesulfonic Acid 103-107 heat shock protein family D (Hsp60) member 1 Homo sapiens 52-57 33100902-1 2020 Aim: To explore the treatment effect of mica on 2,4,6-trinitrobenzenesulfonic acid solution- (TNBS-) induced colitis in mice. Trinitrobenzenesulfonic Acid 48-82 inhibitor of carbonic anhydrase Mus musculus 40-44 33100902-1 2020 Aim: To explore the treatment effect of mica on 2,4,6-trinitrobenzenesulfonic acid solution- (TNBS-) induced colitis in mice. Trinitrobenzenesulfonic Acid 94-98 inhibitor of carbonic anhydrase Mus musculus 40-44 33100902-9 2020 Results: Food intake, activity, and body weight gradually decreased in the TNBS group compared to the control group and the mica group (all P < 0.05). Trinitrobenzenesulfonic Acid 75-79 inhibitor of carbonic anhydrase Mus musculus 124-128 33100902-11 2020 Moreover, the expression of Ang II, ACE2, Ang (1-7), IL-17A, and IL-10 in the TNBS group increased compared to that in the control group. Trinitrobenzenesulfonic Acid 78-82 angiotensinogen (serpin peptidase inhibitor, clade A, member 8) Mus musculus 28-34 32597970-3 2020 The aim of this study is to investigate the effect and the mechanism of RNF8 on UC model induced by trinitrobenzene sulfonic acid (TNBS) in mice. Trinitrobenzenesulfonic Acid 100-129 ring finger protein 8 Mus musculus 72-76 32597970-3 2020 The aim of this study is to investigate the effect and the mechanism of RNF8 on UC model induced by trinitrobenzene sulfonic acid (TNBS) in mice. Trinitrobenzenesulfonic Acid 131-135 ring finger protein 8 Mus musculus 72-76 32597970-10 2020 The TNBS-induced UC mice exhibited colonic damage and inflammation, accompanied by decreased RNF8 expression, impaired autophagy, and increased phosphorylation levels of AKT and mTOR in the colon. Trinitrobenzenesulfonic Acid 4-8 ring finger protein 8 Mus musculus 93-97 32597970-10 2020 The TNBS-induced UC mice exhibited colonic damage and inflammation, accompanied by decreased RNF8 expression, impaired autophagy, and increased phosphorylation levels of AKT and mTOR in the colon. Trinitrobenzenesulfonic Acid 4-8 thymoma viral proto-oncogene 1 Mus musculus 170-173 32597970-10 2020 The TNBS-induced UC mice exhibited colonic damage and inflammation, accompanied by decreased RNF8 expression, impaired autophagy, and increased phosphorylation levels of AKT and mTOR in the colon. Trinitrobenzenesulfonic Acid 4-8 mechanistic target of rapamycin kinase Mus musculus 178-182 32597970-13 2020 Collectively, RNF8 overexpression protects against TNBS-induced UC, which might be due to its enhancement of autophagy by suppressing the AKT/mTOR signaling via AKT1 ubiquitination. Trinitrobenzenesulfonic Acid 51-55 ring finger protein 8 Mus musculus 14-18 32597970-13 2020 Collectively, RNF8 overexpression protects against TNBS-induced UC, which might be due to its enhancement of autophagy by suppressing the AKT/mTOR signaling via AKT1 ubiquitination. Trinitrobenzenesulfonic Acid 51-55 thymoma viral proto-oncogene 1 Mus musculus 138-141 32597970-13 2020 Collectively, RNF8 overexpression protects against TNBS-induced UC, which might be due to its enhancement of autophagy by suppressing the AKT/mTOR signaling via AKT1 ubiquitination. Trinitrobenzenesulfonic Acid 51-55 mechanistic target of rapamycin kinase Mus musculus 142-146 32597970-13 2020 Collectively, RNF8 overexpression protects against TNBS-induced UC, which might be due to its enhancement of autophagy by suppressing the AKT/mTOR signaling via AKT1 ubiquitination. Trinitrobenzenesulfonic Acid 51-55 thymoma viral proto-oncogene 1 Mus musculus 161-165 33100902-11 2020 Moreover, the expression of Ang II, ACE2, Ang (1-7), IL-17A, and IL-10 in the TNBS group increased compared to that in the control group. Trinitrobenzenesulfonic Acid 78-82 angiogenin, ribonuclease, RNase A family, 5 Mus musculus 42-50 33100902-11 2020 Moreover, the expression of Ang II, ACE2, Ang (1-7), IL-17A, and IL-10 in the TNBS group increased compared to that in the control group. Trinitrobenzenesulfonic Acid 78-82 interleukin 17A Mus musculus 53-59 33100902-11 2020 Moreover, the expression of Ang II, ACE2, Ang (1-7), IL-17A, and IL-10 in the TNBS group increased compared to that in the control group. Trinitrobenzenesulfonic Acid 78-82 interleukin 10 Mus musculus 65-70 33100902-12 2020 Compared to the TNBS group, ACE2, Ang (1-7), and IL-10 in the mica group increased, while Ang II and IL-17A decreased (all P < 0.05). Trinitrobenzenesulfonic Acid 16-20 inhibitor of carbonic anhydrase Mus musculus 62-66 33100902-13 2020 Conclusion: Mica can alleviate TNBS-induced colitis in mice by regulating the inflammation process; it reduces Ang II and IL-17A and increases ACE2, IL-10, and Ang (1-7). Trinitrobenzenesulfonic Acid 31-35 inhibitor of carbonic anhydrase Mus musculus 12-16 32607693-3 2020 Expressions of miRNAs and aryl hydrocarbon receptor (AHR) protein were determined in the colitic colon of 2,4,6-trinitrobenzenesulfonic acid (TNBS)-induced colitis mice and CD patients. Trinitrobenzenesulfonic Acid 142-146 aryl-hydrocarbon receptor Mus musculus 53-56 32892648-7 2020 Significant reduced levels of TNF- , IL-6 and IL-10 in drug treated animals signifies inhibition of inflammatory reactions at the TNBS treated site. Trinitrobenzenesulfonic Acid 130-134 tumor necrosis factor Oryctolagus cuniculus 30-33 32892648-7 2020 Significant reduced levels of TNF- , IL-6 and IL-10 in drug treated animals signifies inhibition of inflammatory reactions at the TNBS treated site. Trinitrobenzenesulfonic Acid 130-134 interleukin-6 Oryctolagus cuniculus 37-41 32892648-7 2020 Significant reduced levels of TNF- , IL-6 and IL-10 in drug treated animals signifies inhibition of inflammatory reactions at the TNBS treated site. Trinitrobenzenesulfonic Acid 130-134 interleukin-10 Oryctolagus cuniculus 46-51 32607693-7 2020 MiR-124a-Nju and AHR-/- mice treated with TNBS had more severe intestinal inflammation than WT mice. Trinitrobenzenesulfonic Acid 42-46 microRNA 124-1 Homo sapiens 0-8 32607693-7 2020 MiR-124a-Nju and AHR-/- mice treated with TNBS had more severe intestinal inflammation than WT mice. Trinitrobenzenesulfonic Acid 42-46 aryl-hydrocarbon receptor Mus musculus 17-20 32396274-0 2020 Inhibition of proprotein convertase subtilisin/kexin type 9 attenuates 2,4,6-trinitrobenzenesulfonic acid-induced colitis via repressing toll-like receptor 4/nuclear factor-kappa B. Trinitrobenzenesulfonic Acid 71-105 proprotein convertase subtilisin/kexin type 9 Rattus norvegicus 14-59 33062594-6 2020 Also, the IFN-gamma, IL-1beta, IL-6, Il-23, TNF-alpha, CCL-17, and NF-kB mRNA and protein levels were increased significantly from 1.86-4.91-fold and 1.46-5.50-fold, respectively, in the TNBS-instigated colitis group as compared to the control. Trinitrobenzenesulfonic Acid 187-191 interferon gamma Rattus norvegicus 10-19 33062594-6 2020 Also, the IFN-gamma, IL-1beta, IL-6, Il-23, TNF-alpha, CCL-17, and NF-kB mRNA and protein levels were increased significantly from 1.86-4.91-fold and 1.46-5.50-fold, respectively, in the TNBS-instigated colitis group as compared to the control. Trinitrobenzenesulfonic Acid 187-191 tumor necrosis factor Rattus norvegicus 44-53 33062594-6 2020 Also, the IFN-gamma, IL-1beta, IL-6, Il-23, TNF-alpha, CCL-17, and NF-kB mRNA and protein levels were increased significantly from 1.86-4.91-fold and 1.46-5.50-fold, respectively, in the TNBS-instigated colitis group as compared to the control. Trinitrobenzenesulfonic Acid 187-191 C-C motif chemokine ligand 17 Rattus norvegicus 55-61 33062594-6 2020 Also, the IFN-gamma, IL-1beta, IL-6, Il-23, TNF-alpha, CCL-17, and NF-kB mRNA and protein levels were increased significantly from 1.86-4.91-fold and 1.46-5.50-fold, respectively, in the TNBS-instigated colitis group as compared to the control. Trinitrobenzenesulfonic Acid 187-191 nuclear factor kappa B subunit 1 Rattus norvegicus 67-72 32525764-5 2020 Diosgenin significantly decreased (p < 0.05) TNBS-induced elevated colonic oxido-nitrosative damage, myeloperoxidase, hydroxyproline, mRNA expressions of proinflammatory cytokines (TNF-alpha, IL-1beta, IL-6, and IFN-gamma) and inflammatory markers (iNOs and COX-2) induced by TNBS. Trinitrobenzenesulfonic Acid 45-49 myeloperoxidase Rattus norvegicus 101-116 32525764-5 2020 Diosgenin significantly decreased (p < 0.05) TNBS-induced elevated colonic oxido-nitrosative damage, myeloperoxidase, hydroxyproline, mRNA expressions of proinflammatory cytokines (TNF-alpha, IL-1beta, IL-6, and IFN-gamma) and inflammatory markers (iNOs and COX-2) induced by TNBS. Trinitrobenzenesulfonic Acid 45-49 tumor necrosis factor Rattus norvegicus 181-190 32525764-5 2020 Diosgenin significantly decreased (p < 0.05) TNBS-induced elevated colonic oxido-nitrosative damage, myeloperoxidase, hydroxyproline, mRNA expressions of proinflammatory cytokines (TNF-alpha, IL-1beta, IL-6, and IFN-gamma) and inflammatory markers (iNOs and COX-2) induced by TNBS. Trinitrobenzenesulfonic Acid 45-49 interleukin 1 alpha Rattus norvegicus 192-200 32525764-5 2020 Diosgenin significantly decreased (p < 0.05) TNBS-induced elevated colonic oxido-nitrosative damage, myeloperoxidase, hydroxyproline, mRNA expressions of proinflammatory cytokines (TNF-alpha, IL-1beta, IL-6, and IFN-gamma) and inflammatory markers (iNOs and COX-2) induced by TNBS. Trinitrobenzenesulfonic Acid 45-49 interleukin 6 Rattus norvegicus 202-206 32525764-5 2020 Diosgenin significantly decreased (p < 0.05) TNBS-induced elevated colonic oxido-nitrosative damage, myeloperoxidase, hydroxyproline, mRNA expressions of proinflammatory cytokines (TNF-alpha, IL-1beta, IL-6, and IFN-gamma) and inflammatory markers (iNOs and COX-2) induced by TNBS. Trinitrobenzenesulfonic Acid 45-49 interferon gamma Rattus norvegicus 212-221 32525764-5 2020 Diosgenin significantly decreased (p < 0.05) TNBS-induced elevated colonic oxido-nitrosative damage, myeloperoxidase, hydroxyproline, mRNA expressions of proinflammatory cytokines (TNF-alpha, IL-1beta, IL-6, and IFN-gamma) and inflammatory markers (iNOs and COX-2) induced by TNBS. Trinitrobenzenesulfonic Acid 45-49 nitric oxide synthase 2 Rattus norvegicus 249-253 32525764-5 2020 Diosgenin significantly decreased (p < 0.05) TNBS-induced elevated colonic oxido-nitrosative damage, myeloperoxidase, hydroxyproline, mRNA expressions of proinflammatory cytokines (TNF-alpha, IL-1beta, IL-6, and IFN-gamma) and inflammatory markers (iNOs and COX-2) induced by TNBS. Trinitrobenzenesulfonic Acid 45-49 cytochrome c oxidase II, mitochondrial Rattus norvegicus 258-263 32525764-6 2020 Western blot analysis relevated that TNBS-induced up-regulated protein expressions of NF-kappaB, IkappaBalpha, Bax, and Caspase-1 were markedly decreased (p < 0.05) by diosgenin treatment. Trinitrobenzenesulfonic Acid 37-41 NFKB inhibitor alpha Rattus norvegicus 97-109 32525764-6 2020 Western blot analysis relevated that TNBS-induced up-regulated protein expressions of NF-kappaB, IkappaBalpha, Bax, and Caspase-1 were markedly decreased (p < 0.05) by diosgenin treatment. Trinitrobenzenesulfonic Acid 37-41 BCL2 associated X, apoptosis regulator Rattus norvegicus 111-114 32525764-6 2020 Western blot analysis relevated that TNBS-induced up-regulated protein expressions of NF-kappaB, IkappaBalpha, Bax, and Caspase-1 were markedly decreased (p < 0.05) by diosgenin treatment. Trinitrobenzenesulfonic Acid 37-41 caspase 1 Rattus norvegicus 120-129 32682824-6 2020 Western blotting showed parallel upregulation of mature GDNF and MMP-9 vs control in ISMC isolated on Day 2 of TNBS-induced colitis. Trinitrobenzenesulfonic Acid 111-115 glial cell derived neurotrophic factor Rattus norvegicus 56-60 32682824-6 2020 Western blotting showed parallel upregulation of mature GDNF and MMP-9 vs control in ISMC isolated on Day 2 of TNBS-induced colitis. Trinitrobenzenesulfonic Acid 111-115 matrix metallopeptidase 9 Rattus norvegicus 65-70 32396274-5 2020 Results showed that treatment with TNBS induced a great body weight loss, MPO activity increase, and serious colonic damage, showing an obviously character of IBD. Trinitrobenzenesulfonic Acid 35-39 myeloperoxidase Rattus norvegicus 74-77 32396274-6 2020 PCSK9 was elevated in TNBS-induced rats, and PCSK9 inhibition delivered by adenovirus vector increased the body weight, decreased MPO activity, and ameliorated histological change of colon. Trinitrobenzenesulfonic Acid 22-26 proprotein convertase subtilisin/kexin type 9 Rattus norvegicus 0-5 32396274-7 2020 Second, the protective effect of PCSK9 inhibition against TNBS-induced colitis was accompanied by decrease of proinflammatory factors secretion, including tumor necrosis factor-alpha, interleukin-1beta, interleukin-6, intercellular adhesion molecule 1, and monocyte chemoattractant protein-1. Trinitrobenzenesulfonic Acid 58-62 proprotein convertase subtilisin/kexin type 9 Rattus norvegicus 33-38 32396274-7 2020 Second, the protective effect of PCSK9 inhibition against TNBS-induced colitis was accompanied by decrease of proinflammatory factors secretion, including tumor necrosis factor-alpha, interleukin-1beta, interleukin-6, intercellular adhesion molecule 1, and monocyte chemoattractant protein-1. Trinitrobenzenesulfonic Acid 58-62 intercellular adhesion molecule 1 Rattus norvegicus 218-251 32396274-7 2020 Second, the protective effect of PCSK9 inhibition against TNBS-induced colitis was accompanied by decrease of proinflammatory factors secretion, including tumor necrosis factor-alpha, interleukin-1beta, interleukin-6, intercellular adhesion molecule 1, and monocyte chemoattractant protein-1. Trinitrobenzenesulfonic Acid 58-62 C-C motif chemokine ligand 2 Rattus norvegicus 257-291 32396274-8 2020 TNBS could activate toll-like receptor 4 (TLR4)/nuclear factor-kappa B (NF-kappaB) signaling pathway, while PCSK9 inhibition suppressed activation of TLR4/NF-kappaB in TNBS-induced rats. Trinitrobenzenesulfonic Acid 0-4 toll-like receptor 4 Rattus norvegicus 20-40 32396274-8 2020 TNBS could activate toll-like receptor 4 (TLR4)/nuclear factor-kappa B (NF-kappaB) signaling pathway, while PCSK9 inhibition suppressed activation of TLR4/NF-kappaB in TNBS-induced rats. Trinitrobenzenesulfonic Acid 0-4 toll-like receptor 4 Rattus norvegicus 42-46 32396274-8 2020 TNBS could activate toll-like receptor 4 (TLR4)/nuclear factor-kappa B (NF-kappaB) signaling pathway, while PCSK9 inhibition suppressed activation of TLR4/NF-kappaB in TNBS-induced rats. Trinitrobenzenesulfonic Acid 168-172 proprotein convertase subtilisin/kexin type 9 Rattus norvegicus 108-113 32396274-8 2020 TNBS could activate toll-like receptor 4 (TLR4)/nuclear factor-kappa B (NF-kappaB) signaling pathway, while PCSK9 inhibition suppressed activation of TLR4/NF-kappaB in TNBS-induced rats. Trinitrobenzenesulfonic Acid 168-172 toll-like receptor 4 Rattus norvegicus 150-154 32396274-9 2020 In conclusion, PCSK9 inhibition attenuated TNBS-induced rat colitis through anti-inflammatory effect under inactivation of TLR4/NF-kappaB, suggesting potential therapeutic strategy in IBD. Trinitrobenzenesulfonic Acid 43-47 proprotein convertase subtilisin/kexin type 9 Rattus norvegicus 15-20 32396274-9 2020 In conclusion, PCSK9 inhibition attenuated TNBS-induced rat colitis through anti-inflammatory effect under inactivation of TLR4/NF-kappaB, suggesting potential therapeutic strategy in IBD. Trinitrobenzenesulfonic Acid 43-47 toll-like receptor 4 Rattus norvegicus 123-127 31960283-5 2020 Colon mitochondria of control mice were treated with 5 microM Cur, and TNBS (50, 100 microM)-toxicity was evaluated by measuring swelling, respiration, and aconitase and fumarase activities. Trinitrobenzenesulfonic Acid 71-75 fumarate hydratase 1 Mus musculus 170-178 32703418-8 2020 Increased colonic damage and myeloperoxidase activity after TNBS treatment are elevated by elaidate administration. Trinitrobenzenesulfonic Acid 60-64 myeloperoxidase Mus musculus 29-44 32703418-9 2020 Also, TNBS treatment induces IL-1beta production in colonic mucosa; elaidate administration enhances the induction. Trinitrobenzenesulfonic Acid 6-10 interleukin 1 alpha Mus musculus 29-37 32764411-7 2020 Intravenous administration of DNase I, an enzyme that dissolves the web-like DNA filaments of NETs, during colitis restored the mucosal barrier integrity which reduced the dissemination of luminal bacteria and attenuated intestinal inflammation in both DSS and TNBS models. Trinitrobenzenesulfonic Acid 261-265 deoxyribonuclease I Mus musculus 30-37 32322944-4 2020 We found the DAI scores were significantly increased in the TNBS-treated rats, while reduced in the baicalin-treated group in a dose-dependent manner, accompanied with the alleviation of mucosal injury, the reduction of ZO-1, Occludin, and MUC2 expression. Trinitrobenzenesulfonic Acid 60-64 tight junction protein 1 Rattus norvegicus 220-224 32774055-11 2020 GFP-ADSC delivery significantly antagonized TNBS-induced increased canonical Wnt pathway expression, decreased noncanonical Wnt signaling pathway expression, and increased apoptosis rates and protein level of cleaved caspase-3 in rats. Trinitrobenzenesulfonic Acid 44-48 caspase 3 Rattus norvegicus 217-226 32537016-0 2020 Baicalin alleviates TNBS-induced colitis by inhibiting PI3K/AKT pathway activation. Trinitrobenzenesulfonic Acid 20-24 AKT serine/threonine kinase 1 Homo sapiens 60-63 32537016-5 2020 In the present study, the results revealed that baicalin not only significantly alleviated TNBS-induced colitis by reducing the release of IL-6, TNF-alpha and IL-1beta and increasing the level of IL-10, but promoted the expression of tight-junction proteins ZO-1 and beta-catenin, which may have been achieved by blockage of the PI3K/AKT signaling pathway. Trinitrobenzenesulfonic Acid 91-95 interleukin 6 Homo sapiens 139-143 32537016-5 2020 In the present study, the results revealed that baicalin not only significantly alleviated TNBS-induced colitis by reducing the release of IL-6, TNF-alpha and IL-1beta and increasing the level of IL-10, but promoted the expression of tight-junction proteins ZO-1 and beta-catenin, which may have been achieved by blockage of the PI3K/AKT signaling pathway. Trinitrobenzenesulfonic Acid 91-95 tumor necrosis factor Homo sapiens 145-154 32537016-5 2020 In the present study, the results revealed that baicalin not only significantly alleviated TNBS-induced colitis by reducing the release of IL-6, TNF-alpha and IL-1beta and increasing the level of IL-10, but promoted the expression of tight-junction proteins ZO-1 and beta-catenin, which may have been achieved by blockage of the PI3K/AKT signaling pathway. Trinitrobenzenesulfonic Acid 91-95 tight junction protein 1 Homo sapiens 258-262 32537016-5 2020 In the present study, the results revealed that baicalin not only significantly alleviated TNBS-induced colitis by reducing the release of IL-6, TNF-alpha and IL-1beta and increasing the level of IL-10, but promoted the expression of tight-junction proteins ZO-1 and beta-catenin, which may have been achieved by blockage of the PI3K/AKT signaling pathway. Trinitrobenzenesulfonic Acid 91-95 catenin beta 1 Homo sapiens 267-279 32537016-5 2020 In the present study, the results revealed that baicalin not only significantly alleviated TNBS-induced colitis by reducing the release of IL-6, TNF-alpha and IL-1beta and increasing the level of IL-10, but promoted the expression of tight-junction proteins ZO-1 and beta-catenin, which may have been achieved by blockage of the PI3K/AKT signaling pathway. Trinitrobenzenesulfonic Acid 91-95 AKT serine/threonine kinase 1 Homo sapiens 334-337 32416455-7 2020 RESULTS: The results showed enhanced expression of Ly6G, citrullinated histone H3 (CitH3), and PAD4 in TNBS-induced colitis mice and higher ability of neutrophil to produce NETs in vitro. Trinitrobenzenesulfonic Acid 103-107 lymphocyte antigen 6 complex, locus G Mus musculus 51-55 32516975-3 2020 As the exact pathogenesis of IBD is still unknown and treatment options are limited, we aimed to investigate the effects of sigma1R in 2,4,6-trinitrobenzenesulfonic acid (TNBS)-induced experimental colitis. Trinitrobenzenesulfonic Acid 135-169 sigma non-opioid intracellular receptor 1 Rattus norvegicus 124-131 32516975-3 2020 As the exact pathogenesis of IBD is still unknown and treatment options are limited, we aimed to investigate the effects of sigma1R in 2,4,6-trinitrobenzenesulfonic acid (TNBS)-induced experimental colitis. Trinitrobenzenesulfonic Acid 171-175 sigma non-opioid intracellular receptor 1 Rattus norvegicus 124-131 32322944-4 2020 We found the DAI scores were significantly increased in the TNBS-treated rats, while reduced in the baicalin-treated group in a dose-dependent manner, accompanied with the alleviation of mucosal injury, the reduction of ZO-1, Occludin, and MUC2 expression. Trinitrobenzenesulfonic Acid 60-64 occludin Rattus norvegicus 226-234 32322944-4 2020 We found the DAI scores were significantly increased in the TNBS-treated rats, while reduced in the baicalin-treated group in a dose-dependent manner, accompanied with the alleviation of mucosal injury, the reduction of ZO-1, Occludin, and MUC2 expression. Trinitrobenzenesulfonic Acid 60-64 mucin 2, oligomeric mucus/gel-forming Rattus norvegicus 240-244 32124197-7 2020 A recent study has demonstrated that the treatment with anti-IL-17 antibody significantly alleviated 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colorectal fibrosis in mice by down-regulating the expression of collagen 3 and several pro-fibrogenic cytokines. Trinitrobenzenesulfonic Acid 101-136 interleukin 17A Mus musculus 61-66 32124197-7 2020 A recent study has demonstrated that the treatment with anti-IL-17 antibody significantly alleviated 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colorectal fibrosis in mice by down-regulating the expression of collagen 3 and several pro-fibrogenic cytokines. Trinitrobenzenesulfonic Acid 138-142 interleukin 17A Mus musculus 61-66 31536729-8 2019 Then, intrathecal injection of TRAF6 siRNA attenuated visceral pain, blocked the upregulation of pNF-kappaB, TNF-alpha and IL-1beta levels in the spinal cord in TNBS mice. Trinitrobenzenesulfonic Acid 161-165 TNF receptor-associated factor 6 Mus musculus 31-36 31771884-8 2020 We found that SAU ameliorated TNBS-induced mouse colitis and inflammatory responses in mucosal tissues and peripheral blood CD4+ T cells from IBD patients. Trinitrobenzenesulfonic Acid 30-34 CD4 antigen Mus musculus 124-127 31941937-7 2020 Acute intestinal inflammation due to DSS and TNBS was attenuated in IL-17A knockout mice, whereas chronic colitis was not relieved by T cell transfer from Il17a-/- mice (% of original body weight: wild-type mice vs. Il17a-/- mice, 81.9% vs. 82.2%; P = 0.922). Trinitrobenzenesulfonic Acid 45-49 interleukin 17A Mus musculus 68-74 30657050-8 2020 The increased level of Tumor necrosis factor (TNF ) an expression of colonic Inducible nitric oxide synthase (iNOS) was lowered in treatments as compared to TNBS control. Trinitrobenzenesulfonic Acid 157-161 tumor necrosis factor-like Rattus norvegicus 23-44 30657050-8 2020 The increased level of Tumor necrosis factor (TNF ) an expression of colonic Inducible nitric oxide synthase (iNOS) was lowered in treatments as compared to TNBS control. Trinitrobenzenesulfonic Acid 157-161 tumor necrosis factor-like Rattus norvegicus 46-49 30657050-8 2020 The increased level of Tumor necrosis factor (TNF ) an expression of colonic Inducible nitric oxide synthase (iNOS) was lowered in treatments as compared to TNBS control. Trinitrobenzenesulfonic Acid 157-161 nitric oxide synthase 2 Rattus norvegicus 77-108 30657050-8 2020 The increased level of Tumor necrosis factor (TNF ) an expression of colonic Inducible nitric oxide synthase (iNOS) was lowered in treatments as compared to TNBS control. Trinitrobenzenesulfonic Acid 157-161 nitric oxide synthase 2 Rattus norvegicus 110-114 31889078-1 2019 RNF183 is a ubiquitin ligase containing RING-finger and transmembrane domains, and its expression levels are increased in patients with inflammatory bowel disease (IBD), including Crohn"s disease and ulcerative colitis, and in 2,4,6-trinitrobenzene sulfonic acid-induced colitis mice. Trinitrobenzenesulfonic Acid 227-262 ring finger protein 183 Homo sapiens 0-6 32155506-9 2020 Results demonstrated that GPP attenuates inflammatory and oxidative response in TNBS-induced colitis by downregulating the nuclear factor kappa B pathway and upregulating antioxidant enzymes, with NEP-F being the fraction most likely associated to these protective effects. Trinitrobenzenesulfonic Acid 80-84 membrane metallo-endopeptidase Rattus norvegicus 197-200 32206003-5 2020 AIM: To investigate role of kynurenine 3-monooxygenase (KMO) in TNBS-induced colitis and involvement of Trp metabolites in maintenance of intestinal homeostasis. Trinitrobenzenesulfonic Acid 64-68 kynurenine 3-monooxygenase (kynurenine 3-hydroxylase) Mus musculus 28-54 32206003-5 2020 AIM: To investigate role of kynurenine 3-monooxygenase (KMO) in TNBS-induced colitis and involvement of Trp metabolites in maintenance of intestinal homeostasis. Trinitrobenzenesulfonic Acid 64-68 kynurenine 3-monooxygenase (kynurenine 3-hydroxylase) Mus musculus 56-59 32206003-10 2020 RESULTS: KMO expression levels in the colonic mononuclear phagocytes, including dendritic cells and macrophages increased upon TNBS induction. Trinitrobenzenesulfonic Acid 127-131 kynurenine 3-monooxygenase (kynurenine 3-hydroxylase) Mus musculus 9-12 32206003-11 2020 Notably, KMO deficiency reduced TNBS-induced colitis, resulting in an increased frequency of Foxp3+ regulatory T cells and increased mRNA and protein levels of anti-inflammatory cytokines, including transforming growth factor-beta and interleukin-10. Trinitrobenzenesulfonic Acid 32-36 kynurenine 3-monooxygenase (kynurenine 3-hydroxylase) Mus musculus 9-12 32206003-12 2020 CONCLUSION: Absence of KMO reduced TNBS-induced colitis via generation of Foxp3+ regulatory T cells by producing Kyn. Trinitrobenzenesulfonic Acid 35-39 kynurenine 3-monooxygenase (kynurenine 3-hydroxylase) Mus musculus 23-26 31913697-5 2020 Considering this possibility, we first explored if colitis regulated Olfr-78 expression in the gut, where we observed a significant reduction in the expression of Olfr-78 transcript in mouse models of dextran sodium sulfate (DSS)- and 2,4,6-trinitrobenzenesulfonic acid (TNBS)-induced colitis. Trinitrobenzenesulfonic Acid 235-269 olfactory receptor family 51 subfamily E member 2 Mus musculus 163-170 31913697-5 2020 Considering this possibility, we first explored if colitis regulated Olfr-78 expression in the gut, where we observed a significant reduction in the expression of Olfr-78 transcript in mouse models of dextran sodium sulfate (DSS)- and 2,4,6-trinitrobenzenesulfonic acid (TNBS)-induced colitis. Trinitrobenzenesulfonic Acid 271-275 olfactory receptor family 51 subfamily E member 2 Mus musculus 163-170 31625616-6 2020 TNBS significantly increased myeloperoxidase (MPO) expression, macroscopic colitis scores, and colon shortening. Trinitrobenzenesulfonic Acid 0-4 myeloperoxidase Mus musculus 46-49 32021106-0 2020 KGF Is Delivered to Inflammatory and Induces the Epithelial Hyperplasia in Trinitrobenzene Sulfonic Acid-Induced Ulcerative Colitis Rats. Trinitrobenzenesulfonic Acid 75-104 fibroblast growth factor 7 Rattus norvegicus 0-3 32021106-3 2020 We aimed to explore the therapeutic effect and possible mechanism of KGF gene-modified MSCs on trinitrobenzene sulfonic acid (TNBS)-induced UC rats. Trinitrobenzenesulfonic Acid 95-124 fibroblast growth factor 7 Rattus norvegicus 69-72 32021106-3 2020 We aimed to explore the therapeutic effect and possible mechanism of KGF gene-modified MSCs on trinitrobenzene sulfonic acid (TNBS)-induced UC rats. Trinitrobenzenesulfonic Acid 126-130 fibroblast growth factor 7 Rattus norvegicus 69-72 31586441-5 2020 The expression of iRhom2 and TACE in the colonic tissue of IBD patients and 2,4,6-trinitrobenzenesulfonic acid solution (TNBS)-treated mice was determined by RT-PCR and immunohistochemistry. Trinitrobenzenesulfonic Acid 76-110 rhomboid 5 homolog 2 Homo sapiens 18-24 31536729-8 2019 Then, intrathecal injection of TRAF6 siRNA attenuated visceral pain, blocked the upregulation of pNF-kappaB, TNF-alpha and IL-1beta levels in the spinal cord in TNBS mice. Trinitrobenzenesulfonic Acid 161-165 tumor necrosis factor Mus musculus 109-118 31536729-8 2019 Then, intrathecal injection of TRAF6 siRNA attenuated visceral pain, blocked the upregulation of pNF-kappaB, TNF-alpha and IL-1beta levels in the spinal cord in TNBS mice. Trinitrobenzenesulfonic Acid 161-165 interleukin 1 alpha Mus musculus 123-131 31536729-9 2019 Furthermore, spinal administration of NF-kappaB inhibitor, BAY11-7082 reversed the pain behavior and suppressed spinal TNF-alpha and IL-1beta expression in TNBS mice. Trinitrobenzenesulfonic Acid 156-160 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 38-47 31536729-9 2019 Furthermore, spinal administration of NF-kappaB inhibitor, BAY11-7082 reversed the pain behavior and suppressed spinal TNF-alpha and IL-1beta expression in TNBS mice. Trinitrobenzenesulfonic Acid 156-160 tumor necrosis factor Mus musculus 119-128 31536729-9 2019 Furthermore, spinal administration of NF-kappaB inhibitor, BAY11-7082 reversed the pain behavior and suppressed spinal TNF-alpha and IL-1beta expression in TNBS mice. Trinitrobenzenesulfonic Acid 156-160 interleukin 1 alpha Mus musculus 133-141 31536729-11 2019 Meanwhile, TNBS-induced enhancement of spinal GFAP, TRAF6, pNF-kappaB, TNF-alpha and IL-1beta were reduced by the same treatment of RSV. Trinitrobenzenesulfonic Acid 11-15 glial fibrillary acidic protein Mus musculus 46-50 31536729-11 2019 Meanwhile, TNBS-induced enhancement of spinal GFAP, TRAF6, pNF-kappaB, TNF-alpha and IL-1beta were reduced by the same treatment of RSV. Trinitrobenzenesulfonic Acid 11-15 TNF receptor-associated factor 6 Mus musculus 52-57 31536729-11 2019 Meanwhile, TNBS-induced enhancement of spinal GFAP, TRAF6, pNF-kappaB, TNF-alpha and IL-1beta were reduced by the same treatment of RSV. Trinitrobenzenesulfonic Acid 11-15 tumor necrosis factor Mus musculus 71-80 31536729-11 2019 Meanwhile, TNBS-induced enhancement of spinal GFAP, TRAF6, pNF-kappaB, TNF-alpha and IL-1beta were reduced by the same treatment of RSV. Trinitrobenzenesulfonic Acid 11-15 interleukin 1 alpha Mus musculus 85-93 31731626-2 2019 This study determined the effects of an aqueous extract of Myrciaria jaboticaba peel (EJP) (50 g L-1) on 2,4,6-trinitrobenzenesulfonic acid-induced colitis. Trinitrobenzenesulfonic Acid 105-139 ribosomal protein L4 Rattus norvegicus 97-100 31481750-4 2019 Cell permeable recombined fusion protein TAT-CRYAB was injected intraperitoneally into dextran sulfate sodium (DSS)- or 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis in mice to assess its anti-inflammatory effects. Trinitrobenzenesulfonic Acid 157-161 crystallin, alpha B Mus musculus 45-50 31481750-7 2019 Consistently, administration of TAT-CRYAB fusion protein significantly alleviated DSS- or TNBS-induced colitis in mice and protected intestinal barrier integrity. Trinitrobenzenesulfonic Acid 90-94 crystallin, alpha B Mus musculus 36-41 32550329-14 2019 Conclusion: In TNBS-E-induced rat model of colitis, EPO significantly decreased inflammation and bacterial translocation based on histopathological, biochemical and microbiological parameters. Trinitrobenzenesulfonic Acid 15-19 erythropoietin Rattus norvegicus 52-55 31702041-4 2019 Experimental colitis was induced through intrarectal administration of 2,4,6-trinitrobenzene sulfonic acid (TNBS) in leptin receptor-deficient Zucker rats (LR-D). Trinitrobenzenesulfonic Acid 71-106 leptin receptor Rattus norvegicus 117-132 31702041-4 2019 Experimental colitis was induced through intrarectal administration of 2,4,6-trinitrobenzene sulfonic acid (TNBS) in leptin receptor-deficient Zucker rats (LR-D). Trinitrobenzenesulfonic Acid 108-112 leptin receptor Rattus norvegicus 117-132 31702041-11 2019 In conclusion, activation of the leptin receptor ob-R is an important pathogenic mechanism of UC, and leptin receptor deficiency may provide resistance against TNBS-induced colitis by inhibiting the NF-kappaB and RhoA signaling pathways. Trinitrobenzenesulfonic Acid 160-164 leptin receptor Rattus norvegicus 102-117 31325428-12 2019 Compared to controls, IDO1-TG mice demonstrated an 85% reduction in ileal bacteria (P = .03) when challenged with enteropathogenic E coli, and were protected from immune infiltration, crypt dropout, and ulcers following administration of dextran sodium sulfate or 2,4,6-trinitrobenzenesulfonic acid. Trinitrobenzenesulfonic Acid 264-298 indoleamine 2,3-dioxygenase 1 Mus musculus 22-26 31112869-6 2019 Orally administered irisolidone or kakkalide alleviated colon shortening and myeloperoxidase activity in mice with 2,4,6-trinitrobenzenesulfonic acid (TNBS)-induced colitis. Trinitrobenzenesulfonic Acid 115-149 myeloperoxidase Mus musculus 77-92 31102937-3 2019 A rat UC model was induced with trinitro-benzene-sulfonic acid (TNBS), concentrations of the cytokines IL-1alpha, IL-6, IL-8, IL-1beta, and TNF-alpha were significantly up-regulated and the concentrations of IL-4, IL-10, and IL-13 were significantly down-regulated compared with the control group (P < 0.05). Trinitrobenzenesulfonic Acid 32-62 interleukin 1 alpha Rattus norvegicus 103-112 31102937-3 2019 A rat UC model was induced with trinitro-benzene-sulfonic acid (TNBS), concentrations of the cytokines IL-1alpha, IL-6, IL-8, IL-1beta, and TNF-alpha were significantly up-regulated and the concentrations of IL-4, IL-10, and IL-13 were significantly down-regulated compared with the control group (P < 0.05). Trinitrobenzenesulfonic Acid 32-62 interleukin 4 Rattus norvegicus 208-212 31112869-0 2019 Kakkalide and irisolidone alleviate 2,4,6-trinitrobenzenesulfonic acid-induced colitis in mice by inhibiting lipopolysaccharide binding to toll-like receptor-4 and proteobacteria population. Trinitrobenzenesulfonic Acid 36-70 toll-like receptor 4 Mus musculus 139-159 31132297-4 2019 In an initial series of studies focused on trinitrobenzene sulfonic acid (TNBS)-colitis and dextran sodium sulfate (DSS)-colitis we showed that down-regulation of intestinal RICK expression in NOD2-intact mice by intra-rectal administration of a plasmid expressing RICK-specific siRNA was accompanied by down-regulation of pro-inflammatory cytokine responses in the colon and protection of the mice from experimental colitis. Trinitrobenzenesulfonic Acid 43-72 receptor (TNFRSF)-interacting serine-threonine kinase 2 Mus musculus 174-178 31132297-4 2019 In an initial series of studies focused on trinitrobenzene sulfonic acid (TNBS)-colitis and dextran sodium sulfate (DSS)-colitis we showed that down-regulation of intestinal RICK expression in NOD2-intact mice by intra-rectal administration of a plasmid expressing RICK-specific siRNA was accompanied by down-regulation of pro-inflammatory cytokine responses in the colon and protection of the mice from experimental colitis. Trinitrobenzenesulfonic Acid 43-72 nucleotide-binding oligomerization domain containing 2 Mus musculus 193-197 31078692-10 2019 CONCLUSIONS: SSW effectively attenuated experimental chronic colitis induced by TNBS, which was realized by inhibition of the Wnt/beta-catenin signaling pathway. Trinitrobenzenesulfonic Acid 80-84 Wnt family member 2 Rattus norvegicus 126-129 31078692-10 2019 CONCLUSIONS: SSW effectively attenuated experimental chronic colitis induced by TNBS, which was realized by inhibition of the Wnt/beta-catenin signaling pathway. Trinitrobenzenesulfonic Acid 80-84 catenin beta 1 Rattus norvegicus 130-142 31112869-6 2019 Orally administered irisolidone or kakkalide alleviated colon shortening and myeloperoxidase activity in mice with 2,4,6-trinitrobenzenesulfonic acid (TNBS)-induced colitis. Trinitrobenzenesulfonic Acid 151-155 myeloperoxidase Mus musculus 77-92 31112869-8 2019 Furthermore, they suppressed TNBS-induced expression of M1 macrophage markers TNF-alpha, CD80, CD86, and Arg2 expression while the expression of M2 macrophage markers Arg1, CD163, CD206, and IL-10 was induced. Trinitrobenzenesulfonic Acid 29-33 tumor necrosis factor Mus musculus 78-87 31112869-8 2019 Furthermore, they suppressed TNBS-induced expression of M1 macrophage markers TNF-alpha, CD80, CD86, and Arg2 expression while the expression of M2 macrophage markers Arg1, CD163, CD206, and IL-10 was induced. Trinitrobenzenesulfonic Acid 29-33 arginase type II Mus musculus 105-109 31112869-8 2019 Furthermore, they suppressed TNBS-induced expression of M1 macrophage markers TNF-alpha, CD80, CD86, and Arg2 expression while the expression of M2 macrophage markers Arg1, CD163, CD206, and IL-10 was induced. Trinitrobenzenesulfonic Acid 29-33 arginase, liver Mus musculus 167-171 31112869-8 2019 Furthermore, they suppressed TNBS-induced expression of M1 macrophage markers TNF-alpha, CD80, CD86, and Arg2 expression while the expression of M2 macrophage markers Arg1, CD163, CD206, and IL-10 was induced. Trinitrobenzenesulfonic Acid 29-33 CD163 antigen Mus musculus 173-178 31112869-8 2019 Furthermore, they suppressed TNBS-induced expression of M1 macrophage markers TNF-alpha, CD80, CD86, and Arg2 expression while the expression of M2 macrophage markers Arg1, CD163, CD206, and IL-10 was induced. Trinitrobenzenesulfonic Acid 29-33 mannose receptor, C type 1 Mus musculus 180-185 31112869-8 2019 Furthermore, they suppressed TNBS-induced expression of M1 macrophage markers TNF-alpha, CD80, CD86, and Arg2 expression while the expression of M2 macrophage markers Arg1, CD163, CD206, and IL-10 was induced. Trinitrobenzenesulfonic Acid 29-33 interleukin 10 Mus musculus 191-196 31428451-0 2019 Sustained suppression of IL-18 by employing a vaccine ameliorates intestinal inflammation in TNBS-induced murine colitis. Trinitrobenzenesulfonic Acid 93-97 interleukin 18 Mus musculus 25-30 30580446-7 2019 Moreover, combined ASCs and sulfasalazine therapy effectively inhibited the NF-kappaB signaling pathway, reduced the expression of Bax and prevented the loss of Bcl-2 proteins in colon tissue of the rats with TNBS-induced colitis. Trinitrobenzenesulfonic Acid 209-213 BCL2 associated X, apoptosis regulator Rattus norvegicus 131-134 31324142-6 2019 RESULTS: RNA microarray and quantitative polymerase chain reaction results indicated that miR-34a was downregulated by TNBS induction, but it was upregulated by DEX administration. Trinitrobenzenesulfonic Acid 119-123 microRNA 34a Rattus norvegicus 90-97 29936889-5 2019 The results showed that in Large White pigs, SLA-11 c.754-132 CC sows produced 0.74 and 0.87 more pigs per litter for TNB and NBA of all parities than did TT sows (p < .05); In DIV pigs, SLA-11 c.754-132 CC sows produced 1.17 more pigs per litter for TNB of all parities than did TC sows (p < .05). Trinitrobenzenesulfonic Acid 118-121 SLA-11 Sus scrofa 45-51 29936889-5 2019 The results showed that in Large White pigs, SLA-11 c.754-132 CC sows produced 0.74 and 0.87 more pigs per litter for TNB and NBA of all parities than did TT sows (p < .05); In DIV pigs, SLA-11 c.754-132 CC sows produced 1.17 more pigs per litter for TNB of all parities than did TC sows (p < .05). Trinitrobenzenesulfonic Acid 254-257 SLA-11 Sus scrofa 45-51 29936889-6 2019 In Large White pigs, SLA-11 c.1421 + 38 CC sows produced 0.9 more pigs per litter for TNB of all parities than did TT sows (p < .05), while in DIV pigs SLA-11 c.1421 + 38 CC sows produced 0.84 and 0.7 less pigs per litter for TNB and NBA of all parities than did TT sows (p < .05). Trinitrobenzenesulfonic Acid 86-89 SLA-11 Sus scrofa 21-27 29936889-6 2019 In Large White pigs, SLA-11 c.1421 + 38 CC sows produced 0.9 more pigs per litter for TNB of all parities than did TT sows (p < .05), while in DIV pigs SLA-11 c.1421 + 38 CC sows produced 0.84 and 0.7 less pigs per litter for TNB and NBA of all parities than did TT sows (p < .05). Trinitrobenzenesulfonic Acid 229-232 SLA-11 Sus scrofa 21-27 31059072-7 2019 In addition, the administration of TFA in mice with TNBS-induced colitis led to a significant decrease in the levels of cytokines in the sera and colon tissues; a significant decrease myeloperoxidase activity in the colon tissues was also observed. Trinitrobenzenesulfonic Acid 52-56 myeloperoxidase Mus musculus 184-199 31059072-11 2019 Our findings indicated that TFA could suppress the inflammatory response in mice with TNBS-induced colitis via inhibition of the NF-kappaB and MAPK signaling pathways. Trinitrobenzenesulfonic Acid 86-90 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 129-138 30580446-7 2019 Moreover, combined ASCs and sulfasalazine therapy effectively inhibited the NF-kappaB signaling pathway, reduced the expression of Bax and prevented the loss of Bcl-2 proteins in colon tissue of the rats with TNBS-induced colitis. Trinitrobenzenesulfonic Acid 209-213 BCL2, apoptosis regulator Rattus norvegicus 161-166 30995068-3 2019 We found that renin was highly induced in colonic biopsies from patients with ulcerative colitis or Crohn"s disease, and colonic renin and ANG II levels were markedly increased in a 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis model, indicating that the colonic RAS is activated in colitis. Trinitrobenzenesulfonic Acid 182-217 renin Homo sapiens 14-19 30735453-8 2019 Chronic TNBS induced 1) a visceral hypersensitivity (P = 0.03), 2) an increased colon weight-to-length ratio (P = 0.01), 3) higher inflammatory and fibrosis scores (P = 0.0390 and P = 0.0016, respectively), and 4) a higher colonic IL-6 and IL-10 production (P = 0.008 and P = 0.005, respectively) compared with control rats. Trinitrobenzenesulfonic Acid 8-12 interleukin 6 Rattus norvegicus 231-235 30735453-8 2019 Chronic TNBS induced 1) a visceral hypersensitivity (P = 0.03), 2) an increased colon weight-to-length ratio (P = 0.01), 3) higher inflammatory and fibrosis scores (P = 0.0390 and P = 0.0016, respectively), and 4) a higher colonic IL-6 and IL-10 production (P = 0.008 and P = 0.005, respectively) compared with control rats. Trinitrobenzenesulfonic Acid 8-12 interleukin 10 Rattus norvegicus 240-245 30995068-3 2019 We found that renin was highly induced in colonic biopsies from patients with ulcerative colitis or Crohn"s disease, and colonic renin and ANG II levels were markedly increased in a 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis model, indicating that the colonic RAS is activated in colitis. Trinitrobenzenesulfonic Acid 182-217 renin Homo sapiens 129-134 30995068-3 2019 We found that renin was highly induced in colonic biopsies from patients with ulcerative colitis or Crohn"s disease, and colonic renin and ANG II levels were markedly increased in a 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis model, indicating that the colonic RAS is activated in colitis. Trinitrobenzenesulfonic Acid 182-217 angiotensinogen Homo sapiens 139-145 30995068-3 2019 We found that renin was highly induced in colonic biopsies from patients with ulcerative colitis or Crohn"s disease, and colonic renin and ANG II levels were markedly increased in a 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis model, indicating that the colonic RAS is activated in colitis. Trinitrobenzenesulfonic Acid 219-223 renin Homo sapiens 14-19 30995068-3 2019 We found that renin was highly induced in colonic biopsies from patients with ulcerative colitis or Crohn"s disease, and colonic renin and ANG II levels were markedly increased in a 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis model, indicating that the colonic RAS is activated in colitis. Trinitrobenzenesulfonic Acid 219-223 angiotensinogen Homo sapiens 139-145 30995068-4 2019 Renin transgenic (RenTg) mice exhibited increased phosphorylation in Janus kinase-2 (JAK2) and signal transducer and activator of transcription1/3 (STAT1/3) within colonic mucosa at baseline and following TNBS induction, suggesting that ANG II promotes colonic inflammation via the JAK2/STAT1/3 pathway. Trinitrobenzenesulfonic Acid 205-209 renin Homo sapiens 0-5 30901719-7 2019 Furthermore, the activation of TLR4/NF-kappaB signaling pathway was significantly inhibited by AZA and BJOE treatment when compared with that of TNBS-treated rats. Trinitrobenzenesulfonic Acid 145-149 toll-like receptor 4 Rattus norvegicus 31-35 31114134-4 2019 METHODS: In this study, mice with A20 deletion in intestinal epithelial cells (A20IEC-KO) were utilized to establish a Crohn"s disease mouse model with 2,4,6-trinitrobenzene sulfonic acid (TNBS) administration, as well as wild-type mice. Trinitrobenzenesulfonic Acid 189-193 tumor necrosis factor, alpha-induced protein 3 Mus musculus 34-37 30901719-6 2019 In addition, the elevated mRNA expression of MMP-1, MMP-3 and RAGE induced by TNBS was remarkably inhibited by BJOE, SASP or AZA treatments, while the mRNA expression of PPAR-gamma was significantly enhanced. Trinitrobenzenesulfonic Acid 78-82 matrix metallopeptidase 1 Rattus norvegicus 45-50 30901719-6 2019 In addition, the elevated mRNA expression of MMP-1, MMP-3 and RAGE induced by TNBS was remarkably inhibited by BJOE, SASP or AZA treatments, while the mRNA expression of PPAR-gamma was significantly enhanced. Trinitrobenzenesulfonic Acid 78-82 matrix metallopeptidase 3 Rattus norvegicus 52-57 30901719-6 2019 In addition, the elevated mRNA expression of MMP-1, MMP-3 and RAGE induced by TNBS was remarkably inhibited by BJOE, SASP or AZA treatments, while the mRNA expression of PPAR-gamma was significantly enhanced. Trinitrobenzenesulfonic Acid 78-82 advanced glycosylation end product-specific receptor Rattus norvegicus 62-66 30901719-6 2019 In addition, the elevated mRNA expression of MMP-1, MMP-3 and RAGE induced by TNBS was remarkably inhibited by BJOE, SASP or AZA treatments, while the mRNA expression of PPAR-gamma was significantly enhanced. Trinitrobenzenesulfonic Acid 78-82 peroxisome proliferator-activated receptor gamma Rattus norvegicus 170-180 30779922-11 2019 MIR31-knockout and conditional-knockout mice developed more severe colitis in response to DSS and TNBS, with increased immune responses, compared with control mice. Trinitrobenzenesulfonic Acid 98-102 microRNA 31 Mus musculus 0-5 31019652-6 2019 miR-122 expression was downregulated while SBP1 expression was upregulated under TNBS-induced colitis or oxidative stress. Trinitrobenzenesulfonic Acid 81-85 microRNA 122 Homo sapiens 0-7 30844559-7 2019 This review deals with IL-13 in several experimental colitis models -such as oxazolone-, trinitrobenzene sulfonic acid- or dextran sodium sulphate-induced colitis- and chronic intestinal inflammatory disorders -including celiac disease, UC and Crohn"s disease-, and it also highlights the attempts to modulate IL-13 as therapeutic tool. Trinitrobenzenesulfonic Acid 89-118 interleukin 13 Homo sapiens 23-28 30383440-4 2019 We investigated the effects of hesperetin on tumor necrosis factor-alpha (TNF-alpha), protein tyrosine phosphatase, receptor type C (CD45), caspase-3 and Bax expressions in TNBS in induced colitis model in rats. Trinitrobenzenesulfonic Acid 173-177 BCL2 associated X, apoptosis regulator Rattus norvegicus 154-157 30765845-3 2019 In this report, we found that mTOR inhibitor rapamycin or mTOR deletion in CX3Cr1+ mononuclear phagocytes inhibits expression of interleukin (IL)-23, accompanied by reduced intestinal production of IL-22 and ameliorated fibrosis in the TNBS-induced fibrosis mouse model. Trinitrobenzenesulfonic Acid 236-240 mechanistic target of rapamycin kinase Mus musculus 30-34 30765845-3 2019 In this report, we found that mTOR inhibitor rapamycin or mTOR deletion in CX3Cr1+ mononuclear phagocytes inhibits expression of interleukin (IL)-23, accompanied by reduced intestinal production of IL-22 and ameliorated fibrosis in the TNBS-induced fibrosis mouse model. Trinitrobenzenesulfonic Acid 236-240 mechanistic target of rapamycin kinase Mus musculus 58-62 30765845-3 2019 In this report, we found that mTOR inhibitor rapamycin or mTOR deletion in CX3Cr1+ mononuclear phagocytes inhibits expression of interleukin (IL)-23, accompanied by reduced intestinal production of IL-22 and ameliorated fibrosis in the TNBS-induced fibrosis mouse model. Trinitrobenzenesulfonic Acid 236-240 chemokine (C-X3-C motif) receptor 1 Mus musculus 75-81 30765845-3 2019 In this report, we found that mTOR inhibitor rapamycin or mTOR deletion in CX3Cr1+ mononuclear phagocytes inhibits expression of interleukin (IL)-23, accompanied by reduced intestinal production of IL-22 and ameliorated fibrosis in the TNBS-induced fibrosis mouse model. Trinitrobenzenesulfonic Acid 236-240 interleukin 23, alpha subunit p19 Mus musculus 129-148 30143913-0 2019 Melatonin ameliorates TNBS-induced colitis in rats through the melatonin receptors: involvement of TLR4/MyD88/NF-kappaB signalling pathway. Trinitrobenzenesulfonic Acid 22-26 toll-like receptor 4 Rattus norvegicus 99-103 30143913-0 2019 Melatonin ameliorates TNBS-induced colitis in rats through the melatonin receptors: involvement of TLR4/MyD88/NF-kappaB signalling pathway. Trinitrobenzenesulfonic Acid 22-26 MYD88, innate immune signal transduction adaptor Rattus norvegicus 104-109 30143913-1 2019 AIM: The aim of the present study is to investigate the anti-inflammatory effect of melatonin in trinitrobenzene sulfonic acid (TNBS)-induced rat colitis through the inhibition of Toll-like receptor 4 (TLR4)/nuclear factor kappa B (NF-kappaB) signalling pathway and activation of melatonin receptor. Trinitrobenzenesulfonic Acid 97-126 toll-like receptor 4 Rattus norvegicus 180-200 30143913-1 2019 AIM: The aim of the present study is to investigate the anti-inflammatory effect of melatonin in trinitrobenzene sulfonic acid (TNBS)-induced rat colitis through the inhibition of Toll-like receptor 4 (TLR4)/nuclear factor kappa B (NF-kappaB) signalling pathway and activation of melatonin receptor. Trinitrobenzenesulfonic Acid 97-126 toll-like receptor 4 Rattus norvegicus 202-206 30143913-1 2019 AIM: The aim of the present study is to investigate the anti-inflammatory effect of melatonin in trinitrobenzene sulfonic acid (TNBS)-induced rat colitis through the inhibition of Toll-like receptor 4 (TLR4)/nuclear factor kappa B (NF-kappaB) signalling pathway and activation of melatonin receptor. Trinitrobenzenesulfonic Acid 128-132 toll-like receptor 4 Rattus norvegicus 180-200 30143913-1 2019 AIM: The aim of the present study is to investigate the anti-inflammatory effect of melatonin in trinitrobenzene sulfonic acid (TNBS)-induced rat colitis through the inhibition of Toll-like receptor 4 (TLR4)/nuclear factor kappa B (NF-kappaB) signalling pathway and activation of melatonin receptor. Trinitrobenzenesulfonic Acid 128-132 toll-like receptor 4 Rattus norvegicus 202-206 30143913-12 2019 In addition, melatonin decreased TNBS-induced up-regulation of TLR4, MyD88, and NF-kappaB p65, and increased down-regulation of I-kappaB proteins. Trinitrobenzenesulfonic Acid 33-37 toll-like receptor 4 Rattus norvegicus 63-67 30143913-12 2019 In addition, melatonin decreased TNBS-induced up-regulation of TLR4, MyD88, and NF-kappaB p65, and increased down-regulation of I-kappaB proteins. Trinitrobenzenesulfonic Acid 33-37 MYD88, innate immune signal transduction adaptor Rattus norvegicus 69-74 30143913-12 2019 In addition, melatonin decreased TNBS-induced up-regulation of TLR4, MyD88, and NF-kappaB p65, and increased down-regulation of I-kappaB proteins. Trinitrobenzenesulfonic Acid 33-37 synaptotagmin 1 Rattus norvegicus 90-93 30143913-14 2019 CONCLUSIONS: It seems that the inhibition of TLR4/NF-kappaB signalling pathway may mediate the anti-inflammatory effects of melatonin in TNBS-induced rat colitis. Trinitrobenzenesulfonic Acid 137-141 toll-like receptor 4 Rattus norvegicus 45-49 31406920-6 2019 Results: TNBS-produced colitis manifested as a decrease in the epithelial junctional adhesion molecule-A (JAM-A) and as an increase in trefoil factor-3, ulcerative area, and colon mass index, parameters that collaborate with the gross macroscopic changes in colon tissue. Trinitrobenzenesulfonic Acid 9-13 F11 receptor Rattus norvegicus 74-104 31406920-6 2019 Results: TNBS-produced colitis manifested as a decrease in the epithelial junctional adhesion molecule-A (JAM-A) and as an increase in trefoil factor-3, ulcerative area, and colon mass index, parameters that collaborate with the gross macroscopic changes in colon tissue. Trinitrobenzenesulfonic Acid 9-13 F11 receptor Rattus norvegicus 106-111 31406920-6 2019 Results: TNBS-produced colitis manifested as a decrease in the epithelial junctional adhesion molecule-A (JAM-A) and as an increase in trefoil factor-3, ulcerative area, and colon mass index, parameters that collaborate with the gross macroscopic changes in colon tissue. Trinitrobenzenesulfonic Acid 9-13 trefoil factor 3 Rattus norvegicus 135-151 31406920-7 2019 In addition, TNBS increased hemeoxygenase-1, nuclear factor-kappa B, P-selectin, and myeloperoxidase, as well as the apoptotic ratio of Bax/Bcl-2. Trinitrobenzenesulfonic Acid 13-17 heme oxygenase 1 Rattus norvegicus 28-67 31406920-7 2019 In addition, TNBS increased hemeoxygenase-1, nuclear factor-kappa B, P-selectin, and myeloperoxidase, as well as the apoptotic ratio of Bax/Bcl-2. Trinitrobenzenesulfonic Acid 13-17 selectin P Rattus norvegicus 69-100 31406920-7 2019 In addition, TNBS increased hemeoxygenase-1, nuclear factor-kappa B, P-selectin, and myeloperoxidase, as well as the apoptotic ratio of Bax/Bcl-2. Trinitrobenzenesulfonic Acid 13-17 BCL2 associated X, apoptosis regulator Rattus norvegicus 136-139 31406920-7 2019 In addition, TNBS increased hemeoxygenase-1, nuclear factor-kappa B, P-selectin, and myeloperoxidase, as well as the apoptotic ratio of Bax/Bcl-2. Trinitrobenzenesulfonic Acid 13-17 BCL2, apoptosis regulator Rattus norvegicus 140-145 31019652-6 2019 miR-122 expression was downregulated while SBP1 expression was upregulated under TNBS-induced colitis or oxidative stress. Trinitrobenzenesulfonic Acid 81-85 high mobility group box 1 Homo sapiens 43-47 30800071-4 2019 Meanwhile, serum immunoglobulin G (IgG) was markedly reduced in TNBS treated mice, while 5 and 10 mg/kg matrine alleviated IgG reduction. Trinitrobenzenesulfonic Acid 64-68 immunoglobulin heavy variable V1-62 Mus musculus 17-33 30722992-8 2019 Notably, lentivirus-mediated overexpression of Ascl2 remarkably alleviated the severity of 2,4,6-trinitrobenzenesulfonic acid solution (TNBS)-induced colitis in mice, with decreased level of colonic IL-17A. Trinitrobenzenesulfonic Acid 91-125 achaete-scute family bHLH transcription factor 2 Mus musculus 47-52 30722992-8 2019 Notably, lentivirus-mediated overexpression of Ascl2 remarkably alleviated the severity of 2,4,6-trinitrobenzenesulfonic acid solution (TNBS)-induced colitis in mice, with decreased level of colonic IL-17A. Trinitrobenzenesulfonic Acid 136-140 achaete-scute family bHLH transcription factor 2 Mus musculus 47-52 30227219-4 2019 The present study assessed fecal HMGB1 levels in IBD patients and compared the effects of similar doses of Bifidobacterium longum (Bif) versus VSL#3 on HMGB1 levels in 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced murine colitis. Trinitrobenzenesulfonic Acid 169-204 high mobility group box 1 Homo sapiens 153-158 30654310-5 2019 Collectively, these data elucidated that EVs containing miR-146a ameliorates experimental colitis caused 2,4,6-trinitrobenzenesulfonic acid (TNBS) by targeting TRAF6 and IRAK1. Trinitrobenzenesulfonic Acid 105-139 microRNA 146a Rattus norvegicus 56-64 30654310-5 2019 Collectively, these data elucidated that EVs containing miR-146a ameliorates experimental colitis caused 2,4,6-trinitrobenzenesulfonic acid (TNBS) by targeting TRAF6 and IRAK1. Trinitrobenzenesulfonic Acid 105-139 TNF receptor associated factor 6 Rattus norvegicus 160-165 30654310-5 2019 Collectively, these data elucidated that EVs containing miR-146a ameliorates experimental colitis caused 2,4,6-trinitrobenzenesulfonic acid (TNBS) by targeting TRAF6 and IRAK1. Trinitrobenzenesulfonic Acid 105-139 interleukin-1 receptor-associated kinase 1 Rattus norvegicus 170-175 30654310-5 2019 Collectively, these data elucidated that EVs containing miR-146a ameliorates experimental colitis caused 2,4,6-trinitrobenzenesulfonic acid (TNBS) by targeting TRAF6 and IRAK1. Trinitrobenzenesulfonic Acid 141-145 microRNA 146a Rattus norvegicus 56-64 30654310-5 2019 Collectively, these data elucidated that EVs containing miR-146a ameliorates experimental colitis caused 2,4,6-trinitrobenzenesulfonic acid (TNBS) by targeting TRAF6 and IRAK1. Trinitrobenzenesulfonic Acid 141-145 interleukin-1 receptor-associated kinase 1 Rattus norvegicus 170-175 30800071-4 2019 Meanwhile, serum immunoglobulin G (IgG) was markedly reduced in TNBS treated mice, while 5 and 10 mg/kg matrine alleviated IgG reduction. Trinitrobenzenesulfonic Acid 64-68 immunoglobulin heavy variable V1-62 Mus musculus 35-38 30413272-11 2019 T. spiralis-infected mice induced Th2 immune responses and balanced Th1 immune responses stimulated by TNBS to ameliorate intestinal inflammation. Trinitrobenzenesulfonic Acid 103-107 negative elongation factor complex member C/D, Th1l Mus musculus 68-71 30821556-0 2019 Inhibition of tumor necrosis factor alpha and increased of interleukin 10 by Lactobacillus: a molecular mechanism protection against TNBS-induced ulcerative colitis in chicks. Trinitrobenzenesulfonic Acid 133-137 interleukin 10 Homo sapiens 59-73 30334342-0 2019 Vasopressin augments TNBS-induced colitis through enteric neuronal V1a receptor-mediated COX-2-dependent prostaglandin release from mast cells in mice. Trinitrobenzenesulfonic Acid 21-25 cytochrome c oxidase II, mitochondrial Mus musculus 89-94 30651971-1 2019 Background: Previously, we have demonstrated that IL-33 administration protecting TNBS-induced experimental colitis is associated with facilitation of Th2/Tregs responses in mice. Trinitrobenzenesulfonic Acid 82-86 interleukin 33 Mus musculus 50-55 30651971-10 2019 Conclusions: IL-33 regulates the autophagy is a new immunoregulatory property on TNBS-induced experimental colitis in mice. Trinitrobenzenesulfonic Acid 81-85 interleukin 33 Mus musculus 13-18 30687029-11 2018 TNBS treatment caused a transient up-regulation of CREB-expressing cells at 1 h post-TNBS only. Trinitrobenzenesulfonic Acid 0-4 cAMP responsive element binding protein 1 Rattus norvegicus 51-55 30687029-11 2018 TNBS treatment caused a transient up-regulation of CREB-expressing cells at 1 h post-TNBS only. Trinitrobenzenesulfonic Acid 85-89 cAMP responsive element binding protein 1 Rattus norvegicus 51-55 30687029-12 2018 The number of cells expressing phosphorylated CREB (pS133CREB) did not change at 1 h and 2 h post-TNBS, but was down-regulated by three folds at 6 h post-TNBS. Trinitrobenzenesulfonic Acid 154-158 cAMP responsive element binding protein 1 Rattus norvegicus 46-50 30687029-12 2018 The number of cells expressing phosphorylated CREB (pS133CREB) did not change at 1 h and 2 h post-TNBS, but was down-regulated by three folds at 6 h post-TNBS. Trinitrobenzenesulfonic Acid 154-158 cAMP responsive element binding protein 1 Rattus norvegicus 57-61 30687029-13 2018 Analysis of DRG sections revealed that the number of Mecp2-positive neurons was up-regulated by TNBS treatment, reaching three-fold increase at 2 h post-TNBS, and eight-fold increase at 6 h post-TNBS (p <= 0.05 to control). Trinitrobenzenesulfonic Acid 96-100 methyl CpG binding protein 2 Rattus norvegicus 53-58 30687029-13 2018 Analysis of DRG sections revealed that the number of Mecp2-positive neurons was up-regulated by TNBS treatment, reaching three-fold increase at 2 h post-TNBS, and eight-fold increase at 6 h post-TNBS (p <= 0.05 to control). Trinitrobenzenesulfonic Acid 153-157 methyl CpG binding protein 2 Rattus norvegicus 53-58 30687029-13 2018 Analysis of DRG sections revealed that the number of Mecp2-positive neurons was up-regulated by TNBS treatment, reaching three-fold increase at 2 h post-TNBS, and eight-fold increase at 6 h post-TNBS (p <= 0.05 to control). Trinitrobenzenesulfonic Acid 153-157 methyl CpG binding protein 2 Rattus norvegicus 53-58 30419451-7 2019 The comparison of the TsCystatin + TNBS group with the PBS + TNBS group showed that the DAI score, MPO activity, and colonic macroscopic and microscopic damage significantly reduced, IFN-gamma significantly decreased, IL-4 expression increased, and NF-kappaB expression decreased. Trinitrobenzenesulfonic Acid 35-39 myeloperoxidase Mus musculus 99-102 30503585-7 2019 Moreover, TNBS administration also resulted in activation of p53 and apoptosis. Trinitrobenzenesulfonic Acid 10-14 Wistar clone pR53P1 p53 pseudogene Rattus norvegicus 61-64 30419451-7 2019 The comparison of the TsCystatin + TNBS group with the PBS + TNBS group showed that the DAI score, MPO activity, and colonic macroscopic and microscopic damage significantly reduced, IFN-gamma significantly decreased, IL-4 expression increased, and NF-kappaB expression decreased. Trinitrobenzenesulfonic Acid 61-65 interferon gamma Mus musculus 183-192 30672380-3 2019 Since colocalization of Toll-like receptor 4 (TLR4) and TRPV1 has been observed in primary afferents including the trigeminal sensory neurons and the dorsal root ganglion neurons, we test the hypothesis that TLR4 might regulate the expression and function of TRPV1 in primary afferent neurons in 2,4,6-trinitrobenzene sulfate (TNBS)-induced colitis using the TLR4-deficient and the wild-type C57 mice. Trinitrobenzenesulfonic Acid 327-331 toll-like receptor 4 Mus musculus 24-44 30419451-11 2019 TsCystatin possibly induced a Th2-type immune response in the body, which balanced the Th1-type immune response induced by TNBS administration, thereby relieving colitis. Trinitrobenzenesulfonic Acid 123-127 negative elongation factor complex member C/D, Th1l Mus musculus 87-90 30419451-7 2019 The comparison of the TsCystatin + TNBS group with the PBS + TNBS group showed that the DAI score, MPO activity, and colonic macroscopic and microscopic damage significantly reduced, IFN-gamma significantly decreased, IL-4 expression increased, and NF-kappaB expression decreased. Trinitrobenzenesulfonic Acid 35-39 interferon gamma Mus musculus 183-192 30419451-7 2019 The comparison of the TsCystatin + TNBS group with the PBS + TNBS group showed that the DAI score, MPO activity, and colonic macroscopic and microscopic damage significantly reduced, IFN-gamma significantly decreased, IL-4 expression increased, and NF-kappaB expression decreased. Trinitrobenzenesulfonic Acid 35-39 interleukin 4 Mus musculus 218-222 30672380-3 2019 Since colocalization of Toll-like receptor 4 (TLR4) and TRPV1 has been observed in primary afferents including the trigeminal sensory neurons and the dorsal root ganglion neurons, we test the hypothesis that TLR4 might regulate the expression and function of TRPV1 in primary afferent neurons in 2,4,6-trinitrobenzene sulfate (TNBS)-induced colitis using the TLR4-deficient and the wild-type C57 mice. Trinitrobenzenesulfonic Acid 327-331 toll-like receptor 4 Mus musculus 46-50 30672380-3 2019 Since colocalization of Toll-like receptor 4 (TLR4) and TRPV1 has been observed in primary afferents including the trigeminal sensory neurons and the dorsal root ganglion neurons, we test the hypothesis that TLR4 might regulate the expression and function of TRPV1 in primary afferent neurons in 2,4,6-trinitrobenzene sulfate (TNBS)-induced colitis using the TLR4-deficient and the wild-type C57 mice. Trinitrobenzenesulfonic Acid 327-331 transient receptor potential cation channel, subfamily V, member 1 Mus musculus 56-61 30672380-3 2019 Since colocalization of Toll-like receptor 4 (TLR4) and TRPV1 has been observed in primary afferents including the trigeminal sensory neurons and the dorsal root ganglion neurons, we test the hypothesis that TLR4 might regulate the expression and function of TRPV1 in primary afferent neurons in 2,4,6-trinitrobenzene sulfate (TNBS)-induced colitis using the TLR4-deficient and the wild-type C57 mice. Trinitrobenzenesulfonic Acid 327-331 toll-like receptor 4 Mus musculus 208-212 30672380-3 2019 Since colocalization of Toll-like receptor 4 (TLR4) and TRPV1 has been observed in primary afferents including the trigeminal sensory neurons and the dorsal root ganglion neurons, we test the hypothesis that TLR4 might regulate the expression and function of TRPV1 in primary afferent neurons in 2,4,6-trinitrobenzene sulfate (TNBS)-induced colitis using the TLR4-deficient and the wild-type C57 mice. Trinitrobenzenesulfonic Acid 327-331 toll-like receptor 4 Mus musculus 208-212 30372897-14 2018 The aqueous extract of O. rosea protected the TNBS-induced colonic damage in rats, an effect that could be associated with the presence of polyphenolic compounds, alkaloids, and terpenes; as well as their ability to down-regulate MPO activity. Trinitrobenzenesulfonic Acid 46-50 myeloperoxidase Rattus norvegicus 230-233 29670278-3 2018 Here, we reported that BLT1 regulates trinitrobenzene sulfonic acid (TNBS)-induced colitis, which reflects CD4+ T-cell-dependent adaptive immune mechanisms of IBD. Trinitrobenzenesulfonic Acid 38-67 leukotriene B4 receptor Homo sapiens 23-27 29670278-3 2018 Here, we reported that BLT1 regulates trinitrobenzene sulfonic acid (TNBS)-induced colitis, which reflects CD4+ T-cell-dependent adaptive immune mechanisms of IBD. Trinitrobenzenesulfonic Acid 69-73 leukotriene B4 receptor Homo sapiens 23-27 30478292-2 2018 Here we study the relationship between bacterial antigens and inflammatory stimuli, and miR-146a expression using IEC lines and models of colitis (trinitrobenzenesulfonic acid (TNBS), dextran sulfate sodium (DSS) and the CD4 + CD62L + T cell transfer model). Trinitrobenzenesulfonic Acid 177-181 microRNA 146 Mus musculus 88-96 30478292-2 2018 Here we study the relationship between bacterial antigens and inflammatory stimuli, and miR-146a expression using IEC lines and models of colitis (trinitrobenzenesulfonic acid (TNBS), dextran sulfate sodium (DSS) and the CD4 + CD62L + T cell transfer model). Trinitrobenzenesulfonic Acid 147-175 microRNA 146 Mus musculus 88-96 30478292-7 2018 Intestinal inflammation induced by chemical damage to the epithelium (DSS and TNBS models) induces miR-146a, but no effect is observed in the lymphocyte transfer model. Trinitrobenzenesulfonic Acid 78-82 microRNA 146 Mus musculus 99-107 30386616-7 2018 Results: (1) Hp(2-20) accelerated healing of TNBS-induced colitis compared to controls consistently with the expression of FPRs in colonic mucosa; (2) TNBS upregulated mRNA mucosal expression of COX-2, TNF-alpha, TGF-beta, HB-EGF and t-TG and (3) this, with the exception of HB-EGF, was significantly counteracted by Hp(2-20). Trinitrobenzenesulfonic Acid 151-155 cytochrome c oxidase II, mitochondrial Rattus norvegicus 195-200 30253332-0 2018 MiR-155 inhibition ameliorates 2, 4, 6-Trinitrobenzenesulfonic acid (TNBS)-induced experimental colitis in rat via influencing the differentiation of Th17 cells by Jarid2. Trinitrobenzenesulfonic Acid 31-67 microRNA 155 Rattus norvegicus 0-7 30253332-0 2018 MiR-155 inhibition ameliorates 2, 4, 6-Trinitrobenzenesulfonic acid (TNBS)-induced experimental colitis in rat via influencing the differentiation of Th17 cells by Jarid2. Trinitrobenzenesulfonic Acid 69-73 microRNA 155 Rattus norvegicus 0-7 30253332-0 2018 MiR-155 inhibition ameliorates 2, 4, 6-Trinitrobenzenesulfonic acid (TNBS)-induced experimental colitis in rat via influencing the differentiation of Th17 cells by Jarid2. Trinitrobenzenesulfonic Acid 69-73 jumonji and AT-rich interaction domain containing 2 Rattus norvegicus 164-170 30253332-4 2018 Here, we investigated the role of miR-155 in TNBS-induced rat colitis. Trinitrobenzenesulfonic Acid 45-49 microRNA 155 Rattus norvegicus 34-41 30253332-5 2018 Firstly, we found that the disease activity index (DAI) and Colon pathological changes were significantly reduced (P < 0.05) by using miR-155 inhibition sequences delivered by lentiviral vector, which revealed that miR-155 inhibition ameliorated TNBS-Induced experimental colitis. Trinitrobenzenesulfonic Acid 249-253 microRNA 155 Rattus norvegicus 137-144 30253332-5 2018 Firstly, we found that the disease activity index (DAI) and Colon pathological changes were significantly reduced (P < 0.05) by using miR-155 inhibition sequences delivered by lentiviral vector, which revealed that miR-155 inhibition ameliorated TNBS-Induced experimental colitis. Trinitrobenzenesulfonic Acid 249-253 microRNA 155 Rattus norvegicus 218-225 30253332-6 2018 Then, we carried out flow cytometry, ELISA, qRT-PCR, and found that in TNBS+miR-155 inhibition group, the proportion of Th17 cells in spleens and mesenteric lymph nodes (MLNs) and the level of the Th17 cell-associated cytokines IL-6, IL-17A, IL-17F and IL-21 in colon tissues were significantly reduced (P < 0.05), which revealed that miR-155 inhibition regulated the differentiation and function of Th17 cells. Trinitrobenzenesulfonic Acid 71-75 microRNA 155 Rattus norvegicus 76-83 30253332-6 2018 Then, we carried out flow cytometry, ELISA, qRT-PCR, and found that in TNBS+miR-155 inhibition group, the proportion of Th17 cells in spleens and mesenteric lymph nodes (MLNs) and the level of the Th17 cell-associated cytokines IL-6, IL-17A, IL-17F and IL-21 in colon tissues were significantly reduced (P < 0.05), which revealed that miR-155 inhibition regulated the differentiation and function of Th17 cells. Trinitrobenzenesulfonic Acid 71-75 interleukin 6 Rattus norvegicus 228-232 30253332-6 2018 Then, we carried out flow cytometry, ELISA, qRT-PCR, and found that in TNBS+miR-155 inhibition group, the proportion of Th17 cells in spleens and mesenteric lymph nodes (MLNs) and the level of the Th17 cell-associated cytokines IL-6, IL-17A, IL-17F and IL-21 in colon tissues were significantly reduced (P < 0.05), which revealed that miR-155 inhibition regulated the differentiation and function of Th17 cells. Trinitrobenzenesulfonic Acid 71-75 interleukin 17F Rattus norvegicus 242-248 30253332-6 2018 Then, we carried out flow cytometry, ELISA, qRT-PCR, and found that in TNBS+miR-155 inhibition group, the proportion of Th17 cells in spleens and mesenteric lymph nodes (MLNs) and the level of the Th17 cell-associated cytokines IL-6, IL-17A, IL-17F and IL-21 in colon tissues were significantly reduced (P < 0.05), which revealed that miR-155 inhibition regulated the differentiation and function of Th17 cells. Trinitrobenzenesulfonic Acid 71-75 interleukin 21 Rattus norvegicus 253-258 30253332-6 2018 Then, we carried out flow cytometry, ELISA, qRT-PCR, and found that in TNBS+miR-155 inhibition group, the proportion of Th17 cells in spleens and mesenteric lymph nodes (MLNs) and the level of the Th17 cell-associated cytokines IL-6, IL-17A, IL-17F and IL-21 in colon tissues were significantly reduced (P < 0.05), which revealed that miR-155 inhibition regulated the differentiation and function of Th17 cells. Trinitrobenzenesulfonic Acid 71-75 microRNA 155 Rattus norvegicus 338-345 30253332-8 2018 This study suggests that miR-155 inhibition ameliorates TNBS-induced colitis by regulating the Th17 cells differentiation and function and Jarid2/notch1 is closely related with the process. Trinitrobenzenesulfonic Acid 56-60 microRNA 155 Rattus norvegicus 25-32 30253332-8 2018 This study suggests that miR-155 inhibition ameliorates TNBS-induced colitis by regulating the Th17 cells differentiation and function and Jarid2/notch1 is closely related with the process. Trinitrobenzenesulfonic Acid 56-60 jumonji and AT-rich interaction domain containing 2 Rattus norvegicus 139-145 30253332-8 2018 This study suggests that miR-155 inhibition ameliorates TNBS-induced colitis by regulating the Th17 cells differentiation and function and Jarid2/notch1 is closely related with the process. Trinitrobenzenesulfonic Acid 56-60 notch receptor 1 Rattus norvegicus 146-152 30089249-5 2018 TNBS treatment evoked severe colonic inflammation after 24 h that persisted for 7 days, characterized by weight loss, high levels of myeloperoxidase activity, histological and macroscopic damage, and elevated index of oxidative stress in the blood. Trinitrobenzenesulfonic Acid 0-4 myeloperoxidase Rattus norvegicus 133-148 30386616-7 2018 Results: (1) Hp(2-20) accelerated healing of TNBS-induced colitis compared to controls consistently with the expression of FPRs in colonic mucosa; (2) TNBS upregulated mRNA mucosal expression of COX-2, TNF-alpha, TGF-beta, HB-EGF and t-TG and (3) this, with the exception of HB-EGF, was significantly counteracted by Hp(2-20). Trinitrobenzenesulfonic Acid 151-155 tumor necrosis factor Rattus norvegicus 202-211 30386616-7 2018 Results: (1) Hp(2-20) accelerated healing of TNBS-induced colitis compared to controls consistently with the expression of FPRs in colonic mucosa; (2) TNBS upregulated mRNA mucosal expression of COX-2, TNF-alpha, TGF-beta, HB-EGF and t-TG and (3) this, with the exception of HB-EGF, was significantly counteracted by Hp(2-20). Trinitrobenzenesulfonic Acid 151-155 heparin-binding EGF-like growth factor Rattus norvegicus 223-229 30386616-7 2018 Results: (1) Hp(2-20) accelerated healing of TNBS-induced colitis compared to controls consistently with the expression of FPRs in colonic mucosa; (2) TNBS upregulated mRNA mucosal expression of COX-2, TNF-alpha, TGF-beta, HB-EGF and t-TG and (3) this, with the exception of HB-EGF, was significantly counteracted by Hp(2-20). Trinitrobenzenesulfonic Acid 151-155 heparin-binding EGF-like growth factor Rattus norvegicus 275-281 30301267-4 2018 In trinitrobenzene sulfonic acid-induced IBD rats, 125 to 500 mg/kg of oral CAL significantly alleviated weight loss and diarrhea, decreased colitis inflammatory cell infiltration, and inhibited pro-inflammatory cytokine production. Trinitrobenzenesulfonic Acid 3-32 filamin binding LIM protein 1 Rattus norvegicus 76-79 29113905-8 2018 TRIM21-/- mice had more severe colitis after administration of trinitrobenzene sulfonic acid compared with wild-type mice, which was characterized by increased expression of IFN-gamma, TNF-alpha, and IL-17A in the colon. Trinitrobenzenesulfonic Acid 63-92 tripartite motif-containing 21 Mus musculus 0-6 29113905-8 2018 TRIM21-/- mice had more severe colitis after administration of trinitrobenzene sulfonic acid compared with wild-type mice, which was characterized by increased expression of IFN-gamma, TNF-alpha, and IL-17A in the colon. Trinitrobenzenesulfonic Acid 63-92 interferon gamma Mus musculus 174-183 30100498-4 2018 In this study, we explored the role of kefir grain Lactobacillus-derived EV in modulating inflammation responses via alleviating the production of inflammatory cytokines in tumor necrosis factor-alpha (TNF-alpha)-induced inflammation in Caco-2 cells and the 2,4,6-trinitrobenzene sulfonic acid-induced inflammatory bowel disease mouse model. Trinitrobenzenesulfonic Acid 258-293 tumor necrosis factor Homo sapiens 202-211 29113905-8 2018 TRIM21-/- mice had more severe colitis after administration of trinitrobenzene sulfonic acid compared with wild-type mice, which was characterized by increased expression of IFN-gamma, TNF-alpha, and IL-17A in the colon. Trinitrobenzenesulfonic Acid 63-92 tumor necrosis factor Mus musculus 185-194 29113905-8 2018 TRIM21-/- mice had more severe colitis after administration of trinitrobenzene sulfonic acid compared with wild-type mice, which was characterized by increased expression of IFN-gamma, TNF-alpha, and IL-17A in the colon. Trinitrobenzenesulfonic Acid 63-92 interleukin 17A Mus musculus 200-206 30254408-6 2018 RESULTS: Chronic treatment with TNBS caused more severe inflammation and fibrotic changes in TRPA1-KO than in wild-type mice. Trinitrobenzenesulfonic Acid 32-36 transient receptor potential cation channel, subfamily A, member 1 Mus musculus 93-98 29879627-6 2018 After POL extract treatment, body weights of rats significantly increased, macroscopic and microscopic damage scores reduced, MPO and NOS activity, as well as MDA and NO level significantly decreased, while SOD activity increased in a dose-dependent manner in the TNBS + POL groups compared with the TNBS group. Trinitrobenzenesulfonic Acid 264-268 myeloperoxidase Rattus norvegicus 126-129 30463649-1 2018 Objective To evaluate the therapeutic effect and possible mechanism of PPARgamma agonist rosiglitazone on 2, 4, 6-trinitrobenzenesulfonic acid (TNBS)-induced colitis in mice. Trinitrobenzenesulfonic Acid 106-142 peroxisome proliferator activated receptor gamma Mus musculus 71-80 29551611-5 2018 In addition, GATA3 and ROR-gammat mRNA and protein levels significantly increased but Foxp3 mRNA and protein levels significantly decreased in mice with TNBS treatment compared to mice without TNBS treatment. Trinitrobenzenesulfonic Acid 153-157 GATA binding protein 3 Mus musculus 13-18 29551611-5 2018 In addition, GATA3 and ROR-gammat mRNA and protein levels significantly increased but Foxp3 mRNA and protein levels significantly decreased in mice with TNBS treatment compared to mice without TNBS treatment. Trinitrobenzenesulfonic Acid 153-157 forkhead box P3 Mus musculus 86-91 29704139-14 2018 Both MSCs therapies inhibited the expression of TGF-beta and the phosphorylation of Smad2 and Smad3 after TNBS induction. Trinitrobenzenesulfonic Acid 106-110 SMAD family member 3 Homo sapiens 94-99 29400705-6 2018 Consistent with this, TAOK1 deficiency exacerbates colitis in the 2,4,6-trinitrobenzenesulfonic acid)-induced experimental model of inflammatory bowel disease, likely by its promotion of the IL-17-mediated signaling pathway. Trinitrobenzenesulfonic Acid 66-100 interleukin 17A Homo sapiens 191-196 29788053-2 2018 We reported that mouse p40 peptide-based vaccines ameliorated intestinal inflammation in the prevention of trinitrobenzene sulfonic acid (TNBS)-induced murine colitis model. Trinitrobenzenesulfonic Acid 107-136 interleukin 12b Mus musculus 23-26 29788053-2 2018 We reported that mouse p40 peptide-based vaccines ameliorated intestinal inflammation in the prevention of trinitrobenzene sulfonic acid (TNBS)-induced murine colitis model. Trinitrobenzenesulfonic Acid 138-142 interleukin 12b Mus musculus 23-26 29910080-3 2018 In TNBS (2,4,6-trinitrobenzenesulfonic acid)-induced rat colitis model, oral administration of the compounds 5b and 5d ameliorated colitis with significant recovery in altered expressions of E-cadherin, TNF-alpha and IL-1beta expressions, indicating 5b and 5d as potential agents for therapeutics development against IBD. Trinitrobenzenesulfonic Acid 3-7 cadherin 1 Rattus norvegicus 191-201 29912317-5 2018 Expression of the highly upregulated Yes-associated protein 1 [YAP] was subsequently examined by qRT-PCR, western blotting, and immunohistochemistry in the intestinal tissues of CD patients and the colons of 2,4,6-trinitrobenzene sulphonic acid [TNBS]-induced colitis mice. Trinitrobenzenesulfonic Acid 246-250 Yes1 associated transcriptional regulator Homo sapiens 37-61 29912317-5 2018 Expression of the highly upregulated Yes-associated protein 1 [YAP] was subsequently examined by qRT-PCR, western blotting, and immunohistochemistry in the intestinal tissues of CD patients and the colons of 2,4,6-trinitrobenzene sulphonic acid [TNBS]-induced colitis mice. Trinitrobenzenesulfonic Acid 246-250 Yes1 associated transcriptional regulator Homo sapiens 63-66 29543509-4 2018 Colitis in wild-type and IL-10-, Toll-like receptor 4 (TLR4)-, and myeloid differentiation primary response 88 (MyD88)-deficient mice was induced via the administration of 2,4,6-trinitrobenzene sulfonic acid (TNBS) into the colon. Trinitrobenzenesulfonic Acid 172-207 toll-like receptor 4 Mus musculus 33-53 29543509-4 2018 Colitis in wild-type and IL-10-, Toll-like receptor 4 (TLR4)-, and myeloid differentiation primary response 88 (MyD88)-deficient mice was induced via the administration of 2,4,6-trinitrobenzene sulfonic acid (TNBS) into the colon. Trinitrobenzenesulfonic Acid 172-207 toll-like receptor 4 Mus musculus 55-59 29543509-6 2018 In the TNBS-induced colitis model, guggulsterone reduced disease activity index scores and TREM-1 expression, stimulated IL-10 production, and improved survival in wild-type mice. Trinitrobenzenesulfonic Acid 7-11 triggering receptor expressed on myeloid cells 1 Mus musculus 91-97 29543509-6 2018 In the TNBS-induced colitis model, guggulsterone reduced disease activity index scores and TREM-1 expression, stimulated IL-10 production, and improved survival in wild-type mice. Trinitrobenzenesulfonic Acid 7-11 interleukin 10 Mus musculus 121-126 29704139-14 2018 Both MSCs therapies inhibited the expression of TGF-beta and the phosphorylation of Smad2 and Smad3 after TNBS induction. Trinitrobenzenesulfonic Acid 106-110 SMAD family member 2 Homo sapiens 84-89 29524405-0 2018 Dual expression of CXCR4 and IL-35 enhances the therapeutic effects of BMSCs on TNBS-induced colitis in rats through expansion of Tregs and suppression of Th17 cells. Trinitrobenzenesulfonic Acid 80-84 C-X-C motif chemokine receptor 4 Rattus norvegicus 19-24 29520975-10 2018 Western blotting proved that TNBS infusion down-regulated ChAT but up-regulated NOS expression in the colon MP. Trinitrobenzenesulfonic Acid 29-33 choline O-acetyltransferase Rattus norvegicus 58-62 29933379-9 2018 Colonic IL-1beta concentrations, colonic and systemic CD11b+ cell infiltration, and the number of migrating CD11b+ cells on colonic blood vessels were all increased in TNBS treated mice relative to controls. Trinitrobenzenesulfonic Acid 168-172 interleukin 1 beta Homo sapiens 8-16 29933379-9 2018 Colonic IL-1beta concentrations, colonic and systemic CD11b+ cell infiltration, and the number of migrating CD11b+ cells on colonic blood vessels were all increased in TNBS treated mice relative to controls. Trinitrobenzenesulfonic Acid 168-172 integrin subunit alpha M Homo sapiens 54-59 29933379-9 2018 Colonic IL-1beta concentrations, colonic and systemic CD11b+ cell infiltration, and the number of migrating CD11b+ cells on colonic blood vessels were all increased in TNBS treated mice relative to controls. Trinitrobenzenesulfonic Acid 168-172 integrin subunit alpha M Homo sapiens 108-113 29716766-4 2018 In the present study, ATF3, p53, and p53 target gene Bax expression increased in CD patients; a mouse 2, 4, 6-trinitrobenzenesulfonic acid (TNBS)-induced CD model; and a TNF-alpha-treated HT29 cell colitis model. Trinitrobenzenesulfonic Acid 102-138 activating transcription factor 3 Homo sapiens 22-26 29716766-4 2018 In the present study, ATF3, p53, and p53 target gene Bax expression increased in CD patients; a mouse 2, 4, 6-trinitrobenzenesulfonic acid (TNBS)-induced CD model; and a TNF-alpha-treated HT29 cell colitis model. Trinitrobenzenesulfonic Acid 102-138 tumor protein p53 Homo sapiens 37-40 29716766-4 2018 In the present study, ATF3, p53, and p53 target gene Bax expression increased in CD patients; a mouse 2, 4, 6-trinitrobenzenesulfonic acid (TNBS)-induced CD model; and a TNF-alpha-treated HT29 cell colitis model. Trinitrobenzenesulfonic Acid 102-138 BCL2 associated X, apoptosis regulator Homo sapiens 53-56 29886462-0 2018 [Effects of Pim-1 inhibitor on mouse model of inflammatory bowel disease induced by TNBS]. Trinitrobenzenesulfonic Acid 84-88 proviral integration site 1 Mus musculus 12-17 29577935-7 2018 In addition, lentiviral vector-PTHLH-treated mice were highly sensitive to 2,4,6-trinitrobenzene sulfonic acid, and analysis of the PTHLH-PTH1R axis revealed the involvement of PKA-Runx2 in PTHLH-induced EMT. Trinitrobenzenesulfonic Acid 75-110 parathyroid hormone-like peptide Mus musculus 31-36 29865176-0 2018 Treatment with Obestatin-A Ghrelin Gene-Encoded Peptide-Reduces the Severity of Experimental Colitis Evoked by Trinitrobenzene Sulfonic Acid. Trinitrobenzenesulfonic Acid 111-140 ghrelin and obestatin prepropeptide Rattus norvegicus 27-34 29620246-5 2018 Compared with the control group, TNBS-treated mice had significantly higher secretion of IL-17, higher DAI scores, a lower ratio of Treg, reduced colon lengths and higher histological scores for colon inflammation. Trinitrobenzenesulfonic Acid 33-37 interleukin 17A Mus musculus 89-94 29760423-6 2018 Second, LC27 and LC67 inhibited TNBS-induced NF-kappaB activation, reversed TNBS-suppressed tight junction protein expression, and restored Th17/Treg balance. Trinitrobenzenesulfonic Acid 32-36 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 45-54 29668937-9 2018 TNBS treatment enhanced Smad7 in both colonic epithelial and lamina propria mononuclear cells. Trinitrobenzenesulfonic Acid 0-4 SMAD family member 7 Mus musculus 24-29 29760423-7 2018 Also, treatment with LC27 or LC67 significantly decreased TNBS-induced alanine transaminase [ALT, F(5,30) = 3.50, P < 0.05] and aspartate transaminase [AST, F(5,30) = 12.81, P < 0.05] levels in the blood, as well as t-butylhydroperoxide-induced ALT and AST levels. Trinitrobenzenesulfonic Acid 58-62 glutamic pyruvic transaminase, soluble Mus musculus 93-96 29760423-7 2018 Also, treatment with LC27 or LC67 significantly decreased TNBS-induced alanine transaminase [ALT, F(5,30) = 3.50, P < 0.05] and aspartate transaminase [AST, F(5,30) = 12.81, P < 0.05] levels in the blood, as well as t-butylhydroperoxide-induced ALT and AST levels. Trinitrobenzenesulfonic Acid 58-62 solute carrier family 17 (anion/sugar transporter), member 5 Mus musculus 152-155 29760423-7 2018 Also, treatment with LC27 or LC67 significantly decreased TNBS-induced alanine transaminase [ALT, F(5,30) = 3.50, P < 0.05] and aspartate transaminase [AST, F(5,30) = 12.81, P < 0.05] levels in the blood, as well as t-butylhydroperoxide-induced ALT and AST levels. Trinitrobenzenesulfonic Acid 58-62 glutamic pyruvic transaminase, soluble Mus musculus 245-248 29760423-7 2018 Also, treatment with LC27 or LC67 significantly decreased TNBS-induced alanine transaminase [ALT, F(5,30) = 3.50, P < 0.05] and aspartate transaminase [AST, F(5,30) = 12.81, P < 0.05] levels in the blood, as well as t-butylhydroperoxide-induced ALT and AST levels. Trinitrobenzenesulfonic Acid 58-62 solute carrier family 17 (anion/sugar transporter), member 5 Mus musculus 253-256 29550454-3 2018 In this study, we aimed to explore the potential role of miR-146a-5p (the mature form of miR-146a) in a mouse model of colitis induced by intracolonic injection of trinitrobenzene sulfonic acid (TNBS). Trinitrobenzenesulfonic Acid 164-193 microRNA 146 Mus musculus 57-65 29738575-3 2018 The present study aimed to evaluate the effects of adoptive transfer of DCs obtained from both naive and ovalbumin (OVA)-tolerant mice on the severity of TNBS induced colitis and analyze the eventual protective mechanisms. Trinitrobenzenesulfonic Acid 154-158 serine (or cysteine) peptidase inhibitor, clade B, member 1, pseudogene Mus musculus 105-114 29853790-7 2018 In addition, there was a downregulation of the TNBS-induced increase in the activity of iNOS and levels of Cox-2, TNF-alpha, and IL-1beta while the protein expression of NF-kappaB was significantly unregulated after administration of H-PHL. Trinitrobenzenesulfonic Acid 47-51 cytochrome c oxidase II, mitochondrial Rattus norvegicus 107-112 29853790-7 2018 In addition, there was a downregulation of the TNBS-induced increase in the activity of iNOS and levels of Cox-2, TNF-alpha, and IL-1beta while the protein expression of NF-kappaB was significantly unregulated after administration of H-PHL. Trinitrobenzenesulfonic Acid 47-51 tumor necrosis factor Rattus norvegicus 114-123 29853790-7 2018 In addition, there was a downregulation of the TNBS-induced increase in the activity of iNOS and levels of Cox-2, TNF-alpha, and IL-1beta while the protein expression of NF-kappaB was significantly unregulated after administration of H-PHL. Trinitrobenzenesulfonic Acid 47-51 interleukin 1 beta Rattus norvegicus 129-137 29550454-3 2018 In this study, we aimed to explore the potential role of miR-146a-5p (the mature form of miR-146a) in a mouse model of colitis induced by intracolonic injection of trinitrobenzene sulfonic acid (TNBS). Trinitrobenzenesulfonic Acid 164-193 microRNA 146 Mus musculus 89-97 29550454-3 2018 In this study, we aimed to explore the potential role of miR-146a-5p (the mature form of miR-146a) in a mouse model of colitis induced by intracolonic injection of trinitrobenzene sulfonic acid (TNBS). Trinitrobenzenesulfonic Acid 195-199 microRNA 146 Mus musculus 89-97 29545894-6 2018 In TNBS mice receiving AdTGF-2, the increase in IFN-gamma, tumor necrosis factor-alpha, IL-6, IL-17 and IL-23 was significantly prevented by dexamethasone treatment. Trinitrobenzenesulfonic Acid 3-7 interferon gamma Mus musculus 48-86 29304229-2 2018 We have previously observed that STAT6-/- mice present delayed mucosal recovery after 2,4,6-trinitrobenzenesulfonic acid [TNBS]-induced colitis due to a deficiency in reparatory interleukin-4 [IL4]/STAT6-dependent M2 macrophages, which can be reverted by the exogenous transfer of this cell type. Trinitrobenzenesulfonic Acid 86-120 signal transducer and activator of transcription 6 Mus musculus 33-38 29304229-2 2018 We have previously observed that STAT6-/- mice present delayed mucosal recovery after 2,4,6-trinitrobenzenesulfonic acid [TNBS]-induced colitis due to a deficiency in reparatory interleukin-4 [IL4]/STAT6-dependent M2 macrophages, which can be reverted by the exogenous transfer of this cell type. Trinitrobenzenesulfonic Acid 86-120 interleukin 4 Mus musculus 178-191 29304229-2 2018 We have previously observed that STAT6-/- mice present delayed mucosal recovery after 2,4,6-trinitrobenzenesulfonic acid [TNBS]-induced colitis due to a deficiency in reparatory interleukin-4 [IL4]/STAT6-dependent M2 macrophages, which can be reverted by the exogenous transfer of this cell type. Trinitrobenzenesulfonic Acid 86-120 interleukin 4 Mus musculus 193-196 29304229-2 2018 We have previously observed that STAT6-/- mice present delayed mucosal recovery after 2,4,6-trinitrobenzenesulfonic acid [TNBS]-induced colitis due to a deficiency in reparatory interleukin-4 [IL4]/STAT6-dependent M2 macrophages, which can be reverted by the exogenous transfer of this cell type. Trinitrobenzenesulfonic Acid 122-126 signal transducer and activator of transcription 6 Mus musculus 33-38 29304229-10 2018 Finally, administration of IL4-treated WT macrophages to STAT6-/- mice reduced TNBS-induced fibrosis. Trinitrobenzenesulfonic Acid 79-83 interleukin 4 Mus musculus 27-30 29304229-10 2018 Finally, administration of IL4-treated WT macrophages to STAT6-/- mice reduced TNBS-induced fibrosis. Trinitrobenzenesulfonic Acid 79-83 signal transducer and activator of transcription 6 Mus musculus 57-62 29631607-15 2018 CONCLUSIONS: ASC submucosal endoscopic injection is feasible, safe and ameliorates TNBS-induced colitis in rats, especially stenosis. Trinitrobenzenesulfonic Acid 83-87 PYD and CARD domain containing Rattus norvegicus 13-16 29627390-9 2018 Our data indicated that SB ameliorated the TNBS-induced inflammatory response and intestinal epithelium barrier dysfunction through activating GPR109A and inhibiting the AKT and NF-kappaB p65 signaling pathways. Trinitrobenzenesulfonic Acid 43-47 hydroxycarboxylic acid receptor 2 Mus musculus 143-150 29627390-9 2018 Our data indicated that SB ameliorated the TNBS-induced inflammatory response and intestinal epithelium barrier dysfunction through activating GPR109A and inhibiting the AKT and NF-kappaB p65 signaling pathways. Trinitrobenzenesulfonic Acid 43-47 thymoma viral proto-oncogene 1 Mus musculus 170-173 29627390-9 2018 Our data indicated that SB ameliorated the TNBS-induced inflammatory response and intestinal epithelium barrier dysfunction through activating GPR109A and inhibiting the AKT and NF-kappaB p65 signaling pathways. Trinitrobenzenesulfonic Acid 43-47 v-rel reticuloendotheliosis viral oncogene homolog A (avian) Mus musculus 188-191 29545894-0 2018 Local level of TGF-beta1 determines the effectiveness of dexamethasone through regulating the balance of Treg/Th17 cells in TNBS-induced mouse colitis. Trinitrobenzenesulfonic Acid 124-128 transforming growth factor, beta 1 Mus musculus 15-24 29545894-2 2018 The present study investigated the effects of different local TGF-beta1 levels on the Treg/Th17 balance and on the dexamethasone efficacy in mice with 2,4,6-trinitrobenzenesulfonic acid (TNBS)-induced colitis. Trinitrobenzenesulfonic Acid 187-191 transforming growth factor, beta 1 Mus musculus 62-71 29545894-4 2018 Dexamethasone further decreased colon damage and myeloperoxidase activity in TNBS mice receiving AdTGF-1 and AdTGF-2. Trinitrobenzenesulfonic Acid 77-81 myeloperoxidase Mus musculus 49-64 29516326-10 2018 Functionally, gadolinium chloride (GdCl3), a macrophage selective inhibitor, or LP17, the TREM-1-specific peptide, significantly suppressed the visceral hypersensitivity in trinitrobenzene sulfonic acid (TNBS)-treated mice with IBS-like visceral hypersensitivity. Trinitrobenzenesulfonic Acid 173-202 triggering receptor expressed on myeloid cells 1 Mus musculus 90-96 29516326-10 2018 Functionally, gadolinium chloride (GdCl3), a macrophage selective inhibitor, or LP17, the TREM-1-specific peptide, significantly suppressed the visceral hypersensitivity in trinitrobenzene sulfonic acid (TNBS)-treated mice with IBS-like visceral hypersensitivity. Trinitrobenzenesulfonic Acid 204-208 triggering receptor expressed on myeloid cells 1 Mus musculus 90-96 29545894-6 2018 In TNBS mice receiving AdTGF-2, the increase in IFN-gamma, tumor necrosis factor-alpha, IL-6, IL-17 and IL-23 was significantly prevented by dexamethasone treatment. Trinitrobenzenesulfonic Acid 3-7 interleukin 6 Mus musculus 88-92 29545894-6 2018 In TNBS mice receiving AdTGF-2, the increase in IFN-gamma, tumor necrosis factor-alpha, IL-6, IL-17 and IL-23 was significantly prevented by dexamethasone treatment. Trinitrobenzenesulfonic Acid 3-7 interleukin 17A Mus musculus 94-99 29545894-6 2018 In TNBS mice receiving AdTGF-2, the increase in IFN-gamma, tumor necrosis factor-alpha, IL-6, IL-17 and IL-23 was significantly prevented by dexamethasone treatment. Trinitrobenzenesulfonic Acid 3-7 interleukin 23, alpha subunit p19 Mus musculus 104-109 29545894-8 2018 In mesenteric lymph nodes, AdTGF-1 prevented the TNBS-induced reduction of Tregs and IL-10, and potentially increased the efficacy of dexamethasone. Trinitrobenzenesulfonic Acid 49-53 interleukin 10 Mus musculus 85-90 29545894-9 2018 In addition, dexamethasone further decreased the levels of activated caspase3 in TNBS mice receiving adenoviral TGF-beta1, particularly in the AdTGF-1 group. Trinitrobenzenesulfonic Acid 81-85 caspase 3 Mus musculus 69-77 29545894-9 2018 In addition, dexamethasone further decreased the levels of activated caspase3 in TNBS mice receiving adenoviral TGF-beta1, particularly in the AdTGF-1 group. Trinitrobenzenesulfonic Acid 81-85 transforming growth factor, beta 1 Mus musculus 112-121 29545894-10 2018 The activation of the p38 mitogen-activated protein kinase/c-Jun N-terminal kinase/c-Jun pathway was significantly inhibited by a low amount of TGF-beta1 administered to TNBS-treated mice, which was further decreased by dexamethasone. Trinitrobenzenesulfonic Acid 170-174 jun proto-oncogene Mus musculus 59-64 29545894-10 2018 The activation of the p38 mitogen-activated protein kinase/c-Jun N-terminal kinase/c-Jun pathway was significantly inhibited by a low amount of TGF-beta1 administered to TNBS-treated mice, which was further decreased by dexamethasone. Trinitrobenzenesulfonic Acid 170-174 jun proto-oncogene Mus musculus 83-88 29545894-10 2018 The activation of the p38 mitogen-activated protein kinase/c-Jun N-terminal kinase/c-Jun pathway was significantly inhibited by a low amount of TGF-beta1 administered to TNBS-treated mice, which was further decreased by dexamethasone. Trinitrobenzenesulfonic Acid 170-174 transforming growth factor, beta 1 Mus musculus 144-153 29545894-11 2018 The present study provided evidence that the therapeutic effect of dexamethasone may depend on the local levels of TGF-beta1 in TNBS-induced colitis and may be mediated, at least partially, through promoting the differentiation of Tregs and thus altering the balance of pro- and anti-inflammatory cytokines. Trinitrobenzenesulfonic Acid 128-132 transforming growth factor, beta 1 Mus musculus 115-124 28337639-15 2018 RESULTS: Rats in the TNBS group developed symptoms of colitis, including: body weight loss, colon mass index increase and damage of intestinal tissues with concomitant increase in TNF-alpha, IL-17, MDA levels and decreased SOD activity. Trinitrobenzenesulfonic Acid 21-25 tumor necrosis factor Rattus norvegicus 180-189 29253460-8 2018 miR-31-3p expression was increased in both TNBS- and DSS-induced colitis and human colonic biopsies from ulcerative colitis, compared with controls. Trinitrobenzenesulfonic Acid 43-47 microRNA 31 Homo sapiens 0-6 28337639-15 2018 RESULTS: Rats in the TNBS group developed symptoms of colitis, including: body weight loss, colon mass index increase and damage of intestinal tissues with concomitant increase in TNF-alpha, IL-17, MDA levels and decreased SOD activity. Trinitrobenzenesulfonic Acid 21-25 interleukin 17A Rattus norvegicus 191-196 29572553-7 2018 Galan reduced the TNBS-induced ulceration, colon mass index, colonic MDA, neutrophils adhesion and infiltration (ICAM-1/MPO), inflammatory mediators (NF-kappaB, TNF-alpha, HMGB1, and RAGE), while increased the anti-apoptotic pathway (p-Akt/Bcl-2). Trinitrobenzenesulfonic Acid 18-22 high mobility group box 1 Rattus norvegicus 172-177 29572553-7 2018 Galan reduced the TNBS-induced ulceration, colon mass index, colonic MDA, neutrophils adhesion and infiltration (ICAM-1/MPO), inflammatory mediators (NF-kappaB, TNF-alpha, HMGB1, and RAGE), while increased the anti-apoptotic pathway (p-Akt/Bcl-2). Trinitrobenzenesulfonic Acid 18-22 advanced glycosylation end product-specific receptor Rattus norvegicus 183-187 29572553-7 2018 Galan reduced the TNBS-induced ulceration, colon mass index, colonic MDA, neutrophils adhesion and infiltration (ICAM-1/MPO), inflammatory mediators (NF-kappaB, TNF-alpha, HMGB1, and RAGE), while increased the anti-apoptotic pathway (p-Akt/Bcl-2). Trinitrobenzenesulfonic Acid 18-22 BCL2, apoptosis regulator Rattus norvegicus 240-245 29253460-9 2018 Intracolonic administration of a miR-31-3p chemical inhibitor exacerbated TNBS- and DSS-induced colitis and increased colonic TNF-alpha, CXCL10, and chemokine (C-C motif) ligand 2 (CCL2) mRNA expression. Trinitrobenzenesulfonic Acid 74-78 microRNA 31 Homo sapiens 33-39 29133078-15 2018 REG3A TG mice developed only mild colonic inflammation after exposure to 2,4,6-trinitrobenzene sulfonic acid, compared with control mice. Trinitrobenzenesulfonic Acid 73-108 regenerating islet-derived 3 alpha Mus musculus 0-5 28612842-3 2018 TNBS treatment increased fecal and blood levels of lipopolysaccharide (LPS) and the number of Enterobacteriaceae, particularly Escherichia coli (EC), in the gut microbiota composition, but significantly reduced the number of Lactobacillus johnsonii (LJ). Trinitrobenzenesulfonic Acid 0-4 toll-like receptor 4 Mus musculus 71-74 29790024-2 2018 In colitis caused by trinitrobenzene sulfonate, an increase in TRPV1 expression was more significant in both plexuses. Trinitrobenzenesulfonic Acid 21-46 transient receptor potential cation channel, subfamily V, member 1 Rattus norvegicus 63-68 28582593-4 2018 METHODS: Colitis was induced in wild-type (WT) and SPARC knockout (KO) mice using trinitrobenzene sulfonic acid (TNBS). Trinitrobenzenesulfonic Acid 82-111 secreted acidic cysteine rich glycoprotein Mus musculus 51-56 28582593-9 2018 RESULTS: Trinitrobenzene sulfonic acid exposure significantly reduced bodyweight and increased mucosal inflammation, leukocyte infiltration, and Il17a mRNA expression in WT relative to SPARC KO mice. Trinitrobenzenesulfonic Acid 9-38 interleukin 17A Mus musculus 145-150 28582593-9 2018 RESULTS: Trinitrobenzene sulfonic acid exposure significantly reduced bodyweight and increased mucosal inflammation, leukocyte infiltration, and Il17a mRNA expression in WT relative to SPARC KO mice. Trinitrobenzenesulfonic Acid 9-38 secreted acidic cysteine rich glycoprotein Mus musculus 185-190 28612842-6 2018 Treatment with TNBS or EC induced NF-kappaB activation and tumor necrosis factor-alpha expression in the hippocampus of mice, as well as suppressed brain-derived neurotrophic factor expression. Trinitrobenzenesulfonic Acid 15-19 brain derived neurotrophic factor Mus musculus 148-181 29226383-2 2018 Trinitrobenzene sulfonic acid (TNBS) was used to induce colitis in mice and 1-methyltryptophan (1-MT) to block expression of IDO. Trinitrobenzenesulfonic Acid 0-29 indoleamine 2,3-dioxygenase 1 Mus musculus 125-128 29773105-0 2018 [Protective role of green tea polyphenols in intestinal mucosal barrier function of mice with colitis induced by TNBS through inhibiting JAK2/STAT3 pathway]. Trinitrobenzenesulfonic Acid 113-117 Janus kinase 2 Mus musculus 137-141 29773105-0 2018 [Protective role of green tea polyphenols in intestinal mucosal barrier function of mice with colitis induced by TNBS through inhibiting JAK2/STAT3 pathway]. Trinitrobenzenesulfonic Acid 113-117 signal transducer and activator of transcription 3 Mus musculus 142-147 29773105-13 2018 Conclusion GTP has a significant therapeutic effect on TNBS-induced colitis through down-regulating the JAK2/STAT3 signaling pathway. Trinitrobenzenesulfonic Acid 55-59 Janus kinase 2 Mus musculus 104-108 29773105-13 2018 Conclusion GTP has a significant therapeutic effect on TNBS-induced colitis through down-regulating the JAK2/STAT3 signaling pathway. Trinitrobenzenesulfonic Acid 55-59 signal transducer and activator of transcription 3 Mus musculus 109-114 29456409-1 2018 AIM: To investigate the modulatory effect of recombinant-expressed vasoactive intestinal peptide (VIP) analogue (rVIPa) on trinitrobenzene sulfonic acid (TNBS)-induced colitis in rats. Trinitrobenzenesulfonic Acid 123-152 vasoactive intestinal peptide Rattus norvegicus 98-101 29456409-1 2018 AIM: To investigate the modulatory effect of recombinant-expressed vasoactive intestinal peptide (VIP) analogue (rVIPa) on trinitrobenzene sulfonic acid (TNBS)-induced colitis in rats. Trinitrobenzenesulfonic Acid 154-158 vasoactive intestinal peptide Rattus norvegicus 98-101 29051186-3 2018 Here, the role of Hsp70-mediated intestinal epithelial protection and immune regulation in experimental colitis was examined by using a villin promoter-driven Hsp70 transgene in the 2,4,6-trinitrobenzene sulfonic acid (TNBS) and dextran sodium sulfate (DSS) models and in IL-10/Hsp70 double knockout (IL10-/-/Hsp70-/-) mice. Trinitrobenzenesulfonic Acid 219-223 heat shock protein 1B Mus musculus 18-23 29226383-8 2018 These findings study suggest that Bifidobacteria attenuate TNBS-induced colitis by inducing expression of IDO, which further increases generation of Foxp3+ Treg cells. Trinitrobenzenesulfonic Acid 59-63 indoleamine 2,3-dioxygenase 1 Homo sapiens 106-109 29226383-8 2018 These findings study suggest that Bifidobacteria attenuate TNBS-induced colitis by inducing expression of IDO, which further increases generation of Foxp3+ Treg cells. Trinitrobenzenesulfonic Acid 59-63 forkhead box P3 Homo sapiens 149-154 29081213-4 2018 C29 treatment increased TNBS-suppressed hippocampal brain-derived neurotrophic factor expression and inhibited TNBS-induced hippocampal NF-kappaB activation and blood LPS levels. Trinitrobenzenesulfonic Acid 24-28 brain derived neurotrophic factor Mus musculus 52-85 29129496-4 2018 In this study, Runx2 protein levels were decreased in the intestinal epithelial cells (IECs) of CD patients and in a mouse 2, 4,6-trinitrobenzenesulfonic acid (TNBS)-induced colitis model; in contrast, the expression levels of p53 and Bax, a p53-target gene, were increased. Trinitrobenzenesulfonic Acid 123-158 RUNX family transcription factor 2 Homo sapiens 15-20 29129496-4 2018 In this study, Runx2 protein levels were decreased in the intestinal epithelial cells (IECs) of CD patients and in a mouse 2, 4,6-trinitrobenzenesulfonic acid (TNBS)-induced colitis model; in contrast, the expression levels of p53 and Bax, a p53-target gene, were increased. Trinitrobenzenesulfonic Acid 160-164 RUNX family transcription factor 2 Homo sapiens 15-20 29129496-4 2018 In this study, Runx2 protein levels were decreased in the intestinal epithelial cells (IECs) of CD patients and in a mouse 2, 4,6-trinitrobenzenesulfonic acid (TNBS)-induced colitis model; in contrast, the expression levels of p53 and Bax, a p53-target gene, were increased. Trinitrobenzenesulfonic Acid 160-164 transformation related protein 53, pseudogene Mus musculus 227-230 29129496-4 2018 In this study, Runx2 protein levels were decreased in the intestinal epithelial cells (IECs) of CD patients and in a mouse 2, 4,6-trinitrobenzenesulfonic acid (TNBS)-induced colitis model; in contrast, the expression levels of p53 and Bax, a p53-target gene, were increased. Trinitrobenzenesulfonic Acid 160-164 BCL2-associated X protein Mus musculus 235-238 29129496-4 2018 In this study, Runx2 protein levels were decreased in the intestinal epithelial cells (IECs) of CD patients and in a mouse 2, 4,6-trinitrobenzenesulfonic acid (TNBS)-induced colitis model; in contrast, the expression levels of p53 and Bax, a p53-target gene, were increased. Trinitrobenzenesulfonic Acid 160-164 transformation related protein 53, pseudogene Mus musculus 242-245 29049008-4 2018 In oxazolone-induced intestinal colitis, the expression levels of CRAMP and its receptor FPR2 significantly increased in comparison with those of TNBS-induced mice, vesicle and normal controls. Trinitrobenzenesulfonic Acid 146-150 cathelicidin antimicrobial peptide Mus musculus 66-71 29049008-4 2018 In oxazolone-induced intestinal colitis, the expression levels of CRAMP and its receptor FPR2 significantly increased in comparison with those of TNBS-induced mice, vesicle and normal controls. Trinitrobenzenesulfonic Acid 146-150 formyl peptide receptor 2 Mus musculus 89-93 29552620-13 2018 TRPA1/heat shock protein 47 double-positive cells accumulated in the stenotic intestinal regions of both CD patients and TNBS-treated mice. Trinitrobenzenesulfonic Acid 121-125 transient receptor potential cation channel subfamily A member 1 Homo sapiens 0-5 30518233-9 2018 FRG most potently suppressed TNBS-induced colon shortening, NF- kappa B activation and TNF- alpha and IL-17 expression and increased IL-10 expression. Trinitrobenzenesulfonic Acid 29-33 tumor necrosis factor Mus musculus 87-97 30518233-9 2018 FRG most potently suppressed TNBS-induced colon shortening, NF- kappa B activation and TNF- alpha and IL-17 expression and increased IL-10 expression. Trinitrobenzenesulfonic Acid 29-33 interleukin 17A Mus musculus 102-107 29272492-9 2017 Treating wild-type mice with a DAP-12 inhibitor or a Syk inhibitor caused a robust attenuation of colitis induced by DSS and TNBS. Trinitrobenzenesulfonic Acid 125-129 TYRO protein tyrosine kinase binding protein Mus musculus 31-37 29272492-9 2017 Treating wild-type mice with a DAP-12 inhibitor or a Syk inhibitor caused a robust attenuation of colitis induced by DSS and TNBS. Trinitrobenzenesulfonic Acid 125-129 spleen tyrosine kinase Mus musculus 53-56 28370348-8 2017 RESULTS: MiR-200b-MVs would significantly reverse the morphology in TGF-beta1-treated IEC-6 cells and improve the TNBS-induced colon fibrosis histologically. Trinitrobenzenesulfonic Acid 114-118 microRNA 200b Rattus norvegicus 9-17 29312281-7 2017 gp96-II peptide treatment in the TNBS model limited weight loss to 5% on day 7 compared with prednisolone treatment, whereas placebo-treated animals suffered a 20% weight loss. Trinitrobenzenesulfonic Acid 33-37 heat shock protein 90, beta (Grp94), member 1 Mus musculus 0-4 29285167-0 2017 Effectiveness of C5a aptamers in a TNBS-induced colitis mouse model. Trinitrobenzenesulfonic Acid 35-39 hemolytic complement Mus musculus 17-20 29180692-0 2017 Baicalein ameliorates TNBS-induced colitis by suppressing TLR4/MyD88 signaling cascade and NLRP3 inflammasome activation in mice. Trinitrobenzenesulfonic Acid 22-26 toll-like receptor 4 Mus musculus 58-62 28990050-8 2017 Treatment with n-3 PUFA increased the gene expression of PPAR-gamma in TNBS-treated rats, and reduced the expression of NFAT, which ultimately reduced the release of IL-4 and IL-2 detected by RT-qPCR. Trinitrobenzenesulfonic Acid 71-75 peroxisome proliferator-activated receptor gamma Rattus norvegicus 57-67 28990050-10 2017 In conclusion, the present study demonstrated that dietary n-3 PUFA may attenuate experimental CD induced by TNBS in rats by regulating the expression and activity of the PPAR-gamma/NFAT signaling pathway. Trinitrobenzenesulfonic Acid 109-113 peroxisome proliferator-activated receptor gamma Rattus norvegicus 171-181 28990050-10 2017 In conclusion, the present study demonstrated that dietary n-3 PUFA may attenuate experimental CD induced by TNBS in rats by regulating the expression and activity of the PPAR-gamma/NFAT signaling pathway. Trinitrobenzenesulfonic Acid 109-113 nuclear factor of activated T-cells 5 Rattus norvegicus 182-186 29180692-8 2017 Our study provided evidence for the first time that baicalein attenuated TNBS-induced colitis, at least in part, via inhibition of TLR4/MyD88 signaling cascade as well as inactivation of NLRP3 inflammasome. Trinitrobenzenesulfonic Acid 73-77 toll-like receptor 4 Mus musculus 131-135 29180692-8 2017 Our study provided evidence for the first time that baicalein attenuated TNBS-induced colitis, at least in part, via inhibition of TLR4/MyD88 signaling cascade as well as inactivation of NLRP3 inflammasome. Trinitrobenzenesulfonic Acid 73-77 myeloid differentiation primary response gene 88 Mus musculus 136-141 29180692-0 2017 Baicalein ameliorates TNBS-induced colitis by suppressing TLR4/MyD88 signaling cascade and NLRP3 inflammasome activation in mice. Trinitrobenzenesulfonic Acid 22-26 myeloid differentiation primary response gene 88 Mus musculus 63-68 29180692-0 2017 Baicalein ameliorates TNBS-induced colitis by suppressing TLR4/MyD88 signaling cascade and NLRP3 inflammasome activation in mice. Trinitrobenzenesulfonic Acid 22-26 NLR family, pyrin domain containing 3 Mus musculus 91-96 28854413-3 2017 In this study, novel amphiphilic apo-Tf stearic acid (TfS) conjugates were prepared and characterized by Fourier transform infrared (FTIR) spectroscopy, matrix-assisted laser desorption/ionization-time of flight (MALDI-TOF) mass spectrometry, and trinitrobenzenesulfonic acid (TNBS) assay. Trinitrobenzenesulfonic Acid 247-275 transferrin Homo sapiens 37-39 29167643-8 2017 Conversely, loss of ICCs may explain the lower amounts of adenosine detected in TNBS-treated preparations, since blockade of Cav3 (T-type) channels existing in ICCs with mibefradil (3 muM) or inhibition of the equilibrative nucleoside transporter 1 with dipyridamole (0.5 muM), both decreased extracellular adenosine. Trinitrobenzenesulfonic Acid 80-84 caveolin 3 Rattus norvegicus 125-129 29209161-10 2017 Results: Goats administered with TNBS-ethanol solution showed diarrhea, enhanced VMR and pain behavior response, and increased IL-6, phosphorylated JAK2 and STAT3 (pJAK2 and pSTAT3) in the vlPAG, NRM, NTS and DMV, and their protein and mRNA levels in the SCDH. Trinitrobenzenesulfonic Acid 33-37 interleukin-6 Capra hircus 127-131 29209161-10 2017 Results: Goats administered with TNBS-ethanol solution showed diarrhea, enhanced VMR and pain behavior response, and increased IL-6, phosphorylated JAK2 and STAT3 (pJAK2 and pSTAT3) in the vlPAG, NRM, NTS and DMV, and their protein and mRNA levels in the SCDH. Trinitrobenzenesulfonic Acid 33-37 tyrosine-protein kinase JAK2 Capra hircus 148-152 29209161-10 2017 Results: Goats administered with TNBS-ethanol solution showed diarrhea, enhanced VMR and pain behavior response, and increased IL-6, phosphorylated JAK2 and STAT3 (pJAK2 and pSTAT3) in the vlPAG, NRM, NTS and DMV, and their protein and mRNA levels in the SCDH. Trinitrobenzenesulfonic Acid 33-37 signal transducer and activator of transcription 3 Capra hircus 157-162 29167641-0 2017 alpha7 Nicotinic Agonist AR-R17779 Protects Mice against 2,4,6-Trinitrobenzene Sulfonic Acid-Induced Colitis in a Spleen-Dependent Way. Trinitrobenzenesulfonic Acid 57-92 cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus 0-6 29019857-5 2017 METHODS: We assessed oral delivery of Lactococcus lactis expressing an IL-27 hyperkine on the innate immune response in vivo in a genetically intact, noninfective, acute murine colitis model induced by intrarectal instillation of 2,4,6-trinitrobenzenesulfonic acid in SJL/J mice. Trinitrobenzenesulfonic Acid 230-264 interleukin 27 Mus musculus 71-76 29037608-10 2017 Finally, intrathecal CCL8 neutralizing antibody or CCR5 antagonist DAPTA dose-dependently suppressed TNBS-evoked visceral hyperalgesia and spinal ERK activation. Trinitrobenzenesulfonic Acid 101-105 chemokine (C-C motif) ligand 8 Mus musculus 21-25 29037608-8 2017 Furthermore, TNBS induced the activation of extracellular signal-regulated kinase (ERK) in the spinal cord. Trinitrobenzenesulfonic Acid 13-17 mitogen-activated protein kinase 1 Mus musculus 44-81 29037608-10 2017 Finally, intrathecal CCL8 neutralizing antibody or CCR5 antagonist DAPTA dose-dependently suppressed TNBS-evoked visceral hyperalgesia and spinal ERK activation. Trinitrobenzenesulfonic Acid 101-105 chemokine (C-C motif) receptor 5 Mus musculus 51-55 29037608-8 2017 Furthermore, TNBS induced the activation of extracellular signal-regulated kinase (ERK) in the spinal cord. Trinitrobenzenesulfonic Acid 13-17 mitogen-activated protein kinase 1 Mus musculus 83-86 29037608-9 2017 The induction of visceral pain by TNBS was attenuated by injection of ERK upstream kinase (MEK) inhibitor PD98059. Trinitrobenzenesulfonic Acid 34-38 mitogen-activated protein kinase 1 Mus musculus 70-73 28973050-6 2017 RESULTS: TNBS application to the tongue induced noninflammatory heat hypersensitivity accompanied by the enhancement of p38 phosphorylation in TG neurons innervating the tongue and by an increase in the number of TRPV1 and pp38-immunoreactive (IR) TG neurons innervating the tongue. Trinitrobenzenesulfonic Acid 9-13 mitogen-activated protein kinase 14 Mus musculus 120-123 29037608-9 2017 The induction of visceral pain by TNBS was attenuated by injection of ERK upstream kinase (MEK) inhibitor PD98059. Trinitrobenzenesulfonic Acid 34-38 midkine Mus musculus 91-94 28973050-6 2017 RESULTS: TNBS application to the tongue induced noninflammatory heat hypersensitivity accompanied by the enhancement of p38 phosphorylation in TG neurons innervating the tongue and by an increase in the number of TRPV1 and pp38-immunoreactive (IR) TG neurons innervating the tongue. Trinitrobenzenesulfonic Acid 9-13 transient receptor potential cation channel, subfamily V, member 1 Mus musculus 213-218 28973050-8 2017 CONCLUSION: p38 signaling cascades are involved in tongue heat hyperalgesia in association with TRPV1 upregulation in TG neurons innervating the TNBS-treated tongue. Trinitrobenzenesulfonic Acid 145-149 mitogen-activated protein kinase 14 Mus musculus 12-15 28973050-8 2017 CONCLUSION: p38 signaling cascades are involved in tongue heat hyperalgesia in association with TRPV1 upregulation in TG neurons innervating the TNBS-treated tongue. Trinitrobenzenesulfonic Acid 145-149 transient receptor potential cation channel, subfamily V, member 1 Mus musculus 96-101 29156831-6 2017 Results: In the TNBS-induced colitis in mice, TUNEL-positive and caspase-3-negative cells were observed in the intestinal mucosa, and p-RIPK3 was found to be elevated. Trinitrobenzenesulfonic Acid 16-20 caspase 3 Mus musculus 65-74 28765897-4 2017 In the present study, the effect of TAK-242 on trinitrobenzene sulfonic acid (TNBS)-induced chronic pancreatitis was investigated in rats. Trinitrobenzenesulfonic Acid 47-76 cyclin dependent kinase 9 Homo sapiens 36-39 28765897-4 2017 In the present study, the effect of TAK-242 on trinitrobenzene sulfonic acid (TNBS)-induced chronic pancreatitis was investigated in rats. Trinitrobenzenesulfonic Acid 78-82 cyclin dependent kinase 9 Homo sapiens 36-39 28765897-6 2017 In addition, TAK-242 treatment significantly decreased cell apoptosis, as evidenced by the reduction in Terminal deoxynucleotidyl transferase dUTP nick end labeling-positive cells in pancreas tissue sections, and also promoted cell proliferation in TNBS-treated animals. Trinitrobenzenesulfonic Acid 249-253 cyclin dependent kinase 9 Homo sapiens 13-16 28765897-8 2017 In summary, TAK-242 exhibits protective effects against TNBS-induced chronic pancreatitis and may be a potential therapeutic strategy for the treatment of patients with chronic pancreatitis. Trinitrobenzenesulfonic Acid 56-60 cyclin dependent kinase 9 Homo sapiens 12-15 29156831-6 2017 Results: In the TNBS-induced colitis in mice, TUNEL-positive and caspase-3-negative cells were observed in the intestinal mucosa, and p-RIPK3 was found to be elevated. Trinitrobenzenesulfonic Acid 16-20 receptor interacting serine/threonine kinase 3 Homo sapiens 136-141 28500644-11 2017 Blockade of autophagosome formation by treatment with 3MA, prevented the reduction in protein levels of p62, BCL10, p-IkappaBalpha and NFkappaB-p65 induced by betanin in TNBS-treated mice and weakened the protective effects of betanin on murine colitis. Trinitrobenzenesulfonic Acid 170-174 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 135-143 28955241-12 2017 Moreover, TNBS instillation enhanced local synthesis of inflammatory mediators associated with a neutrophilic response, i.e., CXCL1, CXCL2, and interleukin-6. Trinitrobenzenesulfonic Acid 10-14 chemokine (C-X-C motif) ligand 1 Mus musculus 126-131 28955241-12 2017 Moreover, TNBS instillation enhanced local synthesis of inflammatory mediators associated with a neutrophilic response, i.e., CXCL1, CXCL2, and interleukin-6. Trinitrobenzenesulfonic Acid 10-14 chemokine (C-X-C motif) ligand 2 Mus musculus 133-138 28955241-12 2017 Moreover, TNBS instillation enhanced local synthesis of inflammatory mediators associated with a neutrophilic response, i.e., CXCL1, CXCL2, and interleukin-6. Trinitrobenzenesulfonic Acid 10-14 interleukin 6 Mus musculus 144-157 28286054-14 2017 Co-localization of CRM1 and active caspase-3 in IECs of the TNBS group further indicated the possible involvement of CRM1 in IEC apoptosis. Trinitrobenzenesulfonic Acid 60-64 exportin 1 Homo sapiens 19-23 28286054-14 2017 Co-localization of CRM1 and active caspase-3 in IECs of the TNBS group further indicated the possible involvement of CRM1 in IEC apoptosis. Trinitrobenzenesulfonic Acid 60-64 caspase 3 Homo sapiens 35-44 28286054-14 2017 Co-localization of CRM1 and active caspase-3 in IECs of the TNBS group further indicated the possible involvement of CRM1 in IEC apoptosis. Trinitrobenzenesulfonic Acid 60-64 exportin 1 Homo sapiens 117-121 28666238-0 2017 Protective effects of paeoniflorin on TNBS-induced ulcerative colitis through inhibiting NF-kappaB pathway and apoptosis in mice. Trinitrobenzenesulfonic Acid 38-42 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 89-98 28713999-6 2017 Intestinal and peripheral expression of FGL2 was upregulated in TNBS-induced mice, while the level of FGL2 in the spleen was decreased. Trinitrobenzenesulfonic Acid 64-68 fibrinogen-like protein 2 Mus musculus 40-44 28713999-7 2017 Expression of IL-17 in the plasma, colon and spleen was increased in TNBS-induced mice. Trinitrobenzenesulfonic Acid 69-73 interleukin 17A Mus musculus 14-19 28603288-9 2017 Western blot analysis showed that osthole significantly suppressed the phosphorylation of p38, which was induced by TNBS in mice or by LPS in Raw264.7 cells. Trinitrobenzenesulfonic Acid 116-120 mitogen-activated protein kinase 14 Mus musculus 90-93 28703832-7 2017 iNOS, COX-2, NOX-1, tumor necrosis factor alpha (TNFalpha) and interleukin 1beta (IL1beta) expressions were higher in the mesenteric arteries from TNBS-treated rats, without changes in both eNOS expression and eNOS-Ser1177 phosphorylation. Trinitrobenzenesulfonic Acid 147-151 nitric oxide synthase 2 Rattus norvegicus 0-4 28703832-7 2017 iNOS, COX-2, NOX-1, tumor necrosis factor alpha (TNFalpha) and interleukin 1beta (IL1beta) expressions were higher in the mesenteric arteries from TNBS-treated rats, without changes in both eNOS expression and eNOS-Ser1177 phosphorylation. Trinitrobenzenesulfonic Acid 147-151 cytochrome c oxidase II, mitochondrial Rattus norvegicus 6-11 28703832-7 2017 iNOS, COX-2, NOX-1, tumor necrosis factor alpha (TNFalpha) and interleukin 1beta (IL1beta) expressions were higher in the mesenteric arteries from TNBS-treated rats, without changes in both eNOS expression and eNOS-Ser1177 phosphorylation. Trinitrobenzenesulfonic Acid 147-151 NADPH oxidase 1 Rattus norvegicus 13-18 28703832-7 2017 iNOS, COX-2, NOX-1, tumor necrosis factor alpha (TNFalpha) and interleukin 1beta (IL1beta) expressions were higher in the mesenteric arteries from TNBS-treated rats, without changes in both eNOS expression and eNOS-Ser1177 phosphorylation. Trinitrobenzenesulfonic Acid 147-151 tumor necrosis factor Rattus norvegicus 20-47 28703832-7 2017 iNOS, COX-2, NOX-1, tumor necrosis factor alpha (TNFalpha) and interleukin 1beta (IL1beta) expressions were higher in the mesenteric arteries from TNBS-treated rats, without changes in both eNOS expression and eNOS-Ser1177 phosphorylation. Trinitrobenzenesulfonic Acid 147-151 tumor necrosis factor Rattus norvegicus 49-57 28703832-7 2017 iNOS, COX-2, NOX-1, tumor necrosis factor alpha (TNFalpha) and interleukin 1beta (IL1beta) expressions were higher in the mesenteric arteries from TNBS-treated rats, without changes in both eNOS expression and eNOS-Ser1177 phosphorylation. Trinitrobenzenesulfonic Acid 147-151 interleukin 1 beta Rattus norvegicus 63-80 28703832-7 2017 iNOS, COX-2, NOX-1, tumor necrosis factor alpha (TNFalpha) and interleukin 1beta (IL1beta) expressions were higher in the mesenteric arteries from TNBS-treated rats, without changes in both eNOS expression and eNOS-Ser1177 phosphorylation. Trinitrobenzenesulfonic Acid 147-151 interleukin 1 beta Rattus norvegicus 82-89 28607110-4 2017 In contrast, GPBAR1 activation by BAR501 reversed intestinal inflammation in the trinitrobenzenesulfonic acid and oxazolone models by reducing the trafficking of Ly6C+ monocytes from blood to intestinal mucosa. Trinitrobenzenesulfonic Acid 81-109 G protein-coupled bile acid receptor 1 Mus musculus 13-19 28607110-4 2017 In contrast, GPBAR1 activation by BAR501 reversed intestinal inflammation in the trinitrobenzenesulfonic acid and oxazolone models by reducing the trafficking of Ly6C+ monocytes from blood to intestinal mucosa. Trinitrobenzenesulfonic Acid 81-109 lymphocyte antigen 6 complex, locus C1 Mus musculus 162-166 27901018-3 2017 In this study, IL-25 level was proved to decrease in 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis mice and IL-10 knockout (KO) spontaneous colitis mice. Trinitrobenzenesulfonic Acid 53-88 interleukin 25 Mus musculus 15-20 27901018-7 2017 In addition, the therapeutic effects of anti-miR-31 in TNBS-induced colitis were abolished by colonic treatment with IL-25 antibody or colonic down-expression of IL-25. Trinitrobenzenesulfonic Acid 55-59 interleukin 25 Mus musculus 117-122 27901018-3 2017 In this study, IL-25 level was proved to decrease in 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis mice and IL-10 knockout (KO) spontaneous colitis mice. Trinitrobenzenesulfonic Acid 90-94 interleukin 25 Mus musculus 15-20 27901018-7 2017 In addition, the therapeutic effects of anti-miR-31 in TNBS-induced colitis were abolished by colonic treatment with IL-25 antibody or colonic down-expression of IL-25. Trinitrobenzenesulfonic Acid 55-59 microRNA 31 Mus musculus 45-51 27901018-7 2017 In addition, the therapeutic effects of anti-miR-31 in TNBS-induced colitis were abolished by colonic treatment with IL-25 antibody or colonic down-expression of IL-25. Trinitrobenzenesulfonic Acid 55-59 interleukin 25 Mus musculus 162-167 28619075-10 2017 Further, the CAS treatment also significantly suppressed the mRNA and protein levels of pro-inflammatory cytokines, namely interleukin-1beta and tumor necrosis factor-alpha while enhancing the level of anti-inflammatory cytokine IL-10 in the TNBS-treated rats. Trinitrobenzenesulfonic Acid 242-246 interleukin 10 Rattus norvegicus 229-234 28483526-13 2017 Western blots indicated that CHT1 expression was significantly up-regulated in TNBS-treated rats when compared to naive or sham-operated rats at all time points following surgery. Trinitrobenzenesulfonic Acid 79-83 solute carrier family 5 member 7 Rattus norvegicus 29-33 28483526-14 2017 In the TNBS group, CHT1 expression was higher on day 28 than on day 7 or day 14, but there was no statistical difference in CHT1 expression on day 28 vs. day 21. Trinitrobenzenesulfonic Acid 7-11 solute carrier family 5 member 7 Rattus norvegicus 19-23 28515278-8 2017 Further study demonstrated that blocking the P2Y12 receptor also ameliorated the symptoms of 2,4,6-trinitrobenzenesulfonic acid-induced colitis and multiple low-dose streptozocin-induced type 1 diabetes. Trinitrobenzenesulfonic Acid 93-127 purinergic receptor P2Y, G-protein coupled 12 Mus musculus 45-50 28456627-3 2017 Intrarectal administration of 2.5% 2,4,6-trinitrobenzene sulfonic acid (TNBS) caused inflammation in the colon of wild type mice, but this was less severe in fat-1 transgenic mice that constitutively produce omega-3 PUFAs from omega-6 PUFAs. Trinitrobenzenesulfonic Acid 72-76 FAT atypical cadherin 1 Mus musculus 158-163 28476379-4 2017 In this study, we investigated PRDM5 expression and its potential functions in both human CD (Crohn"s disease) and TNBS (2,4,6-trinitrobenzenesulfonic acid sol)-induced mice experimental colitis. Trinitrobenzenesulfonic Acid 115-119 PR/SET domain 5 Homo sapiens 31-36 28595382-0 2017 Anti-inflammatory properties of Bifidobacterium longum expressing human manganese superoxide dismutase using the TNBS-induced rats model of colitis. Trinitrobenzenesulfonic Acid 113-117 superoxide dismutase 2 Homo sapiens 72-102 28286160-4 2017 P2X7 KO mice were protected against gut inflammation induced by 2,4,6-trinitrobenzenesulfonic acid or oxazolone, with no weight loss or gut histological alterations after treatment. Trinitrobenzenesulfonic Acid 64-98 purinergic receptor P2X, ligand-gated ion channel, 7 Mus musculus 0-4 28476379-4 2017 In this study, we investigated PRDM5 expression and its potential functions in both human CD (Crohn"s disease) and TNBS (2,4,6-trinitrobenzenesulfonic acid sol)-induced mice experimental colitis. Trinitrobenzenesulfonic Acid 121-155 PR/SET domain 5 Homo sapiens 31-36 28476379-5 2017 As shown by western blot and immunohistochemistry, significant up-regulation of PRDM5 was found in the inflamed intestinal tissues of CD patients and TNBS-treated mice, and the molecule was mainly located in IECs. Trinitrobenzenesulfonic Acid 150-154 PR/SET domain 5 Homo sapiens 80-85 28188784-5 2017 Similarly, in TNBS-induced murine colitis model, MAP1S expression was obviously increased. Trinitrobenzenesulfonic Acid 14-18 microtubule-associated protein 1S Mus musculus 49-54 29088747-0 2017 H. pylori attenuates TNBS-induced colitis via increasing mucosal Th2 cells in mice. Trinitrobenzenesulfonic Acid 21-25 heart and neural crest derivatives expressed 2 Mus musculus 65-68 29088747-6 2017 Our results indicate that H. pylori attenuates TNBS-induced colitis mainly through increasing Th2 cells in murine colonic mucosa. Trinitrobenzenesulfonic Acid 47-51 heart and neural crest derivatives expressed 2 Mus musculus 94-97 28341703-3 2017 Specific ablation of DP1 receptor in vascular endothelial cells, colonic epithelium, and myeloid cells augmented DSS/TNBS-induced colitis in mice through increasing vascular permeability, promoting apoptosis of epithelial cells, and stimulating pro-inflammatory cytokine secretion of macrophages, respectively. Trinitrobenzenesulfonic Acid 117-121 receptor accessory protein 5 Mus musculus 21-24 26801887-4 2017 RKIP knockout and wild-type mice were administered dextran sulfate sodium (DSS) or 2,4,6-trinitrobenzenesulfonic acid (TNBS) to induce experimental colitis, and the mice were assessed based on colitis symptoms and biochemical approaches. Trinitrobenzenesulfonic Acid 83-117 phosphatidylethanolamine binding protein 1 Mus musculus 0-4 27824510-5 2017 In the case of RBP4 gene, sows with the AB genotype noted to have significant higher values of TNB and NBA in regard to the respective homozygous genotypes (AA or BB), while the BB genotype showed intermediate results (P < 0.001). Trinitrobenzenesulfonic Acid 95-98 retinol binding protein 4 Sus scrofa 15-19 28137602-3 2017 The method is based on the competition of two substrates for access to the active site of hFMO3 whereby the enzymatic product of the first drug converts nitro-5-thiobenzoate (TNB, yellow) to 5,5"-dithiobis (2-nitrobenzoate) (DTNB, colourless). Trinitrobenzenesulfonic Acid 175-178 dystrobrevin beta Homo sapiens 225-229 26801887-4 2017 RKIP knockout and wild-type mice were administered dextran sulfate sodium (DSS) or 2,4,6-trinitrobenzenesulfonic acid (TNBS) to induce experimental colitis, and the mice were assessed based on colitis symptoms and biochemical approaches. Trinitrobenzenesulfonic Acid 119-123 phosphatidylethanolamine binding protein 1 Mus musculus 0-4 28189973-6 2017 Treatment with ML also inhibited TNBS-induced expression of IL-1beta, IL-17A, and TNF. Trinitrobenzenesulfonic Acid 33-37 interleukin 1 beta Mus musculus 60-68 28189973-6 2017 Treatment with ML also inhibited TNBS-induced expression of IL-1beta, IL-17A, and TNF. Trinitrobenzenesulfonic Acid 33-37 tumor necrosis factor Mus musculus 82-85 28189973-7 2017 While ML reduced the TNBS-induced expression of M1 macrophage markers such as arginase-2 and TNF, it was found to increase the expression of M2 macrophage markers such as arginase-1 and IL-10. Trinitrobenzenesulfonic Acid 21-25 tumor necrosis factor Mus musculus 93-96 27496677-2 2017 in colitis induced by 2,4,6-trinitrobenzene sulfonic acid [TNBS; 2 mg/100 microl 50% ethanol; intrarectally) in mice. Trinitrobenzenesulfonic Acid 22-57 tri-nitrobenzene sulfonic acid susceptible 2 Mus musculus 59-66 27806407-5 2017 Tangeretin also inhibited 2,4,6-trinitrobenzene sulfonic acid-induced differentiation of Th1 and Th17 cells as well as the expression of T-bet, RORgammat, interferon-gamma, IL-12, IL-17, and TNF-alpha. Trinitrobenzenesulfonic Acid 26-61 negative elongation factor complex member C/D, Th1l Mus musculus 89-92 28152446-0 2017 Therapeutic efficacy of carboxyamidotriazole on 2,4,6-trinitrobenzene sulfonic acid-induced colitis model is associated with the inhibition of NLRP3 inflammasome and NF-kappaB activation. Trinitrobenzenesulfonic Acid 48-83 NLR family, pyrin domain containing 3 Rattus norvegicus 143-148 28152446-11 2017 Therefore, CAI attenuates TNBS-induced colitis, which may be attributed to its inhibition of NLRP3 inflammasome and NF-kappaB activation, and down-regulation of proinflammatory cytokines. Trinitrobenzenesulfonic Acid 26-30 NLR family, pyrin domain containing 3 Rattus norvegicus 93-98 27796050-7 2017 Immunohistochemical staining of the distal femur demonstrated that %TNF-alpha+ , %IL-6+ , %RANKL+ , and %OPG+ osteocytes were elevated in cancellous bone in TNBS animals compared to vehicle. Trinitrobenzenesulfonic Acid 157-161 tumor necrosis factor Homo sapiens 68-77 27796050-7 2017 Immunohistochemical staining of the distal femur demonstrated that %TNF-alpha+ , %IL-6+ , %RANKL+ , and %OPG+ osteocytes were elevated in cancellous bone in TNBS animals compared to vehicle. Trinitrobenzenesulfonic Acid 157-161 interleukin 6 Homo sapiens 82-86 27796050-7 2017 Immunohistochemical staining of the distal femur demonstrated that %TNF-alpha+ , %IL-6+ , %RANKL+ , and %OPG+ osteocytes were elevated in cancellous bone in TNBS animals compared to vehicle. Trinitrobenzenesulfonic Acid 157-161 TNF superfamily member 11 Homo sapiens 91-96 27796050-7 2017 Immunohistochemical staining of the distal femur demonstrated that %TNF-alpha+ , %IL-6+ , %RANKL+ , and %OPG+ osteocytes were elevated in cancellous bone in TNBS animals compared to vehicle. Trinitrobenzenesulfonic Acid 157-161 TNF receptor superfamily member 11b Homo sapiens 105-108 27796050-11 2017 Contrary to our hypothesis, %IGF-I+ osteocytes increased in TNBS animals. Trinitrobenzenesulfonic Acid 60-64 insulin like growth factor 1 Homo sapiens 29-34 27806407-4 2017 Tangeretin increased 2,4,6-trinitrobenzene sulfonic acid-suppressed expression of tight junction proteins occludin, claudin-1, and ZO-1. Trinitrobenzenesulfonic Acid 21-56 occludin Mus musculus 106-114 27817132-5 2017 In 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis in rats, weight loss, higher DAI scores, increased visceromotor responses, and inflammatory responses were reversed by application of DPN or ERB-041. Trinitrobenzenesulfonic Acid 3-38 estrogen receptor 2 Rattus norvegicus 203-206 27806407-4 2017 Tangeretin increased 2,4,6-trinitrobenzene sulfonic acid-suppressed expression of tight junction proteins occludin, claudin-1, and ZO-1. Trinitrobenzenesulfonic Acid 21-56 claudin 1 Mus musculus 116-125 27806407-4 2017 Tangeretin increased 2,4,6-trinitrobenzene sulfonic acid-suppressed expression of tight junction proteins occludin, claudin-1, and ZO-1. Trinitrobenzenesulfonic Acid 21-56 tight junction protein 1 Mus musculus 131-135 28300788-4 2017 Following TNBS treatment mRNA levels, protein concentration and immunohistochemical labelling for SphK1 increased significantly. Trinitrobenzenesulfonic Acid 10-14 sphingosine kinase 1 Mus musculus 98-103 28300788-7 2017 Furthermore, TNBS-treated mice exhibited increased phosphorylation of AKT and ERK, and a higher expression of pSTAT3 and the NF-kappaB p65 subunit. Trinitrobenzenesulfonic Acid 13-17 thymoma viral proto-oncogene 1 Mus musculus 70-73 28348486-2 2017 METHODS: We evaluated the suppressive effect of Cur on CD8+CD11c+ cells in spleen and Peyer"s patches (PPs) in colitis induced by trinitrobenzene sulfonic acid. Trinitrobenzenesulfonic Acid 130-159 CD8a molecule Homo sapiens 55-58 27817132-5 2017 In 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis in rats, weight loss, higher DAI scores, increased visceromotor responses, and inflammatory responses were reversed by application of DPN or ERB-041. Trinitrobenzenesulfonic Acid 40-44 estrogen receptor 2 Rattus norvegicus 203-206 28035546-0 2017 Disequilibrium in the CD8+CD28+/CD8+CD28- T Lymphocyte Balance Is Related to Prognosis in Rats with Trinitrobenzenesulfonic Acid-Induced Colitis. Trinitrobenzenesulfonic Acid 100-128 CD8a molecule Homo sapiens 22-25 28035546-0 2017 Disequilibrium in the CD8+CD28+/CD8+CD28- T Lymphocyte Balance Is Related to Prognosis in Rats with Trinitrobenzenesulfonic Acid-Induced Colitis. Trinitrobenzenesulfonic Acid 100-128 Cd28 molecule Rattus norvegicus 26-30 28035546-0 2017 Disequilibrium in the CD8+CD28+/CD8+CD28- T Lymphocyte Balance Is Related to Prognosis in Rats with Trinitrobenzenesulfonic Acid-Induced Colitis. Trinitrobenzenesulfonic Acid 100-128 CD8a molecule Homo sapiens 32-35 28035546-0 2017 Disequilibrium in the CD8+CD28+/CD8+CD28- T Lymphocyte Balance Is Related to Prognosis in Rats with Trinitrobenzenesulfonic Acid-Induced Colitis. Trinitrobenzenesulfonic Acid 100-128 Cd28 molecule Rattus norvegicus 36-40 28035546-2 2017 This investigation will try to identify the changes that occur in the CD8+CD28+/CD8+CD28- T lymphocyte balance during the progression of trinitrobenzenesulfonic acid (TNBS)-induced colitis in rats. Trinitrobenzenesulfonic Acid 137-165 CD8a molecule Homo sapiens 70-73 28035546-2 2017 This investigation will try to identify the changes that occur in the CD8+CD28+/CD8+CD28- T lymphocyte balance during the progression of trinitrobenzenesulfonic acid (TNBS)-induced colitis in rats. Trinitrobenzenesulfonic Acid 137-165 Cd28 molecule Rattus norvegicus 74-78 28035546-2 2017 This investigation will try to identify the changes that occur in the CD8+CD28+/CD8+CD28- T lymphocyte balance during the progression of trinitrobenzenesulfonic acid (TNBS)-induced colitis in rats. Trinitrobenzenesulfonic Acid 137-165 CD8a molecule Homo sapiens 80-83 28035546-2 2017 This investigation will try to identify the changes that occur in the CD8+CD28+/CD8+CD28- T lymphocyte balance during the progression of trinitrobenzenesulfonic acid (TNBS)-induced colitis in rats. Trinitrobenzenesulfonic Acid 137-165 Cd28 molecule Rattus norvegicus 84-88 27817132-6 2017 The higher expressions of P2X3R in dorsal root ganglia (DRG) of CFA-treated rats and those in rectocolon and DRG of TNBS-treated rats were all decreased by injection of DPN or ERB-041. Trinitrobenzenesulfonic Acid 116-120 estrogen receptor 2 Rattus norvegicus 176-179 27778057-5 2017 In the TNBS model was observed reduction in macroscopic and microscopic score, colon weight, neutrophil influx, IL-1beta, MIP-2 and keratinocyte chemoattractant (KC) levels, inhibition of adhesion molecules expression and restoration of IL-10 levels. Trinitrobenzenesulfonic Acid 7-11 interleukin 1 beta Mus musculus 112-120 27579991-3 2017 The main objective of this study was to evaluate the effect of erythropoietin in the TNBS-induced colitis model in mice with a normal intestinal flora. Trinitrobenzenesulfonic Acid 85-89 erythropoietin Mus musculus 63-77 27579991-6 2017 The anti-inflammatory properties of erythropoietin in the TNBS-induced colitis were confirmed by suppression of pro-inflammatory mediators, such as TNF-alpha, IL-1beta and MPO, as well as a significant increase in the anti-inflammatory cytokine, IL-10, was promoted. Trinitrobenzenesulfonic Acid 58-62 erythropoietin Mus musculus 36-50 27579991-6 2017 The anti-inflammatory properties of erythropoietin in the TNBS-induced colitis were confirmed by suppression of pro-inflammatory mediators, such as TNF-alpha, IL-1beta and MPO, as well as a significant increase in the anti-inflammatory cytokine, IL-10, was promoted. Trinitrobenzenesulfonic Acid 58-62 tumor necrosis factor Mus musculus 148-157 27579991-6 2017 The anti-inflammatory properties of erythropoietin in the TNBS-induced colitis were confirmed by suppression of pro-inflammatory mediators, such as TNF-alpha, IL-1beta and MPO, as well as a significant increase in the anti-inflammatory cytokine, IL-10, was promoted. Trinitrobenzenesulfonic Acid 58-62 interleukin 1 beta Mus musculus 159-167 27579991-6 2017 The anti-inflammatory properties of erythropoietin in the TNBS-induced colitis were confirmed by suppression of pro-inflammatory mediators, such as TNF-alpha, IL-1beta and MPO, as well as a significant increase in the anti-inflammatory cytokine, IL-10, was promoted. Trinitrobenzenesulfonic Acid 58-62 interleukin 10 Mus musculus 246-251 27579991-7 2017 These treated mice also presented a reduction in haemoglobin faecal and ALP, suggesting a beneficial effect of erythropoietin in the haemorrhagic focus and destruction of the enterocyte associated with the colon injury induced by TNBS, respectively. Trinitrobenzenesulfonic Acid 230-234 erythropoietin Mus musculus 111-125 27778057-5 2017 In the TNBS model was observed reduction in macroscopic and microscopic score, colon weight, neutrophil influx, IL-1beta, MIP-2 and keratinocyte chemoattractant (KC) levels, inhibition of adhesion molecules expression and restoration of IL-10 levels. Trinitrobenzenesulfonic Acid 7-11 chemokine (C-X-C motif) ligand 2 Mus musculus 122-127 27778057-5 2017 In the TNBS model was observed reduction in macroscopic and microscopic score, colon weight, neutrophil influx, IL-1beta, MIP-2 and keratinocyte chemoattractant (KC) levels, inhibition of adhesion molecules expression and restoration of IL-10 levels. Trinitrobenzenesulfonic Acid 7-11 interleukin 10 Mus musculus 237-242 27778057-7 2017 ET-1 and ET-2 mRNA was decreased 24 h, but ET-2 mRNA was markedly increased at 48 h after TNBS. Trinitrobenzenesulfonic Acid 90-94 endothelin 2 Mus musculus 43-47 27778057-10 2017 CONCLUSIONS: Atrasentan treatment was effective in reducing the severity of colitis in DSS- and TNBS-treated mice, suggesting that ETA receptors might be a potential target for inflammatory bowel diseases. Trinitrobenzenesulfonic Acid 96-100 endothelin receptor type A Mus musculus 131-134 28073341-0 2017 Sijunzi Decoction attenuates 2, 4, 6-trinitrobenzene sulfonic acid (TNBS)-induced colitis in rats and ameliorates TNBS-induced claudin-2 damage via NF-kappaB pathway in Caco2 cells. Trinitrobenzenesulfonic Acid 114-118 claudin 2 Rattus norvegicus 127-136 28127195-6 2017 RESULTS: Colon weight/length ratio, colon COX-2 expression and histological inflammatory score were significantly higher in the TNBS group than in the control group (P = 0.0296, P < 0.0001, P = 0.0007 respectively). Trinitrobenzenesulfonic Acid 128-132 cytochrome c oxidase II, mitochondrial Rattus norvegicus 42-47 28127198-10 2017 AAV-Tbeta4 also modulated colonic TNF-alpha, IL-1beta and IL-10 levels and suppressed the compensatory proliferation of colonic epithelial cells in DSS- and TNBS-treated mice. Trinitrobenzenesulfonic Acid 157-161 thymosin, beta 4, X chromosome Mus musculus 4-10 28099498-3 2017 Here, we evaluated the effects of oral tolerance induced by ingestion of ovalbumin (OVA) on TNBS-induced colitis in mice, an experimental model for human Crohn"s disease. Trinitrobenzenesulfonic Acid 92-96 serine (or cysteine) peptidase inhibitor, clade B, member 1, pseudogene Mus musculus 73-82 28099498-3 2017 Here, we evaluated the effects of oral tolerance induced by ingestion of ovalbumin (OVA) on TNBS-induced colitis in mice, an experimental model for human Crohn"s disease. Trinitrobenzenesulfonic Acid 92-96 serine (or cysteine) peptidase inhibitor, clade B, member 1, pseudogene Mus musculus 84-87 26338824-4 2016 Antisense miR-301a was administered into mice during trinitrobenzene sulphonic acid (TNBS)-induced colitis to determine its role in colitis. Trinitrobenzenesulfonic Acid 85-89 microRNA 301 Mus musculus 10-18 27751819-6 2017 Interestingly, we found that FC9 bound to IFN-gamma R1 and selectively suppressed Th1 but not Th2 immune response in T cells, resulting in an improvement in 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis in mice. Trinitrobenzenesulfonic Acid 157-192 interferon gamma receptor 1 Mus musculus 42-54 27751819-6 2017 Interestingly, we found that FC9 bound to IFN-gamma R1 and selectively suppressed Th1 but not Th2 immune response in T cells, resulting in an improvement in 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis in mice. Trinitrobenzenesulfonic Acid 194-198 interferon gamma receptor 1 Mus musculus 42-54 27754929-0 2017 NOX1/NADPH Oxidase Expressed in Colonic Macrophages Contributes to the Pathogenesis of Colonic Inflammation in Trinitrobenzene Sulfonic Acid-Induced Murine Colitis. Trinitrobenzenesulfonic Acid 111-140 NADPH oxidase 1 Mus musculus 0-4 27754929-3 2017 Intrarectal injection of TNBS caused severe colitis accompanied by body weight loss, diarrhea, and increased myeloperoxidase (MPO) activity in wild-type (WT) mice. Trinitrobenzenesulfonic Acid 25-29 myeloperoxidase Mus musculus 109-124 27754929-3 2017 Intrarectal injection of TNBS caused severe colitis accompanied by body weight loss, diarrhea, and increased myeloperoxidase (MPO) activity in wild-type (WT) mice. Trinitrobenzenesulfonic Acid 25-29 myeloperoxidase Mus musculus 126-129 27754929-5 2017 TNBS-induced upregulation of inflammatory cytokines (tumor necrosis factor (TNF)-alpha and interleukin (IL)-1beta), chemokines (CXCL1 and CXLC2), and inducible nitric oxide synthase (iNOS) was also significantly less in NOX1KO than in WT mice (the inhibitions were 100.8%, 89.0%, 63.5%, 96.7%, and 97.1%, respectively). Trinitrobenzenesulfonic Acid 0-4 tumor necrosis factor Mus musculus 53-86 27754929-5 2017 TNBS-induced upregulation of inflammatory cytokines (tumor necrosis factor (TNF)-alpha and interleukin (IL)-1beta), chemokines (CXCL1 and CXLC2), and inducible nitric oxide synthase (iNOS) was also significantly less in NOX1KO than in WT mice (the inhibitions were 100.8%, 89.0%, 63.5%, 96.7%, and 97.1%, respectively). Trinitrobenzenesulfonic Acid 0-4 interleukin 1 beta Mus musculus 91-113 27754929-5 2017 TNBS-induced upregulation of inflammatory cytokines (tumor necrosis factor (TNF)-alpha and interleukin (IL)-1beta), chemokines (CXCL1 and CXLC2), and inducible nitric oxide synthase (iNOS) was also significantly less in NOX1KO than in WT mice (the inhibitions were 100.8%, 89.0%, 63.5%, 96.7%, and 97.1%, respectively). Trinitrobenzenesulfonic Acid 0-4 chemokine (C-X-C motif) ligand 1 Mus musculus 128-133 27754929-5 2017 TNBS-induced upregulation of inflammatory cytokines (tumor necrosis factor (TNF)-alpha and interleukin (IL)-1beta), chemokines (CXCL1 and CXLC2), and inducible nitric oxide synthase (iNOS) was also significantly less in NOX1KO than in WT mice (the inhibitions were 100.8%, 89.0%, 63.5%, 96.7%, and 97.1%, respectively). Trinitrobenzenesulfonic Acid 0-4 nitric oxide synthase 2, inducible Mus musculus 150-181 27754929-5 2017 TNBS-induced upregulation of inflammatory cytokines (tumor necrosis factor (TNF)-alpha and interleukin (IL)-1beta), chemokines (CXCL1 and CXLC2), and inducible nitric oxide synthase (iNOS) was also significantly less in NOX1KO than in WT mice (the inhibitions were 100.8%, 89.0%, 63.5%, 96.7%, and 97.1%, respectively). Trinitrobenzenesulfonic Acid 0-4 nitric oxide synthase 2, inducible Mus musculus 183-187 27718035-3 2016 In our study, we demonstrated for the first time that GART expression is up-regulated in patients with active CD and in 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced acute colitis model. Trinitrobenzenesulfonic Acid 120-155 phosphoribosylglycinamide formyltransferase, phosphoribosylglycinamide synthetase, phosphoribosylaminoimidazole synthetase Homo sapiens 54-58 27718035-3 2016 In our study, we demonstrated for the first time that GART expression is up-regulated in patients with active CD and in 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced acute colitis model. Trinitrobenzenesulfonic Acid 157-161 phosphoribosylglycinamide formyltransferase, phosphoribosylglycinamide synthetase, phosphoribosylaminoimidazole synthetase Homo sapiens 54-58 26306417-0 2016 Therapeutic and immunoregulatory effect of GATA-binding protein-3/T-box expressed in T-cells ratio of astragalus polysaccharides on 2,4,6-trinitrobenzene sulfonic acid-induced colitis in rats. Trinitrobenzenesulfonic Acid 132-167 GATA binding protein 3 Rattus norvegicus 43-65 26306417-9 2016 TNBS intervention enhanced the expression of both GATA-3 and T-bet, but the expression of T-bet was significantly enhanced than that of GATA-3, resulting in significant reduction of GATA-3/T-bet ratio (P=0.025). Trinitrobenzenesulfonic Acid 0-4 GATA binding protein 3 Rattus norvegicus 50-56 26306417-9 2016 TNBS intervention enhanced the expression of both GATA-3 and T-bet, but the expression of T-bet was significantly enhanced than that of GATA-3, resulting in significant reduction of GATA-3/T-bet ratio (P=0.025). Trinitrobenzenesulfonic Acid 0-4 GATA binding protein 3 Rattus norvegicus 136-142 26306417-9 2016 TNBS intervention enhanced the expression of both GATA-3 and T-bet, but the expression of T-bet was significantly enhanced than that of GATA-3, resulting in significant reduction of GATA-3/T-bet ratio (P=0.025). Trinitrobenzenesulfonic Acid 0-4 GATA binding protein 3 Rattus norvegicus 136-142 27600362-1 2016 To understand the anti-colitic effects of probiotics that up-regulate interleukin (IL)-10 expression in dendritic cells (DCs) and macrophages, we isolated Lactobacillus sakei K17, which potently induced IL-10 expression in DCs and peritoneal macrophages in vitro, among the lactic acid bacteria strains collected from kimchi and investigated its anti-inflammatory effect in mice with 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis. Trinitrobenzenesulfonic Acid 384-419 keratin 17 Mus musculus 175-178 27600362-1 2016 To understand the anti-colitic effects of probiotics that up-regulate interleukin (IL)-10 expression in dendritic cells (DCs) and macrophages, we isolated Lactobacillus sakei K17, which potently induced IL-10 expression in DCs and peritoneal macrophages in vitro, among the lactic acid bacteria strains collected from kimchi and investigated its anti-inflammatory effect in mice with 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis. Trinitrobenzenesulfonic Acid 421-425 keratin 17 Mus musculus 175-178 27600362-3 2016 Treatment with K17 also increased TNBS-suppressed expression of tight junction proteins and IL-10, but inhibited activation of nuclear factor-kappaB (NF-kappaB) and mitogen-activated protein kinases and expression of tumor necrosis factor alpha and IL-17. Trinitrobenzenesulfonic Acid 34-38 keratin 17 Mus musculus 15-18 27600362-3 2016 Treatment with K17 also increased TNBS-suppressed expression of tight junction proteins and IL-10, but inhibited activation of nuclear factor-kappaB (NF-kappaB) and mitogen-activated protein kinases and expression of tumor necrosis factor alpha and IL-17. Trinitrobenzenesulfonic Acid 34-38 interleukin 10 Mus musculus 92-97 27932504-5 2017 Consistent with available microarray data (GEO database) from inflammatory bowel disease (IBD) patients, mouse colonic expression of Cav1.3 was significantly reduced in trinitrobenzene sulfonic acid (TNBS) colitis. Trinitrobenzenesulfonic Acid 169-198 calcium channel, voltage-dependent, L type, alpha 1D subunit Mus musculus 133-139 27932504-5 2017 Consistent with available microarray data (GEO database) from inflammatory bowel disease (IBD) patients, mouse colonic expression of Cav1.3 was significantly reduced in trinitrobenzene sulfonic acid (TNBS) colitis. Trinitrobenzenesulfonic Acid 200-204 calcium channel, voltage-dependent, L type, alpha 1D subunit Mus musculus 133-139 28337946-8 2017 Results We showed that both CXCL12 and CXCR4 were dramatically up-regulated in the dorsal root ganglion in trinitrobenzene sulfonic acid-induced chronic pancreatitis pain model. Trinitrobenzenesulfonic Acid 107-136 C-X-C motif chemokine ligand 12 Rattus norvegicus 28-34 28337946-8 2017 Results We showed that both CXCL12 and CXCR4 were dramatically up-regulated in the dorsal root ganglion in trinitrobenzene sulfonic acid-induced chronic pancreatitis pain model. Trinitrobenzenesulfonic Acid 107-136 C-X-C motif chemokine receptor 4 Rattus norvegicus 39-44 28337946-9 2017 Intrathecal application with AMD3100, a potent and selective CXCR4 inhibitor, reversed the hyperexcitability of dorsal root ganglion neurons innervating the pancreas of rats following trinitrobenzene sulfonic acid injection. Trinitrobenzenesulfonic Acid 184-213 C-X-C motif chemokine receptor 4 Rattus norvegicus 61-66 28337946-10 2017 Furthermore, trinitrobenzene sulfonic acid-induced extracellular signal-regulated kinase activation and Nav1.8 up-regulation in dorsal root ganglias were reversed by intrathecal application with AMD3100 as well as by blockade of extracellular signal-regulated kinase activation by intrathecal U0126. Trinitrobenzenesulfonic Acid 13-42 sodium voltage-gated channel alpha subunit 10 Rattus norvegicus 104-110 28337946-11 2017 More importantly, the trinitrobenzene sulfonic acid-induced persistent pain was significantly suppressed by CXCR4 and extracellular signal-regulated kinase inhibitors. Trinitrobenzenesulfonic Acid 22-51 C-X-C motif chemokine receptor 4 Rattus norvegicus 108-113 27980434-0 2016 TRPA1 in the spinal dorsal horn is involved in post-inflammatory visceral hypersensitivity: in vivo study using TNBS-treated rat model. Trinitrobenzenesulfonic Acid 112-116 transient receptor potential cation channel, subfamily A, member 1 Rattus norvegicus 0-5 27980434-8 2016 Expression of TRPA1 in the SDH (especially in the substantia gelatinosa) and the colon was significantly greater in the TNBS-treated group than in controls (P<0.05). Trinitrobenzenesulfonic Acid 120-124 transient receptor potential cation channel, subfamily A, member 1 Rattus norvegicus 14-19 27980434-9 2016 In the SDH, the number of TRPA1-immunopositive neurons was 25.75+-5.12 in the control group and 34.25+-7.89 in the TNBS-treated group (P=0.023), and integrated optical density values of TRPA1 in the control and TNBS-treated groups were 14,544.63+-6,525.54 and 22,532.75+-7,608.11, respectively (P=0.041). Trinitrobenzenesulfonic Acid 115-119 transient receptor potential cation channel, subfamily A, member 1 Rattus norvegicus 26-31 27980434-9 2016 In the SDH, the number of TRPA1-immunopositive neurons was 25.75+-5.12 in the control group and 34.25+-7.89 in the TNBS-treated group (P=0.023), and integrated optical density values of TRPA1 in the control and TNBS-treated groups were 14,544.63+-6,525.54 and 22,532.75+-7,608.11, respectively (P=0.041). Trinitrobenzenesulfonic Acid 115-119 transient receptor potential cation channel, subfamily A, member 1 Rattus norvegicus 186-191 26948401-8 2016 RESULTS: The administration of EH to TNBS-treated mice prevented (P < 0.05) the loss of body weight and significantly reduced in the colon: a) histological damage score, b) MPO enzymatic activity c) the expression of pro-inflammatory molecules and d) Ikappabeta-alpha degradation and nuclear NF-kappabeta protein levels. Trinitrobenzenesulfonic Acid 37-41 myeloperoxidase Mus musculus 176-179 28164167-8 2016 Following TNBS treatment, IL-6 and artemin mRNA levels were decreased in the distal colon of NMS mice, despite increased MPO activity. Trinitrobenzenesulfonic Acid 10-14 interleukin 6 Mus musculus 26-30 28164167-8 2016 Following TNBS treatment, IL-6 and artemin mRNA levels were decreased in the distal colon of NMS mice, despite increased MPO activity. Trinitrobenzenesulfonic Acid 10-14 myeloperoxidase Mus musculus 121-124 26338824-10 2016 Furthermore, intracolonical administration of antisense miR-301a in TNBS-induced mouse colitis model significantly decreased numbers of interleukin (IL)-17A+ cells and amounts of pro-inflammatory cytokines (eg, IL-17A, TNF-alpha) in inflamed colon. Trinitrobenzenesulfonic Acid 68-72 microRNA 301 Mus musculus 56-64 26338824-10 2016 Furthermore, intracolonical administration of antisense miR-301a in TNBS-induced mouse colitis model significantly decreased numbers of interleukin (IL)-17A+ cells and amounts of pro-inflammatory cytokines (eg, IL-17A, TNF-alpha) in inflamed colon. Trinitrobenzenesulfonic Acid 68-72 interleukin 17A Mus musculus 211-217 26338824-10 2016 Furthermore, intracolonical administration of antisense miR-301a in TNBS-induced mouse colitis model significantly decreased numbers of interleukin (IL)-17A+ cells and amounts of pro-inflammatory cytokines (eg, IL-17A, TNF-alpha) in inflamed colon. Trinitrobenzenesulfonic Acid 68-72 tumor necrosis factor Mus musculus 219-228 27757049-10 2016 RESULTS: The TNBS-treated goats exhibited remarkably increased macroscopic scores, mast-cell counts, myeloperoxidase, and TNFalpha concentrations on days 3 and 7 compared to the saline group, and increased microscopic scores and IL-1beta and IL-6 concentrations on days 3-14. Trinitrobenzenesulfonic Acid 13-17 interleukin-6 Capra hircus 242-246 27585983-0 2016 Fecal Lipocalin-2 as a Sensitive and Noninvasive Biomarker in the TNBS Crohn"s Inflammatory Bowel Disease Model. Trinitrobenzenesulfonic Acid 66-70 lipocalin 2 Mus musculus 6-17 27585983-7 2016 A clear differentiation in Lcn-2 fecal levels between TNBS-treated and vehicle-treated control mice was most noticeable on days 2 and 3. Trinitrobenzenesulfonic Acid 54-58 lipocalin 2 Mus musculus 27-32 26687970-3 2016 Upon induction of colitis with 2,4,6-trinitrobenzenesulfonic acid (TNBS) in rats, we found that the phosphorylation (activation) level of cAMP responsive element-binding (p-CREB) protein, a molecular switch of neuronal plasticity, was increased in specifically labeled bladder afferent neurons in the thoracolumbar and lumbosacral DRGs. Trinitrobenzenesulfonic Acid 31-65 cAMP responsive element binding protein 1 Rattus norvegicus 173-177 26687970-3 2016 Upon induction of colitis with 2,4,6-trinitrobenzenesulfonic acid (TNBS) in rats, we found that the phosphorylation (activation) level of cAMP responsive element-binding (p-CREB) protein, a molecular switch of neuronal plasticity, was increased in specifically labeled bladder afferent neurons in the thoracolumbar and lumbosacral DRGs. Trinitrobenzenesulfonic Acid 67-71 cAMP responsive element binding protein 1 Rattus norvegicus 173-177 27757049-10 2016 RESULTS: The TNBS-treated goats exhibited remarkably increased macroscopic scores, mast-cell counts, myeloperoxidase, and TNFalpha concentrations on days 3 and 7 compared to the saline group, and increased microscopic scores and IL-1beta and IL-6 concentrations on days 3-14. Trinitrobenzenesulfonic Acid 13-17 myeloperoxidase Capra hircus 101-116 27779708-9 2016 The densities of CgA-, PYY-, PP-, Msi1-, Neurog3- and NeuroD1-positive cells were significantly lower in the TNBS group than those in the control group, while those of serotonin-, oxyntomodulin- and somatostatin-positive cells were significantly higher in the TNBS group than those in the control group. Trinitrobenzenesulfonic Acid 109-113 chromogranin A Rattus norvegicus 17-20 27779708-9 2016 The densities of CgA-, PYY-, PP-, Msi1-, Neurog3- and NeuroD1-positive cells were significantly lower in the TNBS group than those in the control group, while those of serotonin-, oxyntomodulin- and somatostatin-positive cells were significantly higher in the TNBS group than those in the control group. Trinitrobenzenesulfonic Acid 109-113 peptide YY Rattus norvegicus 23-26 27779708-9 2016 The densities of CgA-, PYY-, PP-, Msi1-, Neurog3- and NeuroD1-positive cells were significantly lower in the TNBS group than those in the control group, while those of serotonin-, oxyntomodulin- and somatostatin-positive cells were significantly higher in the TNBS group than those in the control group. Trinitrobenzenesulfonic Acid 109-113 musashi RNA-binding protein 1 Rattus norvegicus 34-38 27779708-9 2016 The densities of CgA-, PYY-, PP-, Msi1-, Neurog3- and NeuroD1-positive cells were significantly lower in the TNBS group than those in the control group, while those of serotonin-, oxyntomodulin- and somatostatin-positive cells were significantly higher in the TNBS group than those in the control group. Trinitrobenzenesulfonic Acid 109-113 neurogenin 3 Rattus norvegicus 41-48 27779708-9 2016 The densities of CgA-, PYY-, PP-, Msi1-, Neurog3- and NeuroD1-positive cells were significantly lower in the TNBS group than those in the control group, while those of serotonin-, oxyntomodulin- and somatostatin-positive cells were significantly higher in the TNBS group than those in the control group. Trinitrobenzenesulfonic Acid 109-113 neuronal differentiation 1 Rattus norvegicus 54-61 27779708-9 2016 The densities of CgA-, PYY-, PP-, Msi1-, Neurog3- and NeuroD1-positive cells were significantly lower in the TNBS group than those in the control group, while those of serotonin-, oxyntomodulin- and somatostatin-positive cells were significantly higher in the TNBS group than those in the control group. Trinitrobenzenesulfonic Acid 109-113 somatostatin Rattus norvegicus 199-211 27840918-8 2016 The densities of chromogranin A, peptide YY, and pancreatic polypeptide-producing cells were significantly lower in the TNBS group compared with the control group, whereas the densities of serotonin, oxyntomodulin, and somatostatin-producing cells were significantly higher in the TNBS group. Trinitrobenzenesulfonic Acid 120-124 chromogranin A Rattus norvegicus 17-31 27840918-8 2016 The densities of chromogranin A, peptide YY, and pancreatic polypeptide-producing cells were significantly lower in the TNBS group compared with the control group, whereas the densities of serotonin, oxyntomodulin, and somatostatin-producing cells were significantly higher in the TNBS group. Trinitrobenzenesulfonic Acid 120-124 peptide YY Rattus norvegicus 33-43 27616276-10 2016 Expression of TRPM2 in the mucosa of the distal colon was increased in a trinitrobenzene sulfonic acid-induced colitis model. Trinitrobenzenesulfonic Acid 73-102 transient receptor potential cation channel, subfamily M, member 2 Rattus norvegicus 14-19 27852394-12 2016 Conclusion: ALA may improve the TNBS-induced colitis in mice by inhibiting the phosphorylation of mTOR to promote autophagy. Trinitrobenzenesulfonic Acid 32-36 mechanistic target of rapamycin kinase Mus musculus 98-102 27494685-6 2016 The ratio of CD4(+)CD25(+)CD127dim/CD4(+) of the kappa-carrageenan+TNBS groups was significantly lower than that of the TNBS group. Trinitrobenzenesulfonic Acid 67-71 CD4 antigen Mus musculus 13-16 27494685-6 2016 The ratio of CD4(+)CD25(+)CD127dim/CD4(+) of the kappa-carrageenan+TNBS groups was significantly lower than that of the TNBS group. Trinitrobenzenesulfonic Acid 67-71 CD4 antigen Mus musculus 35-38 27494685-6 2016 The ratio of CD4(+)CD25(+)CD127dim/CD4(+) of the kappa-carrageenan+TNBS groups was significantly lower than that of the TNBS group. Trinitrobenzenesulfonic Acid 120-124 CD4 antigen Mus musculus 13-16 27494685-7 2016 The expression of IL-2, TNF-alpha and IL-6 was significantly increased, whereas the expression of IL-10 was significantly decreased in the kappa-carrageenan+TNBS groups. Trinitrobenzenesulfonic Acid 157-161 interleukin 10 Mus musculus 98-103 27494685-8 2016 In addition, kappa-carrageenan, together with TNBS, decreased the enzyme activity of SOD and GSH-px and up-regulated the expression of TLR4, NF-kappaB, p-ERK, p-JNK, p-Jun., IL-8 and MDA in the colonic mucosa. Trinitrobenzenesulfonic Acid 46-50 toll-like receptor 4 Mus musculus 135-139 27494685-8 2016 In addition, kappa-carrageenan, together with TNBS, decreased the enzyme activity of SOD and GSH-px and up-regulated the expression of TLR4, NF-kappaB, p-ERK, p-JNK, p-Jun., IL-8 and MDA in the colonic mucosa. Trinitrobenzenesulfonic Acid 46-50 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 141-150 27494685-8 2016 In addition, kappa-carrageenan, together with TNBS, decreased the enzyme activity of SOD and GSH-px and up-regulated the expression of TLR4, NF-kappaB, p-ERK, p-JNK, p-Jun., IL-8 and MDA in the colonic mucosa. Trinitrobenzenesulfonic Acid 46-50 eukaryotic translation initiation factor 2 alpha kinase 3 Mus musculus 152-157 27494685-9 2016 CONCLUSIONS: kappa-Carrageenan aggravated the TNBS-induced intestinal inflammation, and such an effect could be associated with the oxidative stress and activation of TLR4-NF-kappaB and MAPK/ERK1/2 pathway. Trinitrobenzenesulfonic Acid 46-50 toll-like receptor 4 Mus musculus 167-171 27494685-9 2016 CONCLUSIONS: kappa-Carrageenan aggravated the TNBS-induced intestinal inflammation, and such an effect could be associated with the oxidative stress and activation of TLR4-NF-kappaB and MAPK/ERK1/2 pathway. Trinitrobenzenesulfonic Acid 46-50 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 172-181 27494685-9 2016 CONCLUSIONS: kappa-Carrageenan aggravated the TNBS-induced intestinal inflammation, and such an effect could be associated with the oxidative stress and activation of TLR4-NF-kappaB and MAPK/ERK1/2 pathway. Trinitrobenzenesulfonic Acid 46-50 mitogen-activated protein kinase 3 Mus musculus 191-197 27757049-10 2016 RESULTS: The TNBS-treated goats exhibited remarkably increased macroscopic scores, mast-cell counts, myeloperoxidase, and TNFalpha concentrations on days 3 and 7 compared to the saline group, and increased microscopic scores and IL-1beta and IL-6 concentrations on days 3-14. Trinitrobenzenesulfonic Acid 13-17 tumor necrosis factor Capra hircus 122-130 27757049-10 2016 RESULTS: The TNBS-treated goats exhibited remarkably increased macroscopic scores, mast-cell counts, myeloperoxidase, and TNFalpha concentrations on days 3 and 7 compared to the saline group, and increased microscopic scores and IL-1beta and IL-6 concentrations on days 3-14. Trinitrobenzenesulfonic Acid 13-17 interleukin-1 beta Capra hircus 229-237 27506642-0 2016 Effects of mimic of manganese superoxide dismutase on 2,4,6-trinitrobenzene sulfonic acid-induced colitis in rats. Trinitrobenzenesulfonic Acid 54-89 superoxide dismutase 2 Rattus norvegicus 20-50 27506642-3 2016 This study was to investigate therapeutic effects and mechanism of MnSODm on 2,4,6-trinitrobenzenesulfonic acid (TNBS) induced colitis model in rats. Trinitrobenzenesulfonic Acid 77-111 superoxide dismutase 2 Rattus norvegicus 67-73 27506642-3 2016 This study was to investigate therapeutic effects and mechanism of MnSODm on 2,4,6-trinitrobenzenesulfonic acid (TNBS) induced colitis model in rats. Trinitrobenzenesulfonic Acid 113-117 superoxide dismutase 2 Rattus norvegicus 67-73 26928963-4 2016 METHODS: Using the 2,4,6-trinitrobenzenesulfonic acid [TNBS]-induced colitis model, involvement of CRTH2 in colitis was investigated by pharmacological antagonism, immunohistochemistry, Western blotting, immunoassay, and leukocyte recruitment. Trinitrobenzenesulfonic Acid 19-53 prostaglandin D2 receptor 2 Homo sapiens 99-104 26928963-4 2016 METHODS: Using the 2,4,6-trinitrobenzenesulfonic acid [TNBS]-induced colitis model, involvement of CRTH2 in colitis was investigated by pharmacological antagonism, immunohistochemistry, Western blotting, immunoassay, and leukocyte recruitment. Trinitrobenzenesulfonic Acid 55-59 prostaglandin D2 receptor 2 Homo sapiens 99-104 27435110-6 2016 AL-1 treatment led to significant reductions in disease activity index (DAI), macroscopic score and colon mucosa damage index (CMDI) associated with TNBS administration. Trinitrobenzenesulfonic Acid 149-153 ephrin A5 Mus musculus 0-4 27206705-2 2016 The aim of this study was to analyze whether and how low doses of haptens, by entry through the skin or gastrointestinal tract, affect the outcome of the predominantly Th1/Th17-mediated 2,4,6-trinitro-benzenesulfonic acid-induced colitis, which mimics an autoimmune bowl disease in man. Trinitrobenzenesulfonic Acid 186-221 negative elongation factor complex member C/D Homo sapiens 168-171 27822176-10 2016 Up-regulated mRNA expression of TNF-alpha, IL-1beta, IL-6, COX-2, and iNOs, as well as down-regulated IL-10 mRNA expressions after TNBS administration, were significantly inhibited by FA (20 and 40 mg/kg) treatment. Trinitrobenzenesulfonic Acid 131-135 tumor necrosis factor Rattus norvegicus 32-41 27822176-10 2016 Up-regulated mRNA expression of TNF-alpha, IL-1beta, IL-6, COX-2, and iNOs, as well as down-regulated IL-10 mRNA expressions after TNBS administration, were significantly inhibited by FA (20 and 40 mg/kg) treatment. Trinitrobenzenesulfonic Acid 131-135 cytochrome c oxidase II, mitochondrial Rattus norvegicus 59-64 27822176-10 2016 Up-regulated mRNA expression of TNF-alpha, IL-1beta, IL-6, COX-2, and iNOs, as well as down-regulated IL-10 mRNA expressions after TNBS administration, were significantly inhibited by FA (20 and 40 mg/kg) treatment. Trinitrobenzenesulfonic Acid 131-135 interleukin 10 Rattus norvegicus 102-107 26939757-17 2016 Finally, SNS prevented the TNBS-induced increases in IL-1beta and IL-4 over time that were observed with sham treatment. Trinitrobenzenesulfonic Acid 27-31 interleukin-1 beta Sus scrofa 53-61 26939757-17 2016 Finally, SNS prevented the TNBS-induced increases in IL-1beta and IL-4 over time that were observed with sham treatment. Trinitrobenzenesulfonic Acid 27-31 interleukin 4 Sus scrofa 66-70 27357734-9 2016 The density of cells expressing CgA, PYY and PP was significantly lower in the TNBS group compared with in the control group, whereas the density of cells expressing serotonin, oxyntomodulin and somatostatin was significantly higher in the TNBS group compared with in the control group. Trinitrobenzenesulfonic Acid 79-83 chromogranin A Rattus norvegicus 32-35 27357734-9 2016 The density of cells expressing CgA, PYY and PP was significantly lower in the TNBS group compared with in the control group, whereas the density of cells expressing serotonin, oxyntomodulin and somatostatin was significantly higher in the TNBS group compared with in the control group. Trinitrobenzenesulfonic Acid 79-83 peptide YY Rattus norvegicus 37-40 27357734-9 2016 The density of cells expressing CgA, PYY and PP was significantly lower in the TNBS group compared with in the control group, whereas the density of cells expressing serotonin, oxyntomodulin and somatostatin was significantly higher in the TNBS group compared with in the control group. Trinitrobenzenesulfonic Acid 79-83 pancreatic polypeptide Rattus norvegicus 45-47 27435110-10 2016 These results indicated that AL-1 could protect intestinal tract from the injury induced by TNBS in mice, suggesting that AL-1 may have potential in treatment for IBD. Trinitrobenzenesulfonic Acid 92-96 ephrin A5 Mus musculus 29-33 27435110-10 2016 These results indicated that AL-1 could protect intestinal tract from the injury induced by TNBS in mice, suggesting that AL-1 may have potential in treatment for IBD. Trinitrobenzenesulfonic Acid 92-96 ephrin A5 Mus musculus 122-126 27418880-3 2016 METHODS: Colitis was induced in CD1 mice by a single intrarectal administration of trinitrobenzene sulfonic acid (TNBS, 4 mg/100 mul in 30 % ethanol) and Abn-CBD and/or the antagonists O-1918 (Abd-CBD), AM251 (CB1 receptor) and AM630 (CB2 receptor), were administered intraperitoneally (all 5 mg/kg, twice daily for 3 days). Trinitrobenzenesulfonic Acid 83-112 CD1 antigen complex Mus musculus 32-35 26601901-4 2016 Our results reveal an impaired mucosal expression of M2 macrophage-associated genes and delayed wound healing in STAT6(-/-) mice treated with 2,4,6-trinitrobenzenesulfonic acid (TNBS). Trinitrobenzenesulfonic Acid 142-176 signal transducer and activator of transcription 6 Mus musculus 113-118 27306412-4 2016 RESULTS: In a rat model with colitis induced by 2,4,6-trinitrobenzene sulfonic acid, we found that endogenously elevated brain-derived neurotrophic factor elicited an up-regulation of calcitonin gene-related peptide in the lumbar L1 dorsal root ganglia. Trinitrobenzenesulfonic Acid 48-83 brain-derived neurotrophic factor Rattus norvegicus 121-154 27478078-10 2016 Similar results were obtained in TNBS-induced colitis at 24 h. Intestinal IL-10 mRNA expression significantly decreased at 12 h and then increased by 6-43 times (p<0.05 to p<0.001) 48h after IA administration. Trinitrobenzenesulfonic Acid 33-37 interleukin 10 Rattus norvegicus 74-79 27478078-12 2016 In the TNBS group, there was 4-12- and 4-7-fold increases in small intestinal IL-10 mRNA expression at 1 and 21 days after colitis induction, respectively (both p<0.01). Trinitrobenzenesulfonic Acid 7-11 interleukin 10 Rattus norvegicus 78-83 27038922-1 2016 AIM: The aim of the present study is to explore whether atorvastatin improves intestinal inflammation through the inhibition of the TLR4/NFkB signaling pathway in TNBS-induced rat colitis. Trinitrobenzenesulfonic Acid 163-167 toll-like receptor 4 Rattus norvegicus 132-136 27038922-9 2016 Furthermore, they inhibited the TNBS-induced expression of TLR4, MyD88 and NF-kappaB p65 proteins. Trinitrobenzenesulfonic Acid 32-36 toll-like receptor 4 Rattus norvegicus 59-63 27038922-9 2016 Furthermore, they inhibited the TNBS-induced expression of TLR4, MyD88 and NF-kappaB p65 proteins. Trinitrobenzenesulfonic Acid 32-36 MYD88, innate immune signal transduction adaptor Rattus norvegicus 65-70 27038922-10 2016 CONCLUSIONS: It is suggested that the anti-inflammatory effect of atorvastatin on TNBS-induced rat colitis may involve the inhibition of the TLR4/NFkB signaling pathway. Trinitrobenzenesulfonic Acid 82-86 toll-like receptor 4 Rattus norvegicus 141-145 27038922-10 2016 CONCLUSIONS: It is suggested that the anti-inflammatory effect of atorvastatin on TNBS-induced rat colitis may involve the inhibition of the TLR4/NFkB signaling pathway. Trinitrobenzenesulfonic Acid 82-86 RELA proto-oncogene, NF-kB subunit Rattus norvegicus 146-150 26802080-4 2016 The influence of differential expressed miR-124 on its putative target, the aryl hydrocarbon receptor (AHR), was investigated in CD patients, intestinal epithelial cells (IECs) and 2,4,6-trinitrobenzene sulphonic acid (TNBS)-induced colitis mice. Trinitrobenzenesulfonic Acid 219-223 aryl hydrocarbon receptor Homo sapiens 76-101 26802080-4 2016 The influence of differential expressed miR-124 on its putative target, the aryl hydrocarbon receptor (AHR), was investigated in CD patients, intestinal epithelial cells (IECs) and 2,4,6-trinitrobenzene sulphonic acid (TNBS)-induced colitis mice. Trinitrobenzenesulfonic Acid 219-223 aryl hydrocarbon receptor Homo sapiens 103-106 26818663-4 2016 Expression of the identified highly up-regulated RNF183 gene was subsequently examined by quantitative reverse transcription polymerase chain reaction [qRT-PCR], western blotting and immunohistochemistry of the intestinal tissues of IBD patients and the colons of trinitrobenzene sulphonic acid [TNBS]-induced colitic mice. Trinitrobenzenesulfonic Acid 296-300 ring finger protein 183 Homo sapiens 49-55 27298558-15 2016 The mRNA expression profile of TGF-betas after repeated TNBS doses was characteristic to CD, TGF-beta 2, but not TGF-beta 3 was up-regulated. Trinitrobenzenesulfonic Acid 56-60 transforming growth factor, beta 2 Rattus norvegicus 93-103 27070821-7 2016 Similarly in mouse keratinocytes in vitro, corticosterone dose dependently suppressed 2,4,6-trinitrobenzenesulfonic acid-induced IL-1alpha and IL-1beta expression. Trinitrobenzenesulfonic Acid 86-120 interleukin 1 alpha Mus musculus 129-138 27070821-7 2016 Similarly in mouse keratinocytes in vitro, corticosterone dose dependently suppressed 2,4,6-trinitrobenzenesulfonic acid-induced IL-1alpha and IL-1beta expression. Trinitrobenzenesulfonic Acid 86-120 interleukin 1 beta Mus musculus 143-151 27109448-0 2016 CD4+ T cell responses in Balb/c mice with food allergy induced by trinitrobenzene sulfonic acid and ovalbumin. Trinitrobenzenesulfonic Acid 66-95 CD4 antigen Mus musculus 0-3 27109448-6 2016 TNBS increased the expression of T cell immunoglobulin and mucin domain-4 and tumor necrosis factor ligand superfamily member 4 in dendritic cells. Trinitrobenzenesulfonic Acid 0-4 tumor necrosis factor (ligand) superfamily, member 4 Mus musculus 59-127 27109448-7 2016 Skewed Th2 cell polarization, extensive expression of interleukin-4, reduced expression of interferon-gamma and forkhead box protein P3 were elicited following concomitant exposure to TNBS and OVA, with reduced regulatory T cells in the mouse intestinal mucosa, whereas a Th1 response was detected when challenged by TNBS or OVA alone. Trinitrobenzenesulfonic Acid 184-188 heart and neural crest derivatives expressed 2 Mus musculus 7-10 27109448-7 2016 Skewed Th2 cell polarization, extensive expression of interleukin-4, reduced expression of interferon-gamma and forkhead box protein P3 were elicited following concomitant exposure to TNBS and OVA, with reduced regulatory T cells in the mouse intestinal mucosa, whereas a Th1 response was detected when challenged by TNBS or OVA alone. Trinitrobenzenesulfonic Acid 184-188 interleukin 4 Mus musculus 54-67 27109448-7 2016 Skewed Th2 cell polarization, extensive expression of interleukin-4, reduced expression of interferon-gamma and forkhead box protein P3 were elicited following concomitant exposure to TNBS and OVA, with reduced regulatory T cells in the mouse intestinal mucosa, whereas a Th1 response was detected when challenged by TNBS or OVA alone. Trinitrobenzenesulfonic Acid 184-188 interferon gamma Mus musculus 91-107 27109448-7 2016 Skewed Th2 cell polarization, extensive expression of interleukin-4, reduced expression of interferon-gamma and forkhead box protein P3 were elicited following concomitant exposure to TNBS and OVA, with reduced regulatory T cells in the mouse intestinal mucosa, whereas a Th1 response was detected when challenged by TNBS or OVA alone. Trinitrobenzenesulfonic Acid 184-188 negative elongation factor complex member C/D, Th1l Mus musculus 272-275 27109448-8 2016 This data suggests that TNBS, as a hapten, combined with food antigens may lead to a Th2 cell response in the intestinal mucosa. Trinitrobenzenesulfonic Acid 24-28 heart and neural crest derivatives expressed 2 Mus musculus 85-88 26601901-4 2016 Our results reveal an impaired mucosal expression of M2 macrophage-associated genes and delayed wound healing in STAT6(-/-) mice treated with 2,4,6-trinitrobenzenesulfonic acid (TNBS). Trinitrobenzenesulfonic Acid 178-182 signal transducer and activator of transcription 6 Mus musculus 113-118 26601901-8 2016 Our results demonstrate that a STAT6-dependent macrophage phenotype promotes mucosal repair in TNBS-treated mice through activation of the Wnt signaling pathway. Trinitrobenzenesulfonic Acid 95-99 signal transducer and activator of transcription 6 Mus musculus 31-36 26601901-8 2016 Our results demonstrate that a STAT6-dependent macrophage phenotype promotes mucosal repair in TNBS-treated mice through activation of the Wnt signaling pathway. Trinitrobenzenesulfonic Acid 95-99 wingless-type MMTV integration site family, member 2B Mus musculus 139-142 27016270-5 2016 GTN treatments inhibited TNBS-induced acute and chronic colitis development in Wistar rats, reducing myeloperoxidase levels and inflammatory cells infiltration in the mucosa. Trinitrobenzenesulfonic Acid 25-29 myeloperoxidase Rattus norvegicus 101-116 27076683-5 2016 Intracolonic 2,4,6-trinitrobenzenesulfonic acid (TNBS) administration (2-d model) increased colonic miR-210 expression that was significantly reduced in NTR1-KO, HIF-1alpha-KO mice, and wild-type mice pretreated intracolonically with locked nucleic acid anti-miR-210. Trinitrobenzenesulfonic Acid 13-47 microRNA 210 Mus musculus 100-107 27076683-7 2016 HIF-1alpha-OE mice had also exacerbated TNBS-induced neovascularization compared with TNBS-exposed wild-type mice. Trinitrobenzenesulfonic Acid 40-44 hypoxia inducible factor 1, alpha subunit Mus musculus 0-10 27076683-7 2016 HIF-1alpha-OE mice had also exacerbated TNBS-induced neovascularization compared with TNBS-exposed wild-type mice. Trinitrobenzenesulfonic Acid 86-90 hypoxia inducible factor 1, alpha subunit Mus musculus 0-10 27076683-5 2016 Intracolonic 2,4,6-trinitrobenzenesulfonic acid (TNBS) administration (2-d model) increased colonic miR-210 expression that was significantly reduced in NTR1-KO, HIF-1alpha-KO mice, and wild-type mice pretreated intracolonically with locked nucleic acid anti-miR-210. Trinitrobenzenesulfonic Acid 13-47 neurotensin receptor 1 Mus musculus 153-160 27076683-8 2016 TNBS-induced neovascularization was attenuated in HIF-1alpha-KO mice, or mice pretreated intracolonically with anti-miR-210. Trinitrobenzenesulfonic Acid 0-4 hypoxia inducible factor 1, alpha subunit Mus musculus 50-60 27076683-8 2016 TNBS-induced neovascularization was attenuated in HIF-1alpha-KO mice, or mice pretreated intracolonically with anti-miR-210. Trinitrobenzenesulfonic Acid 0-4 microRNA 210 Mus musculus 116-123 27076683-9 2016 Intracolonic anti-miR-210 also reduced colitis in response to TNBS (2 d). Trinitrobenzenesulfonic Acid 62-66 microRNA 210 Mus musculus 18-25 27076683-5 2016 Intracolonic 2,4,6-trinitrobenzenesulfonic acid (TNBS) administration (2-d model) increased colonic miR-210 expression that was significantly reduced in NTR1-KO, HIF-1alpha-KO mice, and wild-type mice pretreated intracolonically with locked nucleic acid anti-miR-210. Trinitrobenzenesulfonic Acid 13-47 hypoxia inducible factor 1, alpha subunit Mus musculus 162-172 27076683-5 2016 Intracolonic 2,4,6-trinitrobenzenesulfonic acid (TNBS) administration (2-d model) increased colonic miR-210 expression that was significantly reduced in NTR1-KO, HIF-1alpha-KO mice, and wild-type mice pretreated intracolonically with locked nucleic acid anti-miR-210. Trinitrobenzenesulfonic Acid 13-47 microRNA 210 Mus musculus 259-266 27076683-5 2016 Intracolonic 2,4,6-trinitrobenzenesulfonic acid (TNBS) administration (2-d model) increased colonic miR-210 expression that was significantly reduced in NTR1-KO, HIF-1alpha-KO mice, and wild-type mice pretreated intracolonically with locked nucleic acid anti-miR-210. Trinitrobenzenesulfonic Acid 49-53 microRNA 210 Mus musculus 100-107 27076683-5 2016 Intracolonic 2,4,6-trinitrobenzenesulfonic acid (TNBS) administration (2-d model) increased colonic miR-210 expression that was significantly reduced in NTR1-KO, HIF-1alpha-KO mice, and wild-type mice pretreated intracolonically with locked nucleic acid anti-miR-210. Trinitrobenzenesulfonic Acid 49-53 neurotensin receptor 1 Mus musculus 153-160 27076683-5 2016 Intracolonic 2,4,6-trinitrobenzenesulfonic acid (TNBS) administration (2-d model) increased colonic miR-210 expression that was significantly reduced in NTR1-KO, HIF-1alpha-KO mice, and wild-type mice pretreated intracolonically with locked nucleic acid anti-miR-210. Trinitrobenzenesulfonic Acid 49-53 hypoxia inducible factor 1, alpha subunit Mus musculus 162-172 27076683-5 2016 Intracolonic 2,4,6-trinitrobenzenesulfonic acid (TNBS) administration (2-d model) increased colonic miR-210 expression that was significantly reduced in NTR1-KO, HIF-1alpha-KO mice, and wild-type mice pretreated intracolonically with locked nucleic acid anti-miR-210. Trinitrobenzenesulfonic Acid 49-53 microRNA 210 Mus musculus 259-266 27076683-6 2016 In contrast, HIF-1alpha-OE mice showed increased miR-210 expression at baseline that was further increased following TNBS administration. Trinitrobenzenesulfonic Acid 117-121 hypoxia inducible factor 1, alpha subunit Mus musculus 13-23 27076683-6 2016 In contrast, HIF-1alpha-OE mice showed increased miR-210 expression at baseline that was further increased following TNBS administration. Trinitrobenzenesulfonic Acid 117-121 microRNA 210 Mus musculus 49-56 26997491-4 2016 As shown by Western blot, significant up-regulation of GRHPR was found in TNBS-treated mice as compared with normal controls. Trinitrobenzenesulfonic Acid 74-78 glyoxylate reductase/hydroxypyruvate reductase Mus musculus 55-60 26971225-5 2016 They also suppressed TNBS-induced Th17 cell differentiation and IL-17 expression, but increased TNBS-suppressed Treg cell differentiation and IL-10 expression. Trinitrobenzenesulfonic Acid 21-25 interleukin 17A Mus musculus 64-69 26971225-5 2016 They also suppressed TNBS-induced Th17 cell differentiation and IL-17 expression, but increased TNBS-suppressed Treg cell differentiation and IL-10 expression. Trinitrobenzenesulfonic Acid 96-100 interleukin 10 Mus musculus 142-147 27107073-12 2016 BSQW or Mesalazin significantly inhibited TNBS-induced expression of the TLR4, MyD88 and NF-kappaB P65 genes. Trinitrobenzenesulfonic Acid 42-46 toll-like receptor 4 Rattus norvegicus 73-77 27107073-12 2016 BSQW or Mesalazin significantly inhibited TNBS-induced expression of the TLR4, MyD88 and NF-kappaB P65 genes. Trinitrobenzenesulfonic Acid 42-46 MYD88, innate immune signal transduction adaptor Rattus norvegicus 79-84 26645248-7 2016 RESULTS: TNBS injection significantly upregulated expression of TGF-beta1 in the pancreas and DRGs, and TGF-beta1 receptors in DRGs (T9-T13)in CP rats. Trinitrobenzenesulfonic Acid 9-13 transforming growth factor, beta 1 Rattus norvegicus 64-73 26645248-7 2016 RESULTS: TNBS injection significantly upregulated expression of TGF-beta1 in the pancreas and DRGs, and TGF-beta1 receptors in DRGs (T9-T13)in CP rats. Trinitrobenzenesulfonic Acid 9-13 transforming growth factor, beta 1 Rattus norvegicus 104-113 26911661-2 2016 Some studies have shown that expression of AIF-1 increased in a mouse model of trinitrobenzene sulfonic acid-induced acute colitis and in acute cellular rejection of human cardiac allografts. Trinitrobenzenesulfonic Acid 79-108 allograft inflammatory factor 1 Mus musculus 43-48 27118991-11 2016 CONCLUSIONS: HPM at Tianshu (ST25) and Qihai (RN6) upregulated the expression of occludin, claudin-1, and ZO-1 in TNBS-induced CD model rats. Trinitrobenzenesulfonic Acid 114-118 occludin Rattus norvegicus 81-89 27118991-11 2016 CONCLUSIONS: HPM at Tianshu (ST25) and Qihai (RN6) upregulated the expression of occludin, claudin-1, and ZO-1 in TNBS-induced CD model rats. Trinitrobenzenesulfonic Acid 114-118 tight junction protein 1 Rattus norvegicus 106-110 27274906-5 2016 OBJECTIVE: Investigate the immunomodulatory effect of administering FasL-DCs in the rat trinitrobenzene sulfonic acid (TNBS) model of acute colitis. Trinitrobenzenesulfonic Acid 88-117 Fas ligand Rattus norvegicus 68-76 27274906-5 2016 OBJECTIVE: Investigate the immunomodulatory effect of administering FasL-DCs in the rat trinitrobenzene sulfonic acid (TNBS) model of acute colitis. Trinitrobenzenesulfonic Acid 119-123 Fas ligand Rattus norvegicus 68-76 27047383-4 2016 RESULTS: Blockade of 5-HT1A receptors worsened TNBS-induced local and systemic neutrophil recruitment while 5-HT1A agonist delayed and mitigated the severity of colitis, counteracting the increase in colonic 5-HT content. Trinitrobenzenesulfonic Acid 47-51 5-hydroxytryptamine (serotonin) receptor 1A Mus musculus 21-27 26349931-11 2016 RESULTS: DSS-induced colitis and colitis induced by trinitrobenzene sulfonic acid were markedly exacerbated in GnT-V transgenic mice compared with wild-type mice. Trinitrobenzenesulfonic Acid 52-81 mannoside acetylglucosaminyltransferase 5 Mus musculus 111-116 26926174-9 2016 Mouse TNBS-induced colon shortening, macroscopic score, and myeloperoxidase activity were inhibited by neomangiferin, which also reduced TNBS-induced activation of nuclear factor-kappaB and extracellular signal-regulated kinases, as well as expression of inducible nitric oxide synthase and cyclooxygenase-2. Trinitrobenzenesulfonic Acid 6-10 prostaglandin-endoperoxide synthase 2 Mus musculus 291-307 26926174-9 2016 Mouse TNBS-induced colon shortening, macroscopic score, and myeloperoxidase activity were inhibited by neomangiferin, which also reduced TNBS-induced activation of nuclear factor-kappaB and extracellular signal-regulated kinases, as well as expression of inducible nitric oxide synthase and cyclooxygenase-2. Trinitrobenzenesulfonic Acid 137-141 prostaglandin-endoperoxide synthase 2 Mus musculus 291-307 26926174-10 2016 In addition, neomangiferin inhibited TNBS-induced expression of tumor necrosis factor-alpha, IL-17, IL-6, and IL-1beta, and increased IL-10 expression. Trinitrobenzenesulfonic Acid 37-41 tumor necrosis factor Mus musculus 64-91 26926174-10 2016 In addition, neomangiferin inhibited TNBS-induced expression of tumor necrosis factor-alpha, IL-17, IL-6, and IL-1beta, and increased IL-10 expression. Trinitrobenzenesulfonic Acid 37-41 interleukin 17A Mus musculus 93-98 26926174-10 2016 In addition, neomangiferin inhibited TNBS-induced expression of tumor necrosis factor-alpha, IL-17, IL-6, and IL-1beta, and increased IL-10 expression. Trinitrobenzenesulfonic Acid 37-41 interleukin 6 Mus musculus 100-104 26926174-10 2016 In addition, neomangiferin inhibited TNBS-induced expression of tumor necrosis factor-alpha, IL-17, IL-6, and IL-1beta, and increased IL-10 expression. Trinitrobenzenesulfonic Acid 37-41 interleukin 1 beta Mus musculus 110-118 26926174-10 2016 In addition, neomangiferin inhibited TNBS-induced expression of tumor necrosis factor-alpha, IL-17, IL-6, and IL-1beta, and increased IL-10 expression. Trinitrobenzenesulfonic Acid 37-41 interleukin 10 Mus musculus 134-139 27403031-7 2016 Furthermore, WISP1 expression was also found to be increased in colons from 2,4,6-trinitrobenzenesulfonic acid- (TNBS-) induced mice compared with those from control mice. Trinitrobenzenesulfonic Acid 76-110 cellular communication network factor 4 Mus musculus 13-18 26676112-2 2016 The present study aimed to investigate the protective effects of the AT1R blocker losartan on 2,4,6-trinitrobenzenesulphonic acid (TNBS)-induced colitis. Trinitrobenzenesulfonic Acid 94-129 angiotensin II, type I receptor-associated protein Mus musculus 69-73 26676112-2 2016 The present study aimed to investigate the protective effects of the AT1R blocker losartan on 2,4,6-trinitrobenzenesulphonic acid (TNBS)-induced colitis. Trinitrobenzenesulfonic Acid 131-135 angiotensin II, type I receptor-associated protein Mus musculus 69-73 26676112-9 2016 These results suggested that the AT1R blocker losartan may attenuate TNBS-induced colitis by inhibiting the apoptosis of IECs. Trinitrobenzenesulfonic Acid 69-73 angiotensin II, type I receptor-associated protein Mus musculus 33-37 27403031-7 2016 Furthermore, WISP1 expression was also found to be increased in colons from 2,4,6-trinitrobenzenesulfonic acid- (TNBS-) induced mice compared with those from control mice. Trinitrobenzenesulfonic Acid 113-117 cellular communication network factor 4 Mus musculus 13-18 27403031-8 2016 Further studies confirmed that administration of rWISP1 could aggravate TNBS-induced colitis in vivo. Trinitrobenzenesulfonic Acid 72-76 cellular communication network factor 4 Rattus norvegicus 49-55 26377354-5 2016 In parallel, pro-inflammatory mediators, COX-2, iNOS and CINC-3, elevated by TNBS-induced colitis, were substantially diminished in the inflamed colon. Trinitrobenzenesulfonic Acid 77-81 cytochrome c oxidase II, mitochondrial Rattus norvegicus 41-46 26462538-9 2016 In the TNBS model encenicline reduced the frequency of FoxP3(+) IL-17A(+) T cells in the colon. Trinitrobenzenesulfonic Acid 7-11 forkhead box P3 Mus musculus 55-60 27761147-8 2016 Furthermore, these inhibited TNBS-induced T-bet, RORgammat, TNF-alpha, and IL-17 expression but increased TNBS-suppressed Foxp3 and IL-10 expression. Trinitrobenzenesulfonic Acid 29-33 tumor necrosis factor Mus musculus 60-69 27761147-8 2016 Furthermore, these inhibited TNBS-induced T-bet, RORgammat, TNF-alpha, and IL-17 expression but increased TNBS-suppressed Foxp3 and IL-10 expression. Trinitrobenzenesulfonic Acid 29-33 interleukin 17A Mus musculus 75-80 27761147-8 2016 Furthermore, these inhibited TNBS-induced T-bet, RORgammat, TNF-alpha, and IL-17 expression but increased TNBS-suppressed Foxp3 and IL-10 expression. Trinitrobenzenesulfonic Acid 106-110 forkhead box P3 Mus musculus 122-127 27761147-8 2016 Furthermore, these inhibited TNBS-induced T-bet, RORgammat, TNF-alpha, and IL-17 expression but increased TNBS-suppressed Foxp3 and IL-10 expression. Trinitrobenzenesulfonic Acid 106-110 interleukin 10 Mus musculus 132-137 26377354-5 2016 In parallel, pro-inflammatory mediators, COX-2, iNOS and CINC-3, elevated by TNBS-induced colitis, were substantially diminished in the inflamed colon. Trinitrobenzenesulfonic Acid 77-81 nitric oxide synthase 2 Rattus norvegicus 48-52 26377354-5 2016 In parallel, pro-inflammatory mediators, COX-2, iNOS and CINC-3, elevated by TNBS-induced colitis, were substantially diminished in the inflamed colon. Trinitrobenzenesulfonic Acid 77-81 C-X-C motif chemokine ligand 2 Rattus norvegicus 57-63 26453508-6 2015 CGP treatment also inhibited the TNBS-mediated increases in nitric oxide synthase, cyclooxygenase-2, interleukin-1beta, tumor necrosis factor-alpha, intercellular adhesion molecule-1, and monocyte chemotactic protein-1 proteins or mRNA levels. Trinitrobenzenesulfonic Acid 33-37 prostaglandin-endoperoxide synthase 2 Rattus norvegicus 83-99 26468044-5 2016 METHODS: Myeloperoxidase (MPO) activity determined the extent of inflammation in health, acute trinitrobenzene-sulfonic acid (TNBS) colitis, and in our post-TNBS colitis model of chronic visceral hypersensitivity (CVH). Trinitrobenzenesulfonic Acid 95-124 myeloperoxidase Mus musculus 26-29 26718757-9 2015 TNBS significantly increased the number of TLR9 positive cells compared to control (P<0.010), while 5-ASA, 1,25(OH)D3, and combined treatment with 5-ASA and 1,25(OH)D3 significantly decreased it compared to TNBS group (all P<0.010). Trinitrobenzenesulfonic Acid 0-4 toll-like receptor 9 Rattus norvegicus 43-47 26718757-10 2015 In TNBS group a moderate correlation was observed between MPO activity and the number of TLR9-positive cells (r=0.654, P<0.001). Trinitrobenzenesulfonic Acid 3-7 myeloperoxidase Rattus norvegicus 58-61 26718757-10 2015 In TNBS group a moderate correlation was observed between MPO activity and the number of TLR9-positive cells (r=0.654, P<0.001). Trinitrobenzenesulfonic Acid 3-7 toll-like receptor 9 Rattus norvegicus 89-93 26476684-4 2015 Inflammatory responses in IL-19-deficient mice were assessed using the 2,4,6-trinitrobenzene sulfonic acid (TNBS) model of acute colitis. Trinitrobenzenesulfonic Acid 71-106 interleukin 19 Mus musculus 26-31 26453508-6 2015 CGP treatment also inhibited the TNBS-mediated increases in nitric oxide synthase, cyclooxygenase-2, interleukin-1beta, tumor necrosis factor-alpha, intercellular adhesion molecule-1, and monocyte chemotactic protein-1 proteins or mRNA levels. Trinitrobenzenesulfonic Acid 33-37 interleukin 1 beta Rattus norvegicus 101-147 26453508-6 2015 CGP treatment also inhibited the TNBS-mediated increases in nitric oxide synthase, cyclooxygenase-2, interleukin-1beta, tumor necrosis factor-alpha, intercellular adhesion molecule-1, and monocyte chemotactic protein-1 proteins or mRNA levels. Trinitrobenzenesulfonic Acid 33-37 C-C motif chemokine ligand 2 Rattus norvegicus 188-218 26541861-6 2015 One week after intrarectal challenge with TNBS, HMGB1, IL-17 and IFN-gamma protein levels were remarkably increased following severe colon inflammation. Trinitrobenzenesulfonic Acid 42-46 interferon gamma Mus musculus 65-74 26453508-8 2015 The CGP treatment prevented phosphorylation of p38 mitogen-activated protein kinase, IkappaB-alpha, and DNA-nuclear factor-kappaB binding, all of which were increased in the inflamed colons of TNBS-treated rats. Trinitrobenzenesulfonic Acid 193-197 NFKB inhibitor alpha Rattus norvegicus 85-98 26270588-2 2015 We found that the mRNA expression of Artemin (Artn) in the tongue mucosa of patients with burning mouth syndrome was significantly higher than that of control subjects, and we developed a mouse model of burning mouth syndrome by application of 2,4,6-trinitrobenzene sulfonic acid (TNBS) diluted with 50% ethanol to the dorsum of the tongue. Trinitrobenzenesulfonic Acid 244-279 artemin Homo sapiens 37-44 26270588-5 2015 The number of glial cell line-derived neurotrophic factor family receptor alpha3 (GFRalpha3)-positive and TRPV1-positive trigeminal ganglion (TG) neurons innervating the tongue significantly increased following TNBS treatment and was significantly reduced by successive administration of neutralizing anti-Artn antibody. Trinitrobenzenesulfonic Acid 211-215 GDNF family receptor alpha 3 Homo sapiens 82-91 26270588-2 2015 We found that the mRNA expression of Artemin (Artn) in the tongue mucosa of patients with burning mouth syndrome was significantly higher than that of control subjects, and we developed a mouse model of burning mouth syndrome by application of 2,4,6-trinitrobenzene sulfonic acid (TNBS) diluted with 50% ethanol to the dorsum of the tongue. Trinitrobenzenesulfonic Acid 281-285 artemin Homo sapiens 37-44 26270588-5 2015 The number of glial cell line-derived neurotrophic factor family receptor alpha3 (GFRalpha3)-positive and TRPV1-positive trigeminal ganglion (TG) neurons innervating the tongue significantly increased following TNBS treatment and was significantly reduced by successive administration of neutralizing anti-Artn antibody. Trinitrobenzenesulfonic Acid 211-215 transient receptor potential cation channel subfamily V member 1 Homo sapiens 106-111 26270588-5 2015 The number of glial cell line-derived neurotrophic factor family receptor alpha3 (GFRalpha3)-positive and TRPV1-positive trigeminal ganglion (TG) neurons innervating the tongue significantly increased following TNBS treatment and was significantly reduced by successive administration of neutralizing anti-Artn antibody. Trinitrobenzenesulfonic Acid 211-215 artemin Homo sapiens 306-310 26270588-7 2015 These results suggest that the overexpression of Artn in the TNBS-treated tongue increases the membrane excitability of TG neurons innervating the tongue by increasing TRPV1 sensitivity, which causes heat hyperalgesia. Trinitrobenzenesulfonic Acid 61-65 artemin Homo sapiens 49-53 26270588-7 2015 These results suggest that the overexpression of Artn in the TNBS-treated tongue increases the membrane excitability of TG neurons innervating the tongue by increasing TRPV1 sensitivity, which causes heat hyperalgesia. Trinitrobenzenesulfonic Acid 61-65 transient receptor potential cation channel subfamily V member 1 Homo sapiens 168-173 26270588-2 2015 We found that the mRNA expression of Artemin (Artn) in the tongue mucosa of patients with burning mouth syndrome was significantly higher than that of control subjects, and we developed a mouse model of burning mouth syndrome by application of 2,4,6-trinitrobenzene sulfonic acid (TNBS) diluted with 50% ethanol to the dorsum of the tongue. Trinitrobenzenesulfonic Acid 281-285 artemin Homo sapiens 46-50 26270588-3 2015 TNBS treatment to the tongue induced persistent, week-long, noninflammatory tongue pain and a significant increase in Artn expression in the tongue mucosa and marked tongue heat hyperalgesia. Trinitrobenzenesulfonic Acid 0-4 artemin Homo sapiens 118-122 26224047-0 2015 Berberine ameliorates TNBS induced colitis by inhibiting inflammatory responses and Th1/Th17 differentiation. Trinitrobenzenesulfonic Acid 22-26 negative elongation factor complex member C/D, Th1l Mus musculus 84-87 26404500-4 2015 was characterized in the mouse model of 2,4,6-trinitrobenzenesulfonic acid (TNBS)-induced colitis, based on the assessment of the macroscopic and microscopic total damage scores and determination of myeloperoxidase (MPO) activity and TNF-alpha level in the colon. Trinitrobenzenesulfonic Acid 40-74 myeloperoxidase Mus musculus 199-214 26404500-4 2015 was characterized in the mouse model of 2,4,6-trinitrobenzenesulfonic acid (TNBS)-induced colitis, based on the assessment of the macroscopic and microscopic total damage scores and determination of myeloperoxidase (MPO) activity and TNF-alpha level in the colon. Trinitrobenzenesulfonic Acid 40-74 myeloperoxidase Mus musculus 216-219 26404500-4 2015 was characterized in the mouse model of 2,4,6-trinitrobenzenesulfonic acid (TNBS)-induced colitis, based on the assessment of the macroscopic and microscopic total damage scores and determination of myeloperoxidase (MPO) activity and TNF-alpha level in the colon. Trinitrobenzenesulfonic Acid 40-74 tumor necrosis factor Mus musculus 234-243 26404500-4 2015 was characterized in the mouse model of 2,4,6-trinitrobenzenesulfonic acid (TNBS)-induced colitis, based on the assessment of the macroscopic and microscopic total damage scores and determination of myeloperoxidase (MPO) activity and TNF-alpha level in the colon. Trinitrobenzenesulfonic Acid 76-80 myeloperoxidase Mus musculus 199-214 26404500-4 2015 was characterized in the mouse model of 2,4,6-trinitrobenzenesulfonic acid (TNBS)-induced colitis, based on the assessment of the macroscopic and microscopic total damage scores and determination of myeloperoxidase (MPO) activity and TNF-alpha level in the colon. Trinitrobenzenesulfonic Acid 76-80 myeloperoxidase Mus musculus 216-219 26404500-4 2015 was characterized in the mouse model of 2,4,6-trinitrobenzenesulfonic acid (TNBS)-induced colitis, based on the assessment of the macroscopic and microscopic total damage scores and determination of myeloperoxidase (MPO) activity and TNF-alpha level in the colon. Trinitrobenzenesulfonic Acid 76-80 tumor necrosis factor Mus musculus 234-243 26561804-3 2015 Here, trinitrobenzene sulfonic acid-relapsing (TNBS) colitis was induced in mice; then, we measured the differentiation of Th1/Th2 cells in mouse splenocytes by flow cytometry and the secretion of cytokines in mice with TNBS-induced colitis by real-time polymerase chain reaction and/or enzyme-linked immunosorbent assay (RT-PCR/ELISA). Trinitrobenzenesulfonic Acid 6-35 negative elongation factor complex member C/D, Th1l Mus musculus 123-126 26561804-3 2015 Here, trinitrobenzene sulfonic acid-relapsing (TNBS) colitis was induced in mice; then, we measured the differentiation of Th1/Th2 cells in mouse splenocytes by flow cytometry and the secretion of cytokines in mice with TNBS-induced colitis by real-time polymerase chain reaction and/or enzyme-linked immunosorbent assay (RT-PCR/ELISA). Trinitrobenzenesulfonic Acid 6-35 heart and neural crest derivatives expressed 2 Mus musculus 127-130 26561804-3 2015 Here, trinitrobenzene sulfonic acid-relapsing (TNBS) colitis was induced in mice; then, we measured the differentiation of Th1/Th2 cells in mouse splenocytes by flow cytometry and the secretion of cytokines in mice with TNBS-induced colitis by real-time polymerase chain reaction and/or enzyme-linked immunosorbent assay (RT-PCR/ELISA). Trinitrobenzenesulfonic Acid 47-51 negative elongation factor complex member C/D, Th1l Mus musculus 123-126 26561804-5 2015 Additionally, ELISA showed that the serum levels of IFN-gamma, TNF-alpha, IL-12, IL-6, and IL-1beta were down-regulated in a TNBS model of colitis. Trinitrobenzenesulfonic Acid 125-129 interferon gamma Mus musculus 52-61 26561804-5 2015 Additionally, ELISA showed that the serum levels of IFN-gamma, TNF-alpha, IL-12, IL-6, and IL-1beta were down-regulated in a TNBS model of colitis. Trinitrobenzenesulfonic Acid 125-129 tumor necrosis factor Mus musculus 63-72 26561804-5 2015 Additionally, ELISA showed that the serum levels of IFN-gamma, TNF-alpha, IL-12, IL-6, and IL-1beta were down-regulated in a TNBS model of colitis. Trinitrobenzenesulfonic Acid 125-129 interleukin 6 Mus musculus 81-85 26561804-5 2015 Additionally, ELISA showed that the serum levels of IFN-gamma, TNF-alpha, IL-12, IL-6, and IL-1beta were down-regulated in a TNBS model of colitis. Trinitrobenzenesulfonic Acid 125-129 interleukin 1 beta Mus musculus 91-99 26241646-9 2015 TNBS-induced influx of T-cells and inflammatory monocytes into the colon was higher in Nur77-/- mice, along with increased expression of MCP-1, TNFalpha and IL-6, and decreased Foxp3 RNA expression, compared to wild-type mice. Trinitrobenzenesulfonic Acid 0-4 nuclear receptor subfamily 4, group A, member 1 Mus musculus 87-92 26054809-6 2015 Orally administered ginsenoside Rg1, Rh1, or 20(S)-protopanaxtriol inhibited 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colon shortening, myeloperoxidase activity, and expression of IL-1beta, IL-17, and tumor necrosis factor-alpha in mice with TNBS-induced colitis. Trinitrobenzenesulfonic Acid 77-112 protein phosphatase 1, regulatory subunit 3A Mus musculus 32-35 26054809-6 2015 Orally administered ginsenoside Rg1, Rh1, or 20(S)-protopanaxtriol inhibited 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colon shortening, myeloperoxidase activity, and expression of IL-1beta, IL-17, and tumor necrosis factor-alpha in mice with TNBS-induced colitis. Trinitrobenzenesulfonic Acid 77-112 interleukin 1 beta Mus musculus 190-198 26054809-6 2015 Orally administered ginsenoside Rg1, Rh1, or 20(S)-protopanaxtriol inhibited 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colon shortening, myeloperoxidase activity, and expression of IL-1beta, IL-17, and tumor necrosis factor-alpha in mice with TNBS-induced colitis. Trinitrobenzenesulfonic Acid 77-112 interleukin 17A Mus musculus 200-205 26054809-6 2015 Orally administered ginsenoside Rg1, Rh1, or 20(S)-protopanaxtriol inhibited 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colon shortening, myeloperoxidase activity, and expression of IL-1beta, IL-17, and tumor necrosis factor-alpha in mice with TNBS-induced colitis. Trinitrobenzenesulfonic Acid 77-112 tumor necrosis factor Mus musculus 211-238 26054809-6 2015 Orally administered ginsenoside Rg1, Rh1, or 20(S)-protopanaxtriol inhibited 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colon shortening, myeloperoxidase activity, and expression of IL-1beta, IL-17, and tumor necrosis factor-alpha in mice with TNBS-induced colitis. Trinitrobenzenesulfonic Acid 114-118 protein phosphatase 1, regulatory subunit 3A Mus musculus 32-35 26054809-6 2015 Orally administered ginsenoside Rg1, Rh1, or 20(S)-protopanaxtriol inhibited 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colon shortening, myeloperoxidase activity, and expression of IL-1beta, IL-17, and tumor necrosis factor-alpha in mice with TNBS-induced colitis. Trinitrobenzenesulfonic Acid 114-118 myeloperoxidase Mus musculus 146-161 26054809-6 2015 Orally administered ginsenoside Rg1, Rh1, or 20(S)-protopanaxtriol inhibited 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colon shortening, myeloperoxidase activity, and expression of IL-1beta, IL-17, and tumor necrosis factor-alpha in mice with TNBS-induced colitis. Trinitrobenzenesulfonic Acid 114-118 interleukin 1 beta Mus musculus 190-198 26054809-6 2015 Orally administered ginsenoside Rg1, Rh1, or 20(S)-protopanaxtriol inhibited 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colon shortening, myeloperoxidase activity, and expression of IL-1beta, IL-17, and tumor necrosis factor-alpha in mice with TNBS-induced colitis. Trinitrobenzenesulfonic Acid 114-118 interleukin 17A Mus musculus 200-205 26054809-6 2015 Orally administered ginsenoside Rg1, Rh1, or 20(S)-protopanaxtriol inhibited 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colon shortening, myeloperoxidase activity, and expression of IL-1beta, IL-17, and tumor necrosis factor-alpha in mice with TNBS-induced colitis. Trinitrobenzenesulfonic Acid 114-118 tumor necrosis factor Mus musculus 211-238 26289587-8 2015 and was also reduced in BDNF(+/-) rat treated with TNBS. Trinitrobenzenesulfonic Acid 51-55 brain-derived neurotrophic factor Rattus norvegicus 24-28 26194345-8 2015 Ocotillol treatment increased TNBS-suppressed expression of tight junction proteins ZO-1, occludin, and claudin-1 in the colon. Trinitrobenzenesulfonic Acid 30-34 occludin Mus musculus 90-98 26194345-8 2015 Ocotillol treatment increased TNBS-suppressed expression of tight junction proteins ZO-1, occludin, and claudin-1 in the colon. Trinitrobenzenesulfonic Acid 30-34 claudin 1 Mus musculus 104-113 26194345-9 2015 Treatment with ocotillol inhibited TNBS-induced expression of tumor necrosis factor (TNF)-alpha and IL-1beta, as well as activation of NF-kappaB and MAPKs. Trinitrobenzenesulfonic Acid 35-39 tumor necrosis factor Mus musculus 62-95 26194345-9 2015 Treatment with ocotillol inhibited TNBS-induced expression of tumor necrosis factor (TNF)-alpha and IL-1beta, as well as activation of NF-kappaB and MAPKs. Trinitrobenzenesulfonic Acid 35-39 interleukin 1 beta Mus musculus 100-108 26645045-11 2015 MiR-221-5p expression was increased in both TNBS- and DSS-induced colitis and colonic biopsies from Ulcerative Colitis, but not Crohn"s Disease subjects, compared to controls. Trinitrobenzenesulfonic Acid 44-48 microRNA 221 Homo sapiens 0-7 26645045-12 2015 In mice, intracolonic administration of a miR-221-5p chemical inhibitor, exacerbated TNBS-and DSS-induced colitis, and increased colonic TNF-alpha, Cxcl10, and Col2 alpha 1 mRNA expression. Trinitrobenzenesulfonic Acid 85-89 microRNA 221 Homo sapiens 42-49 26645045-13 2015 In situ hybridization in TNBS-and DSS-exposed colons revealed increased miR-221-5p expression primarily in colonocytes. Trinitrobenzenesulfonic Acid 25-29 microRNA 221 Homo sapiens 72-79 26324318-0 2015 Chronic inflammation up-regulates P-gp in peripheral mononuclear blood cells via the STAT3/Nf-kappab pathway in 2,4,6-trinitrobenzene sulfonic acid-induced colitis mice. Trinitrobenzenesulfonic Acid 112-147 phosphoglycolate phosphatase Mus musculus 34-38 26324318-0 2015 Chronic inflammation up-regulates P-gp in peripheral mononuclear blood cells via the STAT3/Nf-kappab pathway in 2,4,6-trinitrobenzene sulfonic acid-induced colitis mice. Trinitrobenzenesulfonic Acid 112-147 signal transducer and activator of transcription 3 Mus musculus 85-90 26324318-0 2015 Chronic inflammation up-regulates P-gp in peripheral mononuclear blood cells via the STAT3/Nf-kappab pathway in 2,4,6-trinitrobenzene sulfonic acid-induced colitis mice. Trinitrobenzenesulfonic Acid 112-147 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 91-100 26241646-9 2015 TNBS-induced influx of T-cells and inflammatory monocytes into the colon was higher in Nur77-/- mice, along with increased expression of MCP-1, TNFalpha and IL-6, and decreased Foxp3 RNA expression, compared to wild-type mice. Trinitrobenzenesulfonic Acid 0-4 mast cell protease 1 Mus musculus 137-142 26241646-9 2015 TNBS-induced influx of T-cells and inflammatory monocytes into the colon was higher in Nur77-/- mice, along with increased expression of MCP-1, TNFalpha and IL-6, and decreased Foxp3 RNA expression, compared to wild-type mice. Trinitrobenzenesulfonic Acid 0-4 tumor necrosis factor Mus musculus 144-152 26241646-9 2015 TNBS-induced influx of T-cells and inflammatory monocytes into the colon was higher in Nur77-/- mice, along with increased expression of MCP-1, TNFalpha and IL-6, and decreased Foxp3 RNA expression, compared to wild-type mice. Trinitrobenzenesulfonic Acid 0-4 interleukin 6 Mus musculus 157-161 26241646-9 2015 TNBS-induced influx of T-cells and inflammatory monocytes into the colon was higher in Nur77-/- mice, along with increased expression of MCP-1, TNFalpha and IL-6, and decreased Foxp3 RNA expression, compared to wild-type mice. Trinitrobenzenesulfonic Acid 0-4 forkhead box P3 Mus musculus 177-182 25936754-4 2015 Using the trinitrobenzene sulfonic acid-induced mouse models of intestinal inflammation, we observed decreased SGLT1 expression in the inflamed intestine was positively correlated with the mucosal level of epidermal growth factor (EGF) and activated CREB. Trinitrobenzenesulfonic Acid 10-39 solute carrier family 5 (sodium/glucose cotransporter), member 1 Mus musculus 111-116 25936754-4 2015 Using the trinitrobenzene sulfonic acid-induced mouse models of intestinal inflammation, we observed decreased SGLT1 expression in the inflamed intestine was positively correlated with the mucosal level of epidermal growth factor (EGF) and activated CREB. Trinitrobenzenesulfonic Acid 10-39 cAMP responsive element binding protein 1 Mus musculus 250-254 26019446-8 2015 An efficient strategy for IBD therapy is represented by the combination of IL-17A and IL-17F in acute IL-17A knockout TNBS-induced colitis, and also definite decrease of the inflammatory process in IL-17F knockout, DSS-induced colitis have been observed. Trinitrobenzenesulfonic Acid 118-122 interleukin 17A Homo sapiens 75-81 26082774-5 2015 At the beginning, it was known as one of the participants during the development of allergic states and other Th2-mediated responses and it is now accepted that IL-33 contributes to Th1-driven pathologies as demonstrated in animal models of experimental autoimmune encephalomyelitis (EAE), collagen-induced arthritis, and trinitrobenzene sulfonic acid-induced experimental colitis, among others. Trinitrobenzenesulfonic Acid 322-351 interleukin 33 Homo sapiens 161-166 26026060-4 2015 Inhibition of mTORC1 activity by rapamycin treatment or haploinsufficiency of Rheb through genetic modification in mice impaired intestinal cell proliferation and induced cell apoptosis, leading to high mortality in dextran sodium sulfate- and 2,4,6-trinitrobenzene sulfonic acid-induced colitis models. Trinitrobenzenesulfonic Acid 244-279 CREB regulated transcription coactivator 1 Mus musculus 14-20 26026060-4 2015 Inhibition of mTORC1 activity by rapamycin treatment or haploinsufficiency of Rheb through genetic modification in mice impaired intestinal cell proliferation and induced cell apoptosis, leading to high mortality in dextran sodium sulfate- and 2,4,6-trinitrobenzene sulfonic acid-induced colitis models. Trinitrobenzenesulfonic Acid 244-279 Ras homolog enriched in brain Mus musculus 78-82 26218952-18 2015 TNBS significantly increased the spinal expression of HMGB1 and proinflammatory cytokines IL-1beta, TNF-alpha, and IL-6. Trinitrobenzenesulfonic Acid 0-4 high mobility group box 1 Rattus norvegicus 54-59 26218952-18 2015 TNBS significantly increased the spinal expression of HMGB1 and proinflammatory cytokines IL-1beta, TNF-alpha, and IL-6. Trinitrobenzenesulfonic Acid 0-4 interleukin 1 beta Rattus norvegicus 90-98 26218952-18 2015 TNBS significantly increased the spinal expression of HMGB1 and proinflammatory cytokines IL-1beta, TNF-alpha, and IL-6. Trinitrobenzenesulfonic Acid 0-4 tumor necrosis factor Rattus norvegicus 100-109 26218952-18 2015 TNBS significantly increased the spinal expression of HMGB1 and proinflammatory cytokines IL-1beta, TNF-alpha, and IL-6. Trinitrobenzenesulfonic Acid 0-4 interleukin 6 Rattus norvegicus 115-119 26218952-20 2015 Furthermore, TSN IIA, but not the neutralizing anti-HMGB1 antibody, significantly inhibited TNBS-induced spinal TLR4 and GFAP expression. Trinitrobenzenesulfonic Acid 92-96 toll-like receptor 4 Rattus norvegicus 112-116 26218952-20 2015 Furthermore, TSN IIA, but not the neutralizing anti-HMGB1 antibody, significantly inhibited TNBS-induced spinal TLR4 and GFAP expression. Trinitrobenzenesulfonic Acid 92-96 glial fibrillary acidic protein Rattus norvegicus 121-125 25689466-7 2015 Survival rate, TNFalpha, and IL-1beta mRNA were improved in TNBS/Gln compared with TNBS/PBS (p < 0.05). Trinitrobenzenesulfonic Acid 60-64 tumor necrosis factor Rattus norvegicus 15-23 25689466-7 2015 Survival rate, TNFalpha, and IL-1beta mRNA were improved in TNBS/Gln compared with TNBS/PBS (p < 0.05). Trinitrobenzenesulfonic Acid 60-64 interleukin 1 beta Rattus norvegicus 29-37 26020571-7 2015 The solutes normalized the rise in myeloperoxidase, TNFalpha, and IL-1beta induced by TNBS but did not affect levels of reduced glutathione or ICAM-1, while reducing the level of fecal calprotectin, an established marker for inflammatory bowel disease. Trinitrobenzenesulfonic Acid 86-90 myeloperoxidase Rattus norvegicus 35-50 26020571-7 2015 The solutes normalized the rise in myeloperoxidase, TNFalpha, and IL-1beta induced by TNBS but did not affect levels of reduced glutathione or ICAM-1, while reducing the level of fecal calprotectin, an established marker for inflammatory bowel disease. Trinitrobenzenesulfonic Acid 86-90 interleukin 1 beta Rattus norvegicus 66-74 25577335-9 2015 treatment significantly reduced histopathological severity; suppressed expression of COX-2, TNF-alpha, and interleukin-1beta in TNBS-induced mice. Trinitrobenzenesulfonic Acid 128-132 cytochrome c oxidase II, mitochondrial Mus musculus 85-90 25577335-9 2015 treatment significantly reduced histopathological severity; suppressed expression of COX-2, TNF-alpha, and interleukin-1beta in TNBS-induced mice. Trinitrobenzenesulfonic Acid 128-132 tumor necrosis factor Mus musculus 92-101 25577335-9 2015 treatment significantly reduced histopathological severity; suppressed expression of COX-2, TNF-alpha, and interleukin-1beta in TNBS-induced mice. Trinitrobenzenesulfonic Acid 128-132 interleukin 1 beta Mus musculus 107-124 25997679-9 2015 Finally, intracolonically delivered miR-19b decreased the severity of colitis induced with 2,4,6-trinitrobenzene sulphonic acid (TNBS). Trinitrobenzenesulfonic Acid 129-133 microRNA 19b-1 Homo sapiens 36-43 26019446-8 2015 An efficient strategy for IBD therapy is represented by the combination of IL-17A and IL-17F in acute IL-17A knockout TNBS-induced colitis, and also definite decrease of the inflammatory process in IL-17F knockout, DSS-induced colitis have been observed. Trinitrobenzenesulfonic Acid 118-122 interleukin 17F Homo sapiens 86-92 26019446-8 2015 An efficient strategy for IBD therapy is represented by the combination of IL-17A and IL-17F in acute IL-17A knockout TNBS-induced colitis, and also definite decrease of the inflammatory process in IL-17F knockout, DSS-induced colitis have been observed. Trinitrobenzenesulfonic Acid 118-122 interleukin 17A Homo sapiens 102-108 25813397-0 2015 Vitamin D/VDR signaling pathway ameliorates 2,4,6-trinitrobenzene sulfonic acid-induced colitis by inhibiting intestinal epithelial apoptosis. Trinitrobenzenesulfonic Acid 44-79 vitamin D (1,25-dihydroxyvitamin D3) receptor Mus musculus 10-13 25813397-4 2015 Based on the established inhibitory effects of the vitamin D/VDR pathway on IEC apoptosis, we treated mice with 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis with paricalcitol, a vitamin D analog, in order to investigate the mechanisms responsible for the inhibitory effects of the vitamin D/VDR pathway. Trinitrobenzenesulfonic Acid 149-153 vitamin D (1,25-dihydroxyvitamin D3) receptor Mus musculus 61-64 25813397-4 2015 Based on the established inhibitory effects of the vitamin D/VDR pathway on IEC apoptosis, we treated mice with 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis with paricalcitol, a vitamin D analog, in order to investigate the mechanisms responsible for the inhibitory effects of the vitamin D/VDR pathway. Trinitrobenzenesulfonic Acid 149-153 vitamin D (1,25-dihydroxyvitamin D3) receptor Mus musculus 305-308 25311527-9 2015 High-dose liquiritigenin treatment group showed significant decreases in TNBS-induced phosphorylation of IKKbeta, p65, and IkappaB-alpha. Trinitrobenzenesulfonic Acid 73-77 nuclear factor of kappa light polypeptide gene enhancer in B cells inhibitor, alpha Mus musculus 123-136 25698557-6 2015 Oral administration of AIII and sarsasapogenin inhibited 2,3,4-trinitrobenzene sulfonic acid (TNBS)-induced colon shortening and myeloperoxidase activity in mice, along with reducing NF-kappaB activation and interleukin (IL)-1beta, tumor necrosis factor (TNF)-alpha, and IL-6 levels, while simultaneously increasing IL-10. Trinitrobenzenesulfonic Acid 94-98 myeloperoxidase Mus musculus 129-144 25655216-6 2015 In tri-nitrobenzene sulfonic acid (TNBS)-induced colitis, immunocytochemistry showed the selective expression of GDNF in proliferating CSMC, suggesting that smooth muscle proliferation supports the ENS in vivo as well as in vitro. Trinitrobenzenesulfonic Acid 3-33 glial cell derived neurotrophic factor Homo sapiens 113-117 25655216-6 2015 In tri-nitrobenzene sulfonic acid (TNBS)-induced colitis, immunocytochemistry showed the selective expression of GDNF in proliferating CSMC, suggesting that smooth muscle proliferation supports the ENS in vivo as well as in vitro. Trinitrobenzenesulfonic Acid 35-39 glial cell derived neurotrophic factor Homo sapiens 113-117 25311527-9 2015 High-dose liquiritigenin treatment group showed significant decreases in TNBS-induced phosphorylation of IKKbeta, p65, and IkappaB-alpha. Trinitrobenzenesulfonic Acid 73-77 v-rel reticuloendotheliosis viral oncogene homolog A (avian) Mus musculus 114-117 25724769-0 2015 Exogenous carcinoembryonic antigen-related cell adhesion molecule 1 suppresses 2,4,6-trinitrobenzene sulfonic acid-induced ulcerative colitis in mice. Trinitrobenzenesulfonic Acid 79-114 carcinoembryonic antigen-related cell adhesion molecule 1 Mus musculus 10-67 25724769-11 2015 Moreover, exogenous CEACAM1 reduced the levels of inflammatory cytokines, suppressed CD4 T cell infiltration, and effectively inhibited apoptosis in the colon of TNBS-induced UC mice. Trinitrobenzenesulfonic Acid 162-166 carcinoembryonic antigen-related cell adhesion molecule 1 Mus musculus 20-27 25724769-12 2015 CONCLUSIONS: The expression of exogenous CEACAM1 effectively rescues the symptoms of TNBS-induced UC in mice by inhibiting inflammation, T cell infiltration, and apoptosis in the colon. Trinitrobenzenesulfonic Acid 85-89 carcinoembryonic antigen-related cell adhesion molecule 1 Mus musculus 41-48 25634810-10 2015 Interestingly, TNBS injection led to a significant elevation of NE concentration in DRGs and the pancreas, an upregulation of beta2-adrenergic receptor expression in DRGs, and amplification of the NE-induced potentiation of ATP responses. Trinitrobenzenesulfonic Acid 15-19 adrenoceptor beta 2 Rattus norvegicus 126-151 25838986-2 2015 The deficiency of IL-9 suppressed TNBS-induced colitis and led to lower numbers of PU.1 expressing T cells in the lamia propria, suggesting a regulatory role for Th9 cells in the experimental TNBS colitis model. Trinitrobenzenesulfonic Acid 34-38 interleukin 9 Mus musculus 18-22 25838986-7 2015 Surprisingly, the pore-forming molecule Claudin2 revealed equal expression in TNBS-treated wild-type and IL-9-deficient animals. Trinitrobenzenesulfonic Acid 78-82 claudin 2 Mus musculus 40-48 25698557-6 2015 Oral administration of AIII and sarsasapogenin inhibited 2,3,4-trinitrobenzene sulfonic acid (TNBS)-induced colon shortening and myeloperoxidase activity in mice, along with reducing NF-kappaB activation and interleukin (IL)-1beta, tumor necrosis factor (TNF)-alpha, and IL-6 levels, while simultaneously increasing IL-10. Trinitrobenzenesulfonic Acid 94-98 interleukin 1 beta Mus musculus 208-230 25698557-6 2015 Oral administration of AIII and sarsasapogenin inhibited 2,3,4-trinitrobenzene sulfonic acid (TNBS)-induced colon shortening and myeloperoxidase activity in mice, along with reducing NF-kappaB activation and interleukin (IL)-1beta, tumor necrosis factor (TNF)-alpha, and IL-6 levels, while simultaneously increasing IL-10. Trinitrobenzenesulfonic Acid 94-98 tumor necrosis factor Mus musculus 232-265 26019800-7 2015 RESULTS: The results showed that the oral RJ treatment inhibited proinflammatory cytokines, IL-1beta and TNF-alpha secretion, while increasing anti-inflammatory cytokine IL-10 production in the TNBS-induced colitis+RJ group compared with the colitis group not treated with RJ. Trinitrobenzenesulfonic Acid 194-198 interleukin 10 Rattus norvegicus 170-175 25698557-6 2015 Oral administration of AIII and sarsasapogenin inhibited 2,3,4-trinitrobenzene sulfonic acid (TNBS)-induced colon shortening and myeloperoxidase activity in mice, along with reducing NF-kappaB activation and interleukin (IL)-1beta, tumor necrosis factor (TNF)-alpha, and IL-6 levels, while simultaneously increasing IL-10. Trinitrobenzenesulfonic Acid 94-98 interleukin 6 Mus musculus 271-275 25698557-6 2015 Oral administration of AIII and sarsasapogenin inhibited 2,3,4-trinitrobenzene sulfonic acid (TNBS)-induced colon shortening and myeloperoxidase activity in mice, along with reducing NF-kappaB activation and interleukin (IL)-1beta, tumor necrosis factor (TNF)-alpha, and IL-6 levels, while simultaneously increasing IL-10. Trinitrobenzenesulfonic Acid 94-98 interleukin 10 Mus musculus 316-321 25756273-0 2015 The potential protective role of caveolin-1 in intestinal inflammation in TNBS-induced murine colitis. Trinitrobenzenesulfonic Acid 74-78 caveolin 1, caveolae protein Mus musculus 33-43 25756273-3 2015 A recent study showed that Cav-1 is increased and mediates angiogenesis in dextran sodium sulphate-induced colitis, which are contradictory to our pilot findings in 2,4,6-trinitrobenzene sulphonic acid (TNBS)-induced colitis. Trinitrobenzenesulfonic Acid 203-207 caveolin 1, caveolae protein Mus musculus 27-32 25756273-11 2015 Furthermore, after administration of TNBS, Cav-1-/- mice showed significantly increased clinical and colon inflammatory scores and body weight loss when compared with control mice. Trinitrobenzenesulfonic Acid 37-41 caveolin 1, caveolae protein Mus musculus 43-48 25533544-4 2015 In TNBS-induced mouse colitis models, we observed the up-regulation of VPS4B was accompanied with the elevated levels of IEC apoptotic markers (active caspase-3 and cleaved PARP) and phosphorylated p38 in colitis IECs. Trinitrobenzenesulfonic Acid 3-7 vacuolar protein sorting 4B Mus musculus 71-76 25562655-8 2015 In a mouse model, the stereotypic loss of myenteric neurons by Day 4 post-TNBS was abrogated by the selective iNOS inhibitors L-NIL or 1400W without effect on other parameters of intestinal inflammation. Trinitrobenzenesulfonic Acid 74-78 nitric oxide synthase 2, inducible Mus musculus 110-114 25559498-0 2015 Recombinant interleukin-1 receptor antagonist attenuates the severity of chronic pancreatitis induced by TNBS in rats. Trinitrobenzenesulfonic Acid 105-109 interleukin 1 receptor antagonist Rattus norvegicus 12-45 25559498-3 2015 In this study, we attempted to find a connection between interleukin-1beta (IL-1beta) and interleukin-1 receptor antagonist (IL-1Ra) in trinitrobenzene sulfonic acid (TNBS)-induced chronic pancreatitis, and then the therapeutic effect of recombinant IL-1Ra was also detected in the CP model. Trinitrobenzenesulfonic Acid 136-165 interleukin 1 beta Rattus norvegicus 57-74 25559498-3 2015 In this study, we attempted to find a connection between interleukin-1beta (IL-1beta) and interleukin-1 receptor antagonist (IL-1Ra) in trinitrobenzene sulfonic acid (TNBS)-induced chronic pancreatitis, and then the therapeutic effect of recombinant IL-1Ra was also detected in the CP model. Trinitrobenzenesulfonic Acid 136-165 interleukin 1 beta Rattus norvegicus 76-84 25559498-3 2015 In this study, we attempted to find a connection between interleukin-1beta (IL-1beta) and interleukin-1 receptor antagonist (IL-1Ra) in trinitrobenzene sulfonic acid (TNBS)-induced chronic pancreatitis, and then the therapeutic effect of recombinant IL-1Ra was also detected in the CP model. Trinitrobenzenesulfonic Acid 136-165 interleukin 1 receptor antagonist Rattus norvegicus 90-123 25559498-3 2015 In this study, we attempted to find a connection between interleukin-1beta (IL-1beta) and interleukin-1 receptor antagonist (IL-1Ra) in trinitrobenzene sulfonic acid (TNBS)-induced chronic pancreatitis, and then the therapeutic effect of recombinant IL-1Ra was also detected in the CP model. Trinitrobenzenesulfonic Acid 136-165 interleukin 1 receptor antagonist Rattus norvegicus 125-131 25559498-3 2015 In this study, we attempted to find a connection between interleukin-1beta (IL-1beta) and interleukin-1 receptor antagonist (IL-1Ra) in trinitrobenzene sulfonic acid (TNBS)-induced chronic pancreatitis, and then the therapeutic effect of recombinant IL-1Ra was also detected in the CP model. Trinitrobenzenesulfonic Acid 136-165 interleukin 1 receptor antagonist Rattus norvegicus 250-256 25559498-3 2015 In this study, we attempted to find a connection between interleukin-1beta (IL-1beta) and interleukin-1 receptor antagonist (IL-1Ra) in trinitrobenzene sulfonic acid (TNBS)-induced chronic pancreatitis, and then the therapeutic effect of recombinant IL-1Ra was also detected in the CP model. Trinitrobenzenesulfonic Acid 167-171 interleukin 1 beta Rattus norvegicus 57-74 25559498-3 2015 In this study, we attempted to find a connection between interleukin-1beta (IL-1beta) and interleukin-1 receptor antagonist (IL-1Ra) in trinitrobenzene sulfonic acid (TNBS)-induced chronic pancreatitis, and then the therapeutic effect of recombinant IL-1Ra was also detected in the CP model. Trinitrobenzenesulfonic Acid 167-171 interleukin 1 beta Rattus norvegicus 76-84 25559498-3 2015 In this study, we attempted to find a connection between interleukin-1beta (IL-1beta) and interleukin-1 receptor antagonist (IL-1Ra) in trinitrobenzene sulfonic acid (TNBS)-induced chronic pancreatitis, and then the therapeutic effect of recombinant IL-1Ra was also detected in the CP model. Trinitrobenzenesulfonic Acid 167-171 interleukin 1 receptor antagonist Rattus norvegicus 90-123 25559498-3 2015 In this study, we attempted to find a connection between interleukin-1beta (IL-1beta) and interleukin-1 receptor antagonist (IL-1Ra) in trinitrobenzene sulfonic acid (TNBS)-induced chronic pancreatitis, and then the therapeutic effect of recombinant IL-1Ra was also detected in the CP model. Trinitrobenzenesulfonic Acid 167-171 interleukin 1 receptor antagonist Rattus norvegicus 125-131 25559498-3 2015 In this study, we attempted to find a connection between interleukin-1beta (IL-1beta) and interleukin-1 receptor antagonist (IL-1Ra) in trinitrobenzene sulfonic acid (TNBS)-induced chronic pancreatitis, and then the therapeutic effect of recombinant IL-1Ra was also detected in the CP model. Trinitrobenzenesulfonic Acid 167-171 interleukin 1 receptor antagonist Rattus norvegicus 250-256 25562655-3 2015 Here, we demonstrated that the rapid appearance of activated immune cells in the intestinal wall is selectively neurotoxic via iNOS-derived NO, using TNBS-induced colitis in both rats and mice, and a co-culture model of ENS neurons and smooth muscle. Trinitrobenzenesulfonic Acid 150-154 nitric oxide synthase 2 Rattus norvegicus 127-131 25533544-5 2015 Co-localization of VPS4B and active caspase-3 in IECs of the TNBS group further indicated the possible involvement of VPS4B in IEC apoptosis. Trinitrobenzenesulfonic Acid 61-65 vacuolar protein sorting 4 homolog B Homo sapiens 19-24 25533544-5 2015 Co-localization of VPS4B and active caspase-3 in IECs of the TNBS group further indicated the possible involvement of VPS4B in IEC apoptosis. Trinitrobenzenesulfonic Acid 61-65 caspase 3 Homo sapiens 36-45 25533544-5 2015 Co-localization of VPS4B and active caspase-3 in IECs of the TNBS group further indicated the possible involvement of VPS4B in IEC apoptosis. Trinitrobenzenesulfonic Acid 61-65 vacuolar protein sorting 4 homolog B Homo sapiens 118-123 25785006-5 2015 Furthermore, ALA significantly inhibited TNBS-induced apoptosis, which partly due to up-regulation of Bcl-2 expression, reduction of Bax expression and caspase-3, caspase-9 activity. Trinitrobenzenesulfonic Acid 41-45 B cell leukemia/lymphoma 2 Mus musculus 102-107 25445197-8 2015 An increase in myeloperoxidase (MPO) activity was found in the colon, but not in the bladder or urethra after intracolonic TNBS treatment. Trinitrobenzenesulfonic Acid 123-127 myeloperoxidase Rattus norvegicus 15-30 25445197-8 2015 An increase in myeloperoxidase (MPO) activity was found in the colon, but not in the bladder or urethra after intracolonic TNBS treatment. Trinitrobenzenesulfonic Acid 123-127 myeloperoxidase Rattus norvegicus 32-35 25785006-5 2015 Furthermore, ALA significantly inhibited TNBS-induced apoptosis, which partly due to up-regulation of Bcl-2 expression, reduction of Bax expression and caspase-3, caspase-9 activity. Trinitrobenzenesulfonic Acid 41-45 BCL2-associated X protein Mus musculus 133-136 25785006-5 2015 Furthermore, ALA significantly inhibited TNBS-induced apoptosis, which partly due to up-regulation of Bcl-2 expression, reduction of Bax expression and caspase-3, caspase-9 activity. Trinitrobenzenesulfonic Acid 41-45 caspase 3 Mus musculus 152-161 25785006-5 2015 Furthermore, ALA significantly inhibited TNBS-induced apoptosis, which partly due to up-regulation of Bcl-2 expression, reduction of Bax expression and caspase-3, caspase-9 activity. Trinitrobenzenesulfonic Acid 41-45 caspase 9 Mus musculus 163-172 25785006-8 2015 In summary, we demonstrate that ALA has protective properties against TNBS-induced UC through anti-apoptosis, anti-oxidant actions, and mitogen-activated protein kinase (MAPK) signaling pathway. Trinitrobenzenesulfonic Acid 70-74 mitogen-activated protein kinase 1 Mus musculus 170-174 25729764-8 2015 RESULTS: TNBS-induced chronic colitis was associated with increased colonic collagen (col1a2) mRNA expression. Trinitrobenzenesulfonic Acid 9-13 collagen, type I, alpha 2 Mus musculus 86-92 25574088-0 2015 Altered vasoactive intestinal peptides expression in irritable bowel syndrome patients and rats with trinitrobenzene sulfonic acid-induced colitis. Trinitrobenzenesulfonic Acid 101-130 vasoactive intestinal peptide Homo sapiens 8-38 25574088-9 2015 RESULTS: TNBS induced colitis in the rats was confirmed with weight loss (13.7 +- 3.2 g) and increased myeloperoxidase activity. Trinitrobenzenesulfonic Acid 9-13 myeloperoxidase Rattus norvegicus 103-118 25574088-12 2015 The expression of an inflammatory marker myeloperoxidase was significantly elevated in the intracellular granules of neutrophils in rat models following TNBS treatment compared to naive rats. Trinitrobenzenesulfonic Acid 153-157 myeloperoxidase Rattus norvegicus 41-56 25574088-14 2015 VIP plasma concentration was significantly increased in rats following TNBS treatment as compared to naive animals (P < 0.05). Trinitrobenzenesulfonic Acid 71-75 vasoactive intestinal peptide Rattus norvegicus 0-3 25729764-9 2015 Intracolonic cathelicidin (mCRAMP peptide) administration or intravenous delivery of lentivirus-overexpressing cathelicidin gene significantly reduced colonic col1a2 mRNA expression in TNBS-exposed mice, compared to vehicle administration. Trinitrobenzenesulfonic Acid 185-189 collagen, type I, alpha 2 Mus musculus 159-165 26273312-4 2015 Meanwhile, assessments by ELISA revealed an increment in concentrations of IL-2, IL-6, and IL-17 and a reduction in level of TGF-beta after TNBS challenge. Trinitrobenzenesulfonic Acid 140-144 transforming growth factor, beta 1 Rattus norvegicus 125-133 25301381-1 2015 OBJECTIVES: Vasoactive intestinal peptide (VIP) is an immunomodulatory neuropeptide with therapeutic properties in multiple murine models of inflammatory disease including the trinitrobenzene-sulfonic acid (TNBS)-colitis model of Crohn"s disease. Trinitrobenzenesulfonic Acid 176-205 vasoactive intestinal polypeptide Mus musculus 43-46 25821305-8 2015 Simvastatin or rosuvastatin counteracted the reduction in colon length, decreased colon weight, neutrophil accumulation, and tumor necrosis factor-alpha level in TNBS-induced colitis. Trinitrobenzenesulfonic Acid 162-166 tumor necrosis factor Rattus norvegicus 125-152 25301381-4 2015 METHODS: TNBS was intracolonically administered to wild-type (WT) and VIP KO mice, and weight loss and colitis were assessed over time. Trinitrobenzenesulfonic Acid 9-13 vasoactive intestinal polypeptide Mus musculus 70-73 25301381-10 2015 Moreover, splenocytes from TNBS-treated VIP KO mice exhibited an enhanced proliferative response to anti-CD3/CD28 stimulation in vitro. Trinitrobenzenesulfonic Acid 27-31 vasoactive intestinal polypeptide Mus musculus 40-43 25301381-10 2015 Moreover, splenocytes from TNBS-treated VIP KO mice exhibited an enhanced proliferative response to anti-CD3/CD28 stimulation in vitro. Trinitrobenzenesulfonic Acid 27-31 CD3 antigen, epsilon polypeptide Mus musculus 105-108 25301381-10 2015 Moreover, splenocytes from TNBS-treated VIP KO mice exhibited an enhanced proliferative response to anti-CD3/CD28 stimulation in vitro. Trinitrobenzenesulfonic Acid 27-31 CD28 antigen Mus musculus 109-113 25561788-0 2014 2,4,6-trinitrobenzene sulfonic acid-induced chronic colitis with fibrosis and modulation of TGF-beta1 signaling. Trinitrobenzenesulfonic Acid 0-35 transforming growth factor, beta 1 Rattus norvegicus 92-101 25656034-7 2015 Compared with TNBS group, proinflammatory cytokines, including TNF-alpha, IL-12 and VEGF of ADMSC group were significantly reduced, with significant increase of IL-10 expression. Trinitrobenzenesulfonic Acid 14-18 tumor necrosis factor Mus musculus 63-72 25526689-9 2015 We observed significant changes in lymphatic mRNA expression of COX-1, COX-2, MPGES-1, PGIS, EP4 and IP and increases in PGE2 and PGI2 in tissues of TNBS-treated animals. Trinitrobenzenesulfonic Acid 149-153 cytochrome c oxidase I, mitochondrial Rattus norvegicus 64-69 25526689-9 2015 We observed significant changes in lymphatic mRNA expression of COX-1, COX-2, MPGES-1, PGIS, EP4 and IP and increases in PGE2 and PGI2 in tissues of TNBS-treated animals. Trinitrobenzenesulfonic Acid 149-153 cytochrome c oxidase II, mitochondrial Rattus norvegicus 71-76 25526689-9 2015 We observed significant changes in lymphatic mRNA expression of COX-1, COX-2, MPGES-1, PGIS, EP4 and IP and increases in PGE2 and PGI2 in tissues of TNBS-treated animals. Trinitrobenzenesulfonic Acid 149-153 prostaglandin I2 synthase Rattus norvegicus 87-91 25526689-9 2015 We observed significant changes in lymphatic mRNA expression of COX-1, COX-2, MPGES-1, PGIS, EP4 and IP and increases in PGE2 and PGI2 in tissues of TNBS-treated animals. Trinitrobenzenesulfonic Acid 149-153 prostaglandin E receptor 4 Rattus norvegicus 93-96 25526689-10 2015 Changes in mRNA in blood vessels from TNBS-treated animals included differences in COX-1, COX-2, MPGES-1, PGIS, EP1, EP2 and IP expression. Trinitrobenzenesulfonic Acid 38-42 cytochrome c oxidase I, mitochondrial Rattus norvegicus 83-88 25526689-10 2015 Changes in mRNA in blood vessels from TNBS-treated animals included differences in COX-1, COX-2, MPGES-1, PGIS, EP1, EP2 and IP expression. Trinitrobenzenesulfonic Acid 38-42 cytochrome c oxidase II, mitochondrial Rattus norvegicus 90-95 25526689-10 2015 Changes in mRNA in blood vessels from TNBS-treated animals included differences in COX-1, COX-2, MPGES-1, PGIS, EP1, EP2 and IP expression. Trinitrobenzenesulfonic Acid 38-42 prostaglandin I2 synthase Rattus norvegicus 106-110 25526689-10 2015 Changes in mRNA in blood vessels from TNBS-treated animals included differences in COX-1, COX-2, MPGES-1, PGIS, EP1, EP2 and IP expression. Trinitrobenzenesulfonic Acid 38-42 prostaglandin E receptor 1 Rattus norvegicus 112-115 25526689-10 2015 Changes in mRNA in blood vessels from TNBS-treated animals included differences in COX-1, COX-2, MPGES-1, PGIS, EP1, EP2 and IP expression. Trinitrobenzenesulfonic Acid 38-42 prostaglandin E receptor 2 Rattus norvegicus 117-120 25561788-14 2014 Tight junction proteins were modified by repeated TNBS challenge: colon occludin expression rose significantly (P < 0.01), whereas claudin-1 expression fell (P < 0.01). Trinitrobenzenesulfonic Acid 50-54 occludin Rattus norvegicus 72-80 25561788-14 2014 Tight junction proteins were modified by repeated TNBS challenge: colon occludin expression rose significantly (P < 0.01), whereas claudin-1 expression fell (P < 0.01). Trinitrobenzenesulfonic Acid 50-54 claudin 1 Rattus norvegicus 134-143 25561788-11 2014 Colonic production of TGF-beta production tended to be higher in TNBS-treated rats (P < 0.06). Trinitrobenzenesulfonic Acid 65-69 transforming growth factor, beta 1 Rattus norvegicus 22-30 25561788-12 2014 Fibrosis-related proteins such as phospho-p38, phospho-SMAD2/3, and PPARgamma were significantly higher in TNBS-treated rats compared to control rats (all P < 0.05). Trinitrobenzenesulfonic Acid 107-111 peroxisome proliferator-activated receptor gamma Rattus norvegicus 68-77 25561788-13 2014 TNBS rats had a higher expression of Akt compared to control rats (P < 0.01). Trinitrobenzenesulfonic Acid 0-4 AKT serine/threonine kinase 1 Rattus norvegicus 37-40 28247863-9 2015 DSS/TNBS-treated apoA-I KO mice displayed increased mucosal damage upon both colonoscopy and histology, increased intestinal MPO activity and mRNA expression of TNF and ICAM as compared with WT and apoA-I Tg mice. Trinitrobenzenesulfonic Acid 4-8 apolipoprotein A-I Mus musculus 17-23 28247863-5 2015 Mucosal damage from colitis induced by dextran sodium sulphate (DSS) and 2,4,6-trinitrobenzenesulfonic acid (TNBS) was scored by colonoscopy and histology in apoA-I transgenic (Tg) and apoA-I knockout (KO) and wild-type (WT) mice. Trinitrobenzenesulfonic Acid 109-113 apolipoprotein A-I Mus musculus 158-164 28247863-9 2015 DSS/TNBS-treated apoA-I KO mice displayed increased mucosal damage upon both colonoscopy and histology, increased intestinal MPO activity and mRNA expression of TNF and ICAM as compared with WT and apoA-I Tg mice. Trinitrobenzenesulfonic Acid 4-8 myeloperoxidase Mus musculus 125-128 28247863-9 2015 DSS/TNBS-treated apoA-I KO mice displayed increased mucosal damage upon both colonoscopy and histology, increased intestinal MPO activity and mRNA expression of TNF and ICAM as compared with WT and apoA-I Tg mice. Trinitrobenzenesulfonic Acid 4-8 tumor necrosis factor Mus musculus 161-164 28247863-9 2015 DSS/TNBS-treated apoA-I KO mice displayed increased mucosal damage upon both colonoscopy and histology, increased intestinal MPO activity and mRNA expression of TNF and ICAM as compared with WT and apoA-I Tg mice. Trinitrobenzenesulfonic Acid 4-8 apolipoprotein A-I Mus musculus 198-204 25469038-9 2014 The widespread loss of myenteric neurons, and marked but transient HO-1 up-regulation were demonstrated after the first TNBS administration. Trinitrobenzenesulfonic Acid 120-124 heme oxygenase 1 Rattus norvegicus 67-71 25307345-4 2014 We studied NTR1 signaling in colitis-associated angiogenesis using 2,4,6-trinitrobenzenesulfonic acid-treated wild-type and NTR1-knockout mice. Trinitrobenzenesulfonic Acid 67-101 neurotensin receptor 1 Mus musculus 11-15 25307345-6 2014 NTR1-knockout mice had reduced microvascular density and mucosal integrity score compared with wild-type mice after 2,4,6-trinitrobenzenesulfonic acid treatment. Trinitrobenzenesulfonic Acid 116-150 neurotensin receptor 1 Mus musculus 0-4 24550371-10 2014 Treating mice with chronic stress facilitated the initiation of intestinal inflammation by a low dose of TNBS or DSS, which was abolished by pretreatment with an inhibitor of prolactin, the cabergoline. Trinitrobenzenesulfonic Acid 105-109 prolactin Mus musculus 175-184 25561798-9 2014 Colitis was successfully induced by TNBS in mice, characterized by colonic inflammation and aberrant Th1 and Th17 responses. Trinitrobenzenesulfonic Acid 36-40 negative elongation factor complex member C/D, Th1l Mus musculus 101-104 25561798-12 2014 CONCLUSION: B. infantis effectively attenuates TNBS-induced colitis by decreasing Th1 and Th17 responses and increasing Foxp3(+) Treg response in the colonic mucosa. Trinitrobenzenesulfonic Acid 47-51 negative elongation factor complex member C/D, Th1l Mus musculus 82-85 25469038-12 2014 Nevertheless, the HO-1 protein up-regulation after the second TNBS treatment proved to be transient. Trinitrobenzenesulfonic Acid 62-66 heme oxygenase 1 Rattus norvegicus 18-22 24972244-9 2014 Mangiferin furthermore inhibited colon shortening, macroscopic score, and colonic myeloperoxidase activity in TNBS-induced colitic mice. Trinitrobenzenesulfonic Acid 110-114 myeloperoxidase Mus musculus 82-97 25405993-6 2014 The susceptibility to inflammatory experimental colitis induced by intracolonic infusion of TNBS (2,4,6-trinitrobenzenesulphonic acid) was investigated in CORT-nursed rats in comparison with control rats. Trinitrobenzenesulfonic Acid 92-96 cortistatin Rattus norvegicus 155-159 25405993-6 2014 The susceptibility to inflammatory experimental colitis induced by intracolonic infusion of TNBS (2,4,6-trinitrobenzenesulphonic acid) was investigated in CORT-nursed rats in comparison with control rats. Trinitrobenzenesulfonic Acid 98-133 cortistatin Rattus norvegicus 155-159 25192306-7 2014 Cellular neutrophil infiltration, with the subsequent increase in myeloperoxidase levels induced by TNBS, were also reduced after the administration of the lyophilised microalga or (13S)-HOTE. Trinitrobenzenesulfonic Acid 100-104 myeloperoxidase Rattus norvegicus 66-81 24850427-8 2014 SIRT1 was also reduced in mice with colitis induced by 2,4,6-trinitrobenzenesulphonic acid or oxazolone. Trinitrobenzenesulfonic Acid 55-90 sirtuin 1 Mus musculus 0-5 25213465-8 2014 Ursolic acid also suppressed TNBS-induced COX-2 and iNOS expression as well as NF-kappaB activation in colon tissues. Trinitrobenzenesulfonic Acid 29-33 cytochrome c oxidase II, mitochondrial Mus musculus 42-47 25213465-8 2014 Ursolic acid also suppressed TNBS-induced COX-2 and iNOS expression as well as NF-kappaB activation in colon tissues. Trinitrobenzenesulfonic Acid 29-33 nitric oxide synthase 2, inducible Mus musculus 52-56 25213465-9 2014 Ursolic acid (20 mg/kg) also inhibited TNBS-induced IL-1beta, IL-6, TNF-alpha by 93, 86, and 85%, respectively (p < 0.05). Trinitrobenzenesulfonic Acid 39-43 interleukin 1 beta Mus musculus 52-60 25213465-9 2014 Ursolic acid (20 mg/kg) also inhibited TNBS-induced IL-1beta, IL-6, TNF-alpha by 93, 86, and 85%, respectively (p < 0.05). Trinitrobenzenesulfonic Acid 39-43 interleukin 6 Mus musculus 62-66 25213465-9 2014 Ursolic acid (20 mg/kg) also inhibited TNBS-induced IL-1beta, IL-6, TNF-alpha by 93, 86, and 85%, respectively (p < 0.05). Trinitrobenzenesulfonic Acid 39-43 tumor necrosis factor Mus musculus 68-77 25213465-10 2014 However, ursolic acid reversed TNBS-mediated downregulation of IL-10 expression to 79% of the normal control group (p < 0.05). Trinitrobenzenesulfonic Acid 31-35 interleukin 10 Mus musculus 63-68 24972244-10 2014 Mangiferin inhibited TNBS-induced IRAK1 phosphorylation and NF-kappaB activation. Trinitrobenzenesulfonic Acid 21-25 interleukin-1 receptor-associated kinase 1 Mus musculus 34-39 24972244-11 2014 Mangiferin suppressed TNBS-induced up-regulation of cyclooxygenase-2 and inducible NO synthase. Trinitrobenzenesulfonic Acid 22-26 prostaglandin-endoperoxide synthase 2 Mus musculus 52-68 24972244-11 2014 Mangiferin suppressed TNBS-induced up-regulation of cyclooxygenase-2 and inducible NO synthase. Trinitrobenzenesulfonic Acid 22-26 nitric oxide synthase 2, inducible Mus musculus 73-94 25118782-6 2014 Pre-administration of 10(7)CFU/day EcN to TNBS-treated rats resulted in a significant protection against inflammatory response and colons isolated from these rats exhibited a more pronounced expression of ZO-1 than the other groups. Trinitrobenzenesulfonic Acid 42-46 tight junction protein 1 Rattus norvegicus 205-209 24944202-5 2014 TNBS treatment in vivo and IL-1beta and TNF-alpha in vitro induced inducible nitric oxide synthase (iNOS) expression, stimulated ERK1/2 activity, caused iNOS-mediated S-nitrosylation and inhibition of AC5/6, and induced phosphorylation of PDE4D5 and stimulated its activity. Trinitrobenzenesulfonic Acid 0-4 nitric oxide synthase 2, inducible Mus musculus 67-98 25070376-2 2014 The present study aimed to evaluate the effects of targeting the IL-23/IL-17 pathway using the anti-IL-23p19 monoclonal antibody (mAb) on 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced CD rats. Trinitrobenzenesulfonic Acid 138-173 interleukin 17A Rattus norvegicus 71-76 25070376-2 2014 The present study aimed to evaluate the effects of targeting the IL-23/IL-17 pathway using the anti-IL-23p19 monoclonal antibody (mAb) on 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced CD rats. Trinitrobenzenesulfonic Acid 138-173 interleukin 23 subunit alpha Rattus norvegicus 100-108 25070376-2 2014 The present study aimed to evaluate the effects of targeting the IL-23/IL-17 pathway using the anti-IL-23p19 monoclonal antibody (mAb) on 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced CD rats. Trinitrobenzenesulfonic Acid 175-179 interleukin 17A Rattus norvegicus 71-76 25070376-2 2014 The present study aimed to evaluate the effects of targeting the IL-23/IL-17 pathway using the anti-IL-23p19 monoclonal antibody (mAb) on 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced CD rats. Trinitrobenzenesulfonic Acid 175-179 interleukin 23 subunit alpha Rattus norvegicus 100-108 25070376-7 2014 Anti-IL-23p19 mAb attenuated TNBS-induced CD in model rats. Trinitrobenzenesulfonic Acid 29-33 interleukin 23 subunit alpha Rattus norvegicus 5-13 25146101-5 2014 The results showed that GdCl3 had no macrophage depletion effect in colonic mucosa, but significantly suppressed TNBS and DSS-induced TNFalpha, IL-1beta and IL-6 secretions. Trinitrobenzenesulfonic Acid 113-117 interleukin 1 beta Mus musculus 144-152 24912557-5 2014 Expressions of the IL-6 and FasL genes appeared to be down-regulated by the formulation in TNBS-treated colon tissues, suggesting that the suppression of those genes may be involved in the anti-inflammatory activity of the formulation. Trinitrobenzenesulfonic Acid 91-95 interleukin 6 Mus musculus 19-23 24912557-5 2014 Expressions of the IL-6 and FasL genes appeared to be down-regulated by the formulation in TNBS-treated colon tissues, suggesting that the suppression of those genes may be involved in the anti-inflammatory activity of the formulation. Trinitrobenzenesulfonic Acid 91-95 Fas ligand (TNF superfamily, member 6) Mus musculus 28-32 24944202-5 2014 TNBS treatment in vivo and IL-1beta and TNF-alpha in vitro induced inducible nitric oxide synthase (iNOS) expression, stimulated ERK1/2 activity, caused iNOS-mediated S-nitrosylation and inhibition of AC5/6, and induced phosphorylation of PDE4D5 and stimulated its activity. Trinitrobenzenesulfonic Acid 0-4 nitric oxide synthase 2, inducible Mus musculus 100-104 24944202-5 2014 TNBS treatment in vivo and IL-1beta and TNF-alpha in vitro induced inducible nitric oxide synthase (iNOS) expression, stimulated ERK1/2 activity, caused iNOS-mediated S-nitrosylation and inhibition of AC5/6, and induced phosphorylation of PDE4D5 and stimulated its activity. Trinitrobenzenesulfonic Acid 0-4 mitogen-activated protein kinase 3 Mus musculus 129-135 24944202-5 2014 TNBS treatment in vivo and IL-1beta and TNF-alpha in vitro induced inducible nitric oxide synthase (iNOS) expression, stimulated ERK1/2 activity, caused iNOS-mediated S-nitrosylation and inhibition of AC5/6, and induced phosphorylation of PDE4D5 and stimulated its activity. Trinitrobenzenesulfonic Acid 0-4 nitric oxide synthase 2, inducible Mus musculus 153-157 24944202-5 2014 TNBS treatment in vivo and IL-1beta and TNF-alpha in vitro induced inducible nitric oxide synthase (iNOS) expression, stimulated ERK1/2 activity, caused iNOS-mediated S-nitrosylation and inhibition of AC5/6, and induced phosphorylation of PDE4D5 and stimulated its activity. Trinitrobenzenesulfonic Acid 0-4 adenylate cyclase 6 Mus musculus 201-206 24875097-7 2014 In two mice models of trinitrobenzene sulfonic acid (TNBS)- and dextran sulfate sodium (DSS)-induced colitis, the colonic expression of GLP-2R mRNA was decreased by 60% compared with control mice. Trinitrobenzenesulfonic Acid 22-51 glucagon-like peptide 2 receptor Mus musculus 136-142 24875097-7 2014 In two mice models of trinitrobenzene sulfonic acid (TNBS)- and dextran sulfate sodium (DSS)-induced colitis, the colonic expression of GLP-2R mRNA was decreased by 60% compared with control mice. Trinitrobenzenesulfonic Acid 53-57 glucagon-like peptide 2 receptor Mus musculus 136-142 24875097-9 2014 Therapeutically, GLP-2 showed a weak restorative effect on intestinal inflammation during TNBS-induced colitis as assessed by macroscopic score and inflammatory markers. Trinitrobenzenesulfonic Acid 90-94 glucagon-like peptide 2 receptor Mus musculus 17-22 24832648-9 2014 The number of TRPM8 nerve fibers in mucosa of DSS- or 2,4,6-trinitrobenzene sulfonic acid-induced colitis model mice drastically increased compared with control mice. Trinitrobenzenesulfonic Acid 54-89 transient receptor potential cation channel, subfamily M, member 8 Mus musculus 14-19 24000293-8 2014 Upregulation or downregulation of miR-141 in the TNBS-induced or IL-10 KO colitic colon regulated leukocyte infiltration and alleviated or aggravated experimental colitis, respectively. Trinitrobenzenesulfonic Acid 49-53 microRNA 141 Homo sapiens 34-41 24815859-6 2014 CLP-0611 also inhibited TNBS-induced expression of TNF-alpha, IL-1beta, and IL-6. Trinitrobenzenesulfonic Acid 24-28 tumor necrosis factor Mus musculus 51-60 25177159-6 2014 TNBS elicits Th-1 driven immune response, whereas oxazolone predominantly exhibits immune response of Th-2 phenotype. Trinitrobenzenesulfonic Acid 0-4 negative elongation factor complex member C/D Homo sapiens 13-17 24815859-6 2014 CLP-0611 also inhibited TNBS-induced expression of TNF-alpha, IL-1beta, and IL-6. Trinitrobenzenesulfonic Acid 24-28 interleukin 1 beta Mus musculus 62-70 24815859-6 2014 CLP-0611 also inhibited TNBS-induced expression of TNF-alpha, IL-1beta, and IL-6. Trinitrobenzenesulfonic Acid 24-28 interleukin 6 Mus musculus 76-80 24758288-7 2014 The expression of toll-like receptor 3 (TLR3) and the TLRs signaling pathway molecules MyD88 and TRIF, the activation of NF-kappaB, and the production of inflammatory cytokine tumor necrosis factor-alpha were stimulated in TNBS-treated zebrafish but there was no corresponding alteration in germ-free fish. Trinitrobenzenesulfonic Acid 223-227 toll-like receptor 3 Danio rerio 18-38 24740538-4 2014 LARG expression was increased in longitudinal muscle cells isolated from muscle strips cultured for 24 h with IL-1beta or TNF-alpha or obtained from the colon of TNBS-treated mice. Trinitrobenzenesulfonic Acid 162-166 Rho guanine nucleotide exchange factor (GEF) 12 Mus musculus 0-4 24740538-7 2014 Expression of the MLCP activator, telokin, and MLCP activity were also decreased in longitudinal muscle cells from TNBS-treated mice or from strips treated with IL-1beta or TNF-alpha. Trinitrobenzenesulfonic Acid 115-119 tumor necrosis factor Mus musculus 173-182 24740538-9 2014 In colonic circular smooth muscle cells isolated from TNBS-treated mice or from strips treated with IL-1beta or TNF-alpha, CPI-17 expression and sustained muscle contraction were decreased. Trinitrobenzenesulfonic Acid 54-58 interleukin 1 beta Mus musculus 100-108 24740538-9 2014 In colonic circular smooth muscle cells isolated from TNBS-treated mice or from strips treated with IL-1beta or TNF-alpha, CPI-17 expression and sustained muscle contraction were decreased. Trinitrobenzenesulfonic Acid 54-58 protein phosphatase 1, regulatory inhibitor subunit 14A Mus musculus 123-129 24704625-10 2014 In summary, these results suggest that andrographolide sulfonate ameliorated TNBS-induced colitis in mice through inhibiting Th1/Th17 response. Trinitrobenzenesulfonic Acid 77-81 negative elongation factor complex member C/D, Th1l Mus musculus 125-128 24758288-7 2014 The expression of toll-like receptor 3 (TLR3) and the TLRs signaling pathway molecules MyD88 and TRIF, the activation of NF-kappaB, and the production of inflammatory cytokine tumor necrosis factor-alpha were stimulated in TNBS-treated zebrafish but there was no corresponding alteration in germ-free fish. Trinitrobenzenesulfonic Acid 223-227 toll-like receptor 3 Danio rerio 40-44 24758288-7 2014 The expression of toll-like receptor 3 (TLR3) and the TLRs signaling pathway molecules MyD88 and TRIF, the activation of NF-kappaB, and the production of inflammatory cytokine tumor necrosis factor-alpha were stimulated in TNBS-treated zebrafish but there was no corresponding alteration in germ-free fish. Trinitrobenzenesulfonic Acid 223-227 tumor necrosis factor a (TNF superfamily, member 2) Danio rerio 176-203 24627565-3 2014 We investigated whether satellite glial cell (SGC) and tumor necrosis factor-alpha (TNF-alpha) activation in DRG participates in a 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced rat model of visceral hyperalgesia. Trinitrobenzenesulfonic Acid 168-172 tumor necrosis factor Rattus norvegicus 84-93 24627565-4 2014 In TNBS-treated rats, TNF-alpha expression increased in DRG and was colocalized to SGCs enveloping a given neuron. Trinitrobenzenesulfonic Acid 3-7 tumor necrosis factor Rattus norvegicus 22-31 24627565-6 2014 When nerves attached to DRG (L6-S1) were stimulated with a series of electrical stimulations, TNF-alpha were released from DRG in TNBS-treated animals compared with controls. Trinitrobenzenesulfonic Acid 130-134 tumor necrosis factor Rattus norvegicus 94-103 24524998-8 2014 However, 5-HT combined with a low dose of 2,4,6-trinitrobenzene sulfonic acid (TNBS), the level of which caused a minimal level of colitis, exaggerated colon inflammation accompanied by much more enhanced induction of inflammatory cytokines, IL-6, IL-8, and MCP-1, indicating that colon epithelial cells directly exposed to 5-HT are primed toward inflammation. Trinitrobenzenesulfonic Acid 42-77 interleukin 6 Mus musculus 242-246 24782617-9 2014 RESULTS: Collagen I and IGF-1 expression was increased, and SIRT1 expression was decreased (0.67 +- 0.04 vs 1.05 +- 0.07, P < 0.001) in TNBS-induced colitis compared with the control group. Trinitrobenzenesulfonic Acid 139-143 sirtuin 1 Rattus norvegicus 60-65 24764672-0 2014 Hepcidin expression in colon during trinitrobenzene sulfonic acid-induced colitis in rats. Trinitrobenzenesulfonic Acid 36-65 hepcidin antimicrobial peptide Rattus norvegicus 0-8 24524998-8 2014 However, 5-HT combined with a low dose of 2,4,6-trinitrobenzene sulfonic acid (TNBS), the level of which caused a minimal level of colitis, exaggerated colon inflammation accompanied by much more enhanced induction of inflammatory cytokines, IL-6, IL-8, and MCP-1, indicating that colon epithelial cells directly exposed to 5-HT are primed toward inflammation. Trinitrobenzenesulfonic Acid 42-77 chemokine (C-X-C motif) ligand 15 Mus musculus 248-252 24524998-8 2014 However, 5-HT combined with a low dose of 2,4,6-trinitrobenzene sulfonic acid (TNBS), the level of which caused a minimal level of colitis, exaggerated colon inflammation accompanied by much more enhanced induction of inflammatory cytokines, IL-6, IL-8, and MCP-1, indicating that colon epithelial cells directly exposed to 5-HT are primed toward inflammation. Trinitrobenzenesulfonic Acid 42-77 mast cell protease 1 Mus musculus 258-263 24524998-8 2014 However, 5-HT combined with a low dose of 2,4,6-trinitrobenzene sulfonic acid (TNBS), the level of which caused a minimal level of colitis, exaggerated colon inflammation accompanied by much more enhanced induction of inflammatory cytokines, IL-6, IL-8, and MCP-1, indicating that colon epithelial cells directly exposed to 5-HT are primed toward inflammation. Trinitrobenzenesulfonic Acid 79-83 interleukin 6 Mus musculus 242-246 24524998-8 2014 However, 5-HT combined with a low dose of 2,4,6-trinitrobenzene sulfonic acid (TNBS), the level of which caused a minimal level of colitis, exaggerated colon inflammation accompanied by much more enhanced induction of inflammatory cytokines, IL-6, IL-8, and MCP-1, indicating that colon epithelial cells directly exposed to 5-HT are primed toward inflammation. Trinitrobenzenesulfonic Acid 79-83 chemokine (C-X-C motif) ligand 15 Mus musculus 248-252 24524998-8 2014 However, 5-HT combined with a low dose of 2,4,6-trinitrobenzene sulfonic acid (TNBS), the level of which caused a minimal level of colitis, exaggerated colon inflammation accompanied by much more enhanced induction of inflammatory cytokines, IL-6, IL-8, and MCP-1, indicating that colon epithelial cells directly exposed to 5-HT are primed toward inflammation. Trinitrobenzenesulfonic Acid 79-83 mast cell protease 1 Mus musculus 258-263 24412990-6 2014 P2X7-R C57BL/6 mice were treated with trinitrobenzene sulfonic acid or dextran sulfate sodium (DSS) for inducing colitis. Trinitrobenzenesulfonic Acid 38-67 purinergic receptor P2X, ligand-gated ion channel, 7 Mus musculus 0-6 24122226-4 2014 The present study was designed to investigate the role of SDF-1alpha/CXCR4 axis in the therapeutic effects of lentivirus-preconditioned BMSCs for 2,4,6-trinitrobenzene sulfonic acid (TNBS)-colitis rats. Trinitrobenzenesulfonic Acid 146-181 C-X-C motif chemokine receptor 4 Rattus norvegicus 69-74 24122226-4 2014 The present study was designed to investigate the role of SDF-1alpha/CXCR4 axis in the therapeutic effects of lentivirus-preconditioned BMSCs for 2,4,6-trinitrobenzene sulfonic acid (TNBS)-colitis rats. Trinitrobenzenesulfonic Acid 183-187 C-X-C motif chemokine receptor 4 Rattus norvegicus 69-74 24931258-21 2014 On day 7 the expressions of TNF-alpha and IL-1beta in the thalidomide treatment group were lower than in the TNBS model group. Trinitrobenzenesulfonic Acid 109-113 tumor necrosis factor Rattus norvegicus 28-37 23962873-3 2014 In addition, we found that Nod2-/- mice manifest decreased severity of 2,4,6-trinitrobenzene sulfonic acid (TNBS)-colitis and that TNBS-colitis in Nod2-/- or Nod2+/+ mice is ameliorated by adoptive transfer of LP cells from ethanol-treated mice before, but not after, depletion of LAP+ T cells. Trinitrobenzenesulfonic Acid 71-106 nucleotide-binding oligomerization domain containing 2 Mus musculus 27-31 24504372-2 2014 The latest study showed that ginsenoside Rb1 and its metabolites could inhibit TNBS-induced colitis injury. Trinitrobenzenesulfonic Acid 79-83 RB transcriptional corepressor 1 Mus musculus 41-44 23307618-9 2014 On the other hand, colonic mRNA expression and the serum concentration of MCP-1 were significantly higher in the TNBS-treated rats than in the control animals. Trinitrobenzenesulfonic Acid 113-117 C-C motif chemokine ligand 2 Rattus norvegicus 74-79 24116743-7 2014 In addition, 2,4,6-trinitrobenzene sulfonic acid-induced colitis and SAMP1/Yit mice, a model of spontaneous Crohn"s disease, also exhibited increased mucosal TnC in colon and ilea respectively. Trinitrobenzenesulfonic Acid 13-48 tenascin C Mus musculus 158-161 24285285-8 2014 The level of CD11b(+)Gr-1(+) myeloid-derived suppressor cells (MDSCs) was increased in all tested tissues of the TNBS- and DSS-treated groups, apart from the basal membrane (BM) in the DSS-induced colitis groups and the lamina propria (LP) in the DSS-induced chronic colitis group. Trinitrobenzenesulfonic Acid 113-117 integrin alpha M Mus musculus 13-18 24286754-0 2014 Aquaporin 3 and 8 are down-regulated in TNBS-induced rat colitis. Trinitrobenzenesulfonic Acid 40-44 aquaporin 3 (Gill blood group) Rattus norvegicus 0-17 24286754-5 2014 As a result, exposure to TNBS+ethanol resulted in a marked decrease in both the mRNA and protein expression of AQP3 and AQP8, with the exception of AQP8 protein which was negative in the distal colon in all three groups. Trinitrobenzenesulfonic Acid 25-29 aquaporin 3 (Gill blood group) Rattus norvegicus 111-115 24286754-5 2014 As a result, exposure to TNBS+ethanol resulted in a marked decrease in both the mRNA and protein expression of AQP3 and AQP8, with the exception of AQP8 protein which was negative in the distal colon in all three groups. Trinitrobenzenesulfonic Acid 25-29 aquaporin 8 Rattus norvegicus 120-124 23771723-6 2014 Compared with rats in the model controls, TGP (50 or 100 mg/kg/day)-treated rats with TNBS/ethanol-induced colitis showed significant improvements of DAI, CMDI, HPS, and MPO activity. Trinitrobenzenesulfonic Acid 86-90 myeloperoxidase Rattus norvegicus 170-173 24931258-21 2014 On day 7 the expressions of TNF-alpha and IL-1beta in the thalidomide treatment group were lower than in the TNBS model group. Trinitrobenzenesulfonic Acid 109-113 interleukin 1 beta Rattus norvegicus 42-50 24931258-25 2014 In the TNBS model group, the IL-10 expression peaked later than in the thalidomide treatment group. Trinitrobenzenesulfonic Acid 7-11 interleukin 10 Rattus norvegicus 29-34 24314293-0 2013 Effects of interleukin-4 or interleukin-10 gene therapy on trinitrobenzenesulfonic acid-induced murine colitis. Trinitrobenzenesulfonic Acid 59-87 interleukin 10 Mus musculus 28-42 24683438-6 2014 Furthermore, 6 weeks of running significantly decreased TNBS-induced inflammatory markers, including extent of lesions, severity of mucosal damage, and gene expression of IL-1beta, CXCL1, and MPO activity, while IL-10 gene expression and cNOS activity were increased. Trinitrobenzenesulfonic Acid 56-60 interleukin 1 beta Rattus norvegicus 171-179 24683438-6 2014 Furthermore, 6 weeks of running significantly decreased TNBS-induced inflammatory markers, including extent of lesions, severity of mucosal damage, and gene expression of IL-1beta, CXCL1, and MPO activity, while IL-10 gene expression and cNOS activity were increased. Trinitrobenzenesulfonic Acid 56-60 C-X-C motif chemokine ligand 1 Rattus norvegicus 181-186 24683438-6 2014 Furthermore, 6 weeks of running significantly decreased TNBS-induced inflammatory markers, including extent of lesions, severity of mucosal damage, and gene expression of IL-1beta, CXCL1, and MPO activity, while IL-10 gene expression and cNOS activity were increased. Trinitrobenzenesulfonic Acid 56-60 myeloperoxidase Rattus norvegicus 192-195 25452234-10 2014 In TNBS-treated rats, Cav3.2 was upregulated in the dorsal root ganglia, while CSE was downregulated in the colon. Trinitrobenzenesulfonic Acid 3-7 cystathionine gamma-lyase Rattus norvegicus 79-82 24376661-2 2013 Expression of MCH is upregulated in inflamed intestinal mucosa in humans with colitis and MCH-deficient mice treated with trinitrobenzene-sulfonic acid (TNBS) develop an attenuated form of colitis compared to wild type animals. Trinitrobenzenesulfonic Acid 122-151 pro-melanin concentrating hormone Homo sapiens 14-17 24376661-2 2013 Expression of MCH is upregulated in inflamed intestinal mucosa in humans with colitis and MCH-deficient mice treated with trinitrobenzene-sulfonic acid (TNBS) develop an attenuated form of colitis compared to wild type animals. Trinitrobenzenesulfonic Acid 153-157 pro-melanin concentrating hormone Homo sapiens 14-17 24376661-10 2013 Most importantly, and in analogy to human IBD and TNBS-induced mouse experimental colitis, we found increased intestinal expression of MCH and its receptor in TNBS-treated zebrafish. Trinitrobenzenesulfonic Acid 50-54 pro-melanin concentrating hormone Homo sapiens 135-138 24376661-10 2013 Most importantly, and in analogy to human IBD and TNBS-induced mouse experimental colitis, we found increased intestinal expression of MCH and its receptor in TNBS-treated zebrafish. Trinitrobenzenesulfonic Acid 159-163 pro-melanin concentrating hormone Homo sapiens 135-138 24314293-8 2013 Injections of IL-4 or IL-10 significantly inhibited TNBS-induced colon tissue damage, disease activity index (DAI) and body weight loss compared to the control mice. Trinitrobenzenesulfonic Acid 52-56 interleukin 4 Mus musculus 14-18 24314293-8 2013 Injections of IL-4 or IL-10 significantly inhibited TNBS-induced colon tissue damage, disease activity index (DAI) and body weight loss compared to the control mice. Trinitrobenzenesulfonic Acid 52-56 interleukin 10 Mus musculus 22-27 24314293-11 2013 CONCLUSIONS: These data suggest that intraperitoneal injection of IL-4 or IL-10 plasmid was a potential strategy in control of TNBS-induced murine colitis, but their combination had less effect. Trinitrobenzenesulfonic Acid 127-131 interleukin 4 Mus musculus 66-70 24314293-11 2013 CONCLUSIONS: These data suggest that intraperitoneal injection of IL-4 or IL-10 plasmid was a potential strategy in control of TNBS-induced murine colitis, but their combination had less effect. Trinitrobenzenesulfonic Acid 127-131 interleukin 10 Mus musculus 74-79 23892357-7 2013 Rectal administration of CAPE ameliorated 2,4,6-trinitrobenzene sulfonic acid-induced rat colitis and activated the Nrf2 pathway in the inflamed colon, and incubation of CAPE in the lumen of the inflamed distal colon generated Oxi-CAPE. Trinitrobenzenesulfonic Acid 42-77 structural maintenance of chromosomes 2 Rattus norvegicus 25-29 24441193-3 2013 The present study evaluated the expression of TGFbeta, Smad3, alphavbeta6 integrin, mTOR and PPARgamma in 2,4,6-trinitrobenzenesulphonic acid (TNBS)-induced colorectal fibrosis in Smad3 wild-type (WT) and null mice. Trinitrobenzenesulfonic Acid 106-141 mechanistic target of rapamycin kinase Mus musculus 84-88 24441193-3 2013 The present study evaluated the expression of TGFbeta, Smad3, alphavbeta6 integrin, mTOR and PPARgamma in 2,4,6-trinitrobenzenesulphonic acid (TNBS)-induced colorectal fibrosis in Smad3 wild-type (WT) and null mice. Trinitrobenzenesulfonic Acid 106-141 peroxisome proliferator activated receptor gamma Mus musculus 93-102 24441193-3 2013 The present study evaluated the expression of TGFbeta, Smad3, alphavbeta6 integrin, mTOR and PPARgamma in 2,4,6-trinitrobenzenesulphonic acid (TNBS)-induced colorectal fibrosis in Smad3 wild-type (WT) and null mice. Trinitrobenzenesulfonic Acid 106-141 SMAD family member 3 Mus musculus 180-185 24441193-3 2013 The present study evaluated the expression of TGFbeta, Smad3, alphavbeta6 integrin, mTOR and PPARgamma in 2,4,6-trinitrobenzenesulphonic acid (TNBS)-induced colorectal fibrosis in Smad3 wild-type (WT) and null mice. Trinitrobenzenesulfonic Acid 143-147 transforming growth factor, beta 1 Mus musculus 46-53 24441193-3 2013 The present study evaluated the expression of TGFbeta, Smad3, alphavbeta6 integrin, mTOR and PPARgamma in 2,4,6-trinitrobenzenesulphonic acid (TNBS)-induced colorectal fibrosis in Smad3 wild-type (WT) and null mice. Trinitrobenzenesulfonic Acid 143-147 mechanistic target of rapamycin kinase Mus musculus 84-88 24441193-3 2013 The present study evaluated the expression of TGFbeta, Smad3, alphavbeta6 integrin, mTOR and PPARgamma in 2,4,6-trinitrobenzenesulphonic acid (TNBS)-induced colorectal fibrosis in Smad3 wild-type (WT) and null mice. Trinitrobenzenesulfonic Acid 143-147 peroxisome proliferator activated receptor gamma Mus musculus 93-102 24441193-3 2013 The present study evaluated the expression of TGFbeta, Smad3, alphavbeta6 integrin, mTOR and PPARgamma in 2,4,6-trinitrobenzenesulphonic acid (TNBS)-induced colorectal fibrosis in Smad3 wild-type (WT) and null mice. Trinitrobenzenesulfonic Acid 143-147 SMAD family member 3 Mus musculus 180-185 24441193-4 2013 Smad3 WT mice treated with TNBS developed a marked colorectal fibrosis and showed a concomitant up-regulation of TGFbeta, Smad3, alphavbeta6 and mTOR and a reduction of PPARgamma expression. Trinitrobenzenesulfonic Acid 27-31 SMAD family member 3 Mus musculus 0-5 24441193-4 2013 Smad3 WT mice treated with TNBS developed a marked colorectal fibrosis and showed a concomitant up-regulation of TGFbeta, Smad3, alphavbeta6 and mTOR and a reduction of PPARgamma expression. Trinitrobenzenesulfonic Acid 27-31 transforming growth factor, beta 1 Mus musculus 113-120 24441193-4 2013 Smad3 WT mice treated with TNBS developed a marked colorectal fibrosis and showed a concomitant up-regulation of TGFbeta, Smad3, alphavbeta6 and mTOR and a reduction of PPARgamma expression. Trinitrobenzenesulfonic Acid 27-31 SMAD family member 3 Mus musculus 122-127 24441193-4 2013 Smad3 WT mice treated with TNBS developed a marked colorectal fibrosis and showed a concomitant up-regulation of TGFbeta, Smad3, alphavbeta6 and mTOR and a reduction of PPARgamma expression. Trinitrobenzenesulfonic Acid 27-31 mechanistic target of rapamycin kinase Mus musculus 145-149 24441193-4 2013 Smad3 WT mice treated with TNBS developed a marked colorectal fibrosis and showed a concomitant up-regulation of TGFbeta, Smad3, alphavbeta6 and mTOR and a reduction of PPARgamma expression. Trinitrobenzenesulfonic Acid 27-31 peroxisome proliferator activated receptor gamma Mus musculus 169-178 24441193-5 2013 On the other hand, Smad3 Null mice similarly treated with TNBS did not develop fibrosis and showed a very low or even absent expression of TGFbeta, Smad3, alphavbeta6 and mTOR and a marked over-expression of PPARgamma. Trinitrobenzenesulfonic Acid 58-62 SMAD family member 3 Mus musculus 19-24 24441193-5 2013 On the other hand, Smad3 Null mice similarly treated with TNBS did not develop fibrosis and showed a very low or even absent expression of TGFbeta, Smad3, alphavbeta6 and mTOR and a marked over-expression of PPARgamma. Trinitrobenzenesulfonic Acid 58-62 transforming growth factor, beta 1 Mus musculus 139-146 24441193-5 2013 On the other hand, Smad3 Null mice similarly treated with TNBS did not develop fibrosis and showed a very low or even absent expression of TGFbeta, Smad3, alphavbeta6 and mTOR and a marked over-expression of PPARgamma. Trinitrobenzenesulfonic Acid 58-62 SMAD family member 3 Mus musculus 148-153 24441193-5 2013 On the other hand, Smad3 Null mice similarly treated with TNBS did not develop fibrosis and showed a very low or even absent expression of TGFbeta, Smad3, alphavbeta6 and mTOR and a marked over-expression of PPARgamma. Trinitrobenzenesulfonic Acid 58-62 mechanistic target of rapamycin kinase Mus musculus 171-175 24441193-5 2013 On the other hand, Smad3 Null mice similarly treated with TNBS did not develop fibrosis and showed a very low or even absent expression of TGFbeta, Smad3, alphavbeta6 and mTOR and a marked over-expression of PPARgamma. Trinitrobenzenesulfonic Acid 58-62 peroxisome proliferator activated receptor gamma Mus musculus 208-217 24441193-6 2013 At the same time the expression of alpha-smooth muscle actin (a marker of activated myofibroblasts), collagen I-III and connective tissue growth factor (a downstream effector of TGFbeta/Smad3-induced extracellular matrix proteins) were up-regulated in Smad3 WT mice treated with TNBS compared to Null TNBS-treated mice. Trinitrobenzenesulfonic Acid 279-283 transforming growth factor, beta 1 Mus musculus 178-185 24441193-6 2013 At the same time the expression of alpha-smooth muscle actin (a marker of activated myofibroblasts), collagen I-III and connective tissue growth factor (a downstream effector of TGFbeta/Smad3-induced extracellular matrix proteins) were up-regulated in Smad3 WT mice treated with TNBS compared to Null TNBS-treated mice. Trinitrobenzenesulfonic Acid 279-283 SMAD family member 3 Mus musculus 186-191 24441193-6 2013 At the same time the expression of alpha-smooth muscle actin (a marker of activated myofibroblasts), collagen I-III and connective tissue growth factor (a downstream effector of TGFbeta/Smad3-induced extracellular matrix proteins) were up-regulated in Smad3 WT mice treated with TNBS compared to Null TNBS-treated mice. Trinitrobenzenesulfonic Acid 301-305 transforming growth factor, beta 1 Mus musculus 178-185 24441193-6 2013 At the same time the expression of alpha-smooth muscle actin (a marker of activated myofibroblasts), collagen I-III and connective tissue growth factor (a downstream effector of TGFbeta/Smad3-induced extracellular matrix proteins) were up-regulated in Smad3 WT mice treated with TNBS compared to Null TNBS-treated mice. Trinitrobenzenesulfonic Acid 301-305 SMAD family member 3 Mus musculus 186-191 23794034-3 2013 The aim of the present study is to determine the changes in the expression of calponin, caldesmon, tropomyosin, and smoothelin in colonic smooth muscle from trinitrobenzene sulphonic acid (TNBS)- and dextran sodium sulphate (DSS)-induced colitis in mice. Trinitrobenzenesulfonic Acid 189-193 smoothelin Mus musculus 116-126 23772040-7 2013 Finally, IL-10(+)CD8(+) T cells played a protective role in the TNBS-induced murine colitis model, indicating a critical role of this population of CD8(+) T cells in regulatory immune responses. Trinitrobenzenesulfonic Acid 64-68 interleukin 10 Mus musculus 9-14 23786412-0 2013 Recovery from TNBS-induced colitis leads to the resistance to recurrent colitis and an increased ratio of FOXP3 to CD3 mRNA. Trinitrobenzenesulfonic Acid 14-18 forkhead box P3 Mus musculus 106-111 23786412-0 2013 Recovery from TNBS-induced colitis leads to the resistance to recurrent colitis and an increased ratio of FOXP3 to CD3 mRNA. Trinitrobenzenesulfonic Acid 14-18 CD3 antigen, epsilon polypeptide Mus musculus 115-118 23786412-11 2013 CONCLUSIONS: Mice that recovered from TNBS-induced acute colitis with intestinal epithelial disruption are resistant to recurrent colitis, which is associated with an increased ratio of FOXP3 to CD3 mRNA expression. Trinitrobenzenesulfonic Acid 38-42 forkhead box P3 Mus musculus 186-191 23786412-11 2013 CONCLUSIONS: Mice that recovered from TNBS-induced acute colitis with intestinal epithelial disruption are resistant to recurrent colitis, which is associated with an increased ratio of FOXP3 to CD3 mRNA expression. Trinitrobenzenesulfonic Acid 38-42 CD3 antigen, epsilon polypeptide Mus musculus 195-198 23819906-0 2013 Antifibrotic role of chemokine CXCL9 in experimental chronic pancreatitis induced by trinitrobenzene sulfonic acid in rats. Trinitrobenzenesulfonic Acid 85-114 C-X-C motif chemokine ligand 9 Rattus norvegicus 31-36 24062413-6 2013 Notably, recovery of IELs by adoptive transfer could reduce the susceptibility of Nod2(-/-) mice to the 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis. Trinitrobenzenesulfonic Acid 104-139 nucleotide-binding oligomerization domain containing 2 Mus musculus 82-86 24062413-6 2013 Notably, recovery of IELs by adoptive transfer could reduce the susceptibility of Nod2(-/-) mice to the 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis. Trinitrobenzenesulfonic Acid 141-145 nucleotide-binding oligomerization domain containing 2 Mus musculus 82-86 23819906-7 2013 Chronic pancreatic injury in rats was induced after TNBS treatment and CXCL9 protein was markedly upregulated during TNBS-induced chronic pancreatitis. Trinitrobenzenesulfonic Acid 117-121 C-X-C motif chemokine ligand 9 Rattus norvegicus 71-76 23819906-8 2013 Although parenchymal injury in the pancreas was not obviously affected after rCXCL9 and neutralizing antibody administration, rCXCL9 could attenuate fibrogenesis in TNBS-induced chronic pancreatitis in vivo and exerted antifibrotic effects in vitro, suppressing collagen production in activated PSCs. Trinitrobenzenesulfonic Acid 165-169 C-X-C motif chemokine ligand 9 Rattus norvegicus 126-132 23742179-8 2013 Treatment with TNBS caused colon shortening; increased myeloperoxidase activity; and increased IL-1beta, IL-6 and TNF-alpha expression in mice. Trinitrobenzenesulfonic Acid 15-19 interleukin 1 beta Mus musculus 95-103 24066068-10 2013 Our findings suggest that sinomenine has anti-inflammatory effects on TNBS-induced colitis by down-regulating the levels of miR-155 and several related inflammatory cytokines. Trinitrobenzenesulfonic Acid 70-74 microRNA 155 Mus musculus 124-131 24142717-2 2013 This study aimed to investigate the impact of probiotics (Lactobacillus, Bifidobacterium) on the expression of TLR4 and tumor necrosis factor-alpha (TNF-alpha) in the colon mucosa of rat experimental ulcerative colitis model induced by trinitrobenzene sulfonic acid (TNBS)/ethanol and immune complexes. Trinitrobenzenesulfonic Acid 236-265 toll-like receptor 4 Rattus norvegicus 111-115 24142717-2 2013 This study aimed to investigate the impact of probiotics (Lactobacillus, Bifidobacterium) on the expression of TLR4 and tumor necrosis factor-alpha (TNF-alpha) in the colon mucosa of rat experimental ulcerative colitis model induced by trinitrobenzene sulfonic acid (TNBS)/ethanol and immune complexes. Trinitrobenzenesulfonic Acid 236-265 tumor necrosis factor Rattus norvegicus 149-158 23956437-4 2013 In this study, we investigated the role of IDO in 2,4,6-trinitrobenzene sulfate (TNBS)-induced colitis in mice by gene deletion and pharmacological inhibition. Trinitrobenzenesulfonic Acid 81-85 indoleamine 2,3-dioxygenase 1 Mus musculus 43-46 23956437-5 2013 TNBS treatment induced significantly more severe colitis in Ido1 gene-deficient (Ido1-/-) mice than in Ido1 wild-type (Ido1+/+) mice, indicating a role for IDO1 in suppression of acute colitis. Trinitrobenzenesulfonic Acid 0-4 indoleamine 2,3-dioxygenase 1 Mus musculus 60-64 23956437-5 2013 TNBS treatment induced significantly more severe colitis in Ido1 gene-deficient (Ido1-/-) mice than in Ido1 wild-type (Ido1+/+) mice, indicating a role for IDO1 in suppression of acute colitis. Trinitrobenzenesulfonic Acid 0-4 indoleamine 2,3-dioxygenase 1 Mus musculus 81-85 23956437-5 2013 TNBS treatment induced significantly more severe colitis in Ido1 gene-deficient (Ido1-/-) mice than in Ido1 wild-type (Ido1+/+) mice, indicating a role for IDO1 in suppression of acute colitis. Trinitrobenzenesulfonic Acid 0-4 indoleamine 2,3-dioxygenase 1 Mus musculus 81-85 23956437-5 2013 TNBS treatment induced significantly more severe colitis in Ido1 gene-deficient (Ido1-/-) mice than in Ido1 wild-type (Ido1+/+) mice, indicating a role for IDO1 in suppression of acute colitis. Trinitrobenzenesulfonic Acid 0-4 indoleamine 2,3-dioxygenase 1 Mus musculus 81-85 23956437-5 2013 TNBS treatment induced significantly more severe colitis in Ido1 gene-deficient (Ido1-/-) mice than in Ido1 wild-type (Ido1+/+) mice, indicating a role for IDO1 in suppression of acute colitis. Trinitrobenzenesulfonic Acid 0-4 indoleamine 2,3-dioxygenase 1 Mus musculus 156-160 23956437-6 2013 Consistent with this, the expression of Ido1 was increased in the colonic interstitial tissues of TNBS-treated Ido1+/+ mice. Trinitrobenzenesulfonic Acid 98-102 indoleamine 2,3-dioxygenase 1 Mus musculus 40-44 23956437-6 2013 Consistent with this, the expression of Ido1 was increased in the colonic interstitial tissues of TNBS-treated Ido1+/+ mice. Trinitrobenzenesulfonic Acid 98-102 indoleamine 2,3-dioxygenase 1 Mus musculus 111-115 23747339-10 2013 The effects of cytokines on TRPV5 were not observed in cells stably transfected with membrane-bound Klotho; TRPV5 expression was preserved when colitis was induced with TNBS in transgenic mice that overexpressed Klotho or in mice with T-cell transfer colitis injected with soluble recombinant Klotho. Trinitrobenzenesulfonic Acid 169-173 transient receptor potential cation channel, subfamily V, member 5 Mus musculus 108-113 23747339-11 2013 CONCLUSIONS: After induction of colitis in mice via TNBS administration or T-cell transfer, tumor necrosis factor and interferon-gamma reduced the expression and activity of Klotho, which otherwise would protect TRPV5 from hypersialylation and cytokine-induced TRPV5 endocytosis, UBR4-dependent ubiquitination, degradation, and urinary wasting of Ca(2+). Trinitrobenzenesulfonic Acid 52-56 interferon gamma Mus musculus 118-134 23747339-11 2013 CONCLUSIONS: After induction of colitis in mice via TNBS administration or T-cell transfer, tumor necrosis factor and interferon-gamma reduced the expression and activity of Klotho, which otherwise would protect TRPV5 from hypersialylation and cytokine-induced TRPV5 endocytosis, UBR4-dependent ubiquitination, degradation, and urinary wasting of Ca(2+). Trinitrobenzenesulfonic Acid 52-56 klotho Mus musculus 174-180 23742179-11 2013 Lactobacillus brevis G-101 inhibited TNBS-induced IRAK-1 phosphorylation and NF-kappaB activation, as well as the expression of COX-2 and iNOS. Trinitrobenzenesulfonic Acid 37-41 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 77-86 23742179-8 2013 Treatment with TNBS caused colon shortening; increased myeloperoxidase activity; and increased IL-1beta, IL-6 and TNF-alpha expression in mice. Trinitrobenzenesulfonic Acid 15-19 interleukin 6 Mus musculus 105-109 23742179-8 2013 Treatment with TNBS caused colon shortening; increased myeloperoxidase activity; and increased IL-1beta, IL-6 and TNF-alpha expression in mice. Trinitrobenzenesulfonic Acid 15-19 tumor necrosis factor Mus musculus 114-123 23945234-5 2013 In experimental colitis models induced by 2,4,6-trinitrobenzenesulfonic acid, dextran sulfate sodium, or CD4(+)CD45RB(hi) T cell transfer, transgenic mice expressing hVDR in IECs were highly resistant to colitis, as manifested by marked reductions in clinical colitis scores, colonic histological damage, and colonic inflammation compared with WT mice. Trinitrobenzenesulfonic Acid 42-76 vitamin D receptor Homo sapiens 166-170 23188093-12 2013 TNBS treatment induced TNF-alpha expression, and AGO administration suppressed induction. Trinitrobenzenesulfonic Acid 0-4 tumor necrosis factor Mus musculus 23-32 23748116-6 2013 In a rat model of trinitrobenzene sulfonic acid (TNBS)-induced visceral hypersensitivity, orally administered uroguanylin increased colonic thresholds required to elicit abdominal contractions in response to colorectal distension (CRD). Trinitrobenzenesulfonic Acid 18-47 guanylate cyclase activator 2B Rattus norvegicus 110-121 23748116-6 2013 In a rat model of trinitrobenzene sulfonic acid (TNBS)-induced visceral hypersensitivity, orally administered uroguanylin increased colonic thresholds required to elicit abdominal contractions in response to colorectal distension (CRD). Trinitrobenzenesulfonic Acid 49-53 guanylate cyclase activator 2B Rattus norvegicus 110-121 23748116-7 2013 Oral administration of cGMP mimicked the antihyperalgesic effects of uroguanylin, significantly decreasing TNBS- and restraint stress-induced visceromotor response to graded CRD in rats. Trinitrobenzenesulfonic Acid 107-111 guanylate cyclase activator 2B Rattus norvegicus 69-80 23679814-5 2013 MALDI-TOF analysis revealed that heat-shock protein 70 (HSP70) was one of the carbonylated proteins induced by TNBS. Trinitrobenzenesulfonic Acid 111-115 heat shock protein 1B Mus musculus 33-54 23679814-5 2013 MALDI-TOF analysis revealed that heat-shock protein 70 (HSP70) was one of the carbonylated proteins induced by TNBS. Trinitrobenzenesulfonic Acid 111-115 heat shock protein 1B Mus musculus 56-61 23679814-6 2013 To verify the role of HSP70 in TNBS-treated XS106 cell, we fused protein transduction domain (PTD) with HSP70 to facilitate protein delivery into the cell. Trinitrobenzenesulfonic Acid 31-35 heat shock protein 1B Mus musculus 22-27 23188093-16 2013 CONCLUSIONS: We infer that AGO administration inhibits TNBS-induced colitis in mice through HO-1 induction in macrophages. Trinitrobenzenesulfonic Acid 55-59 heme oxygenase 1 Mus musculus 92-96 23665276-7 2013 RESULTS: GPR41(-/-) and GPR43(-/-) mice had reduced inflammatory responses after administration of ethanol or TNBS compared with control mice, and had a slower immune response against C rodentium infection, clearing the bacteria more slowly. Trinitrobenzenesulfonic Acid 110-114 free fatty acid receptor 3 Mus musculus 9-14 23665276-7 2013 RESULTS: GPR41(-/-) and GPR43(-/-) mice had reduced inflammatory responses after administration of ethanol or TNBS compared with control mice, and had a slower immune response against C rodentium infection, clearing the bacteria more slowly. Trinitrobenzenesulfonic Acid 110-114 free fatty acid receptor 2 Mus musculus 24-29 23558009-5 2013 We induced CP by injecting the chemical agent trinitrobenzene sulfonic acid (TNBS), which causes severe acute pancreatitis, into the pancreatic duct of C57BL/6 trpa1(+/+) and trpa1(-/-) mice. Trinitrobenzenesulfonic Acid 46-75 transient receptor potential cation channel, subfamily A, member 1 Mus musculus 160-165 24101390-0 2013 A study comparing the efficacy of antimicrobial agents versus enzyme (P-gp) inducers in the treatment of 2,4,6 trinitrobenzenesulfonic acid-induced colitis in rats. Trinitrobenzenesulfonic Acid 105-139 ATP-binding cassette, subfamily B (MDR/TAP), member 1B Rattus norvegicus 70-74 23772025-3 2013 Trinitrobenzene sulfonic acid-induced colitis was attenuated by the administration of PON-1. Trinitrobenzenesulfonic Acid 0-29 paraoxonase 1 Homo sapiens 86-91 23558009-5 2013 We induced CP by injecting the chemical agent trinitrobenzene sulfonic acid (TNBS), which causes severe acute pancreatitis, into the pancreatic duct of C57BL/6 trpa1(+/+) and trpa1(-/-) mice. Trinitrobenzenesulfonic Acid 77-81 transient receptor potential cation channel, subfamily A, member 1 Mus musculus 160-165 23602915-0 2013 Brazilian propolis ameliorates trinitrobenzene sulfonic acid-induced colitis in mice by inhibiting Th1 differentiation. Trinitrobenzenesulfonic Acid 31-60 negative elongation factor complex member C/D, Th1l Mus musculus 99-102 23352442-4 2013 CL BuOH extract also inhibited colon shortening and myeloperoxidase activity in TNBS-induced colitic mice. Trinitrobenzenesulfonic Acid 80-84 myeloperoxidase Mus musculus 52-67 22814364-8 2013 RESULTS: TNBS increased the expression of T-cell immunoglobulin and mucin domain-4 and CD80 and decreased the levels of interleukin-12 in dendritic cells. Trinitrobenzenesulfonic Acid 9-13 CD80 antigen Mus musculus 87-91 22814364-9 2013 Higher serum levels of OVA-specific immunoglobulin E, histamine expression and skewed antigen-specific Th2 polarization in the intestinal tissue were detected in mice sensitized with TNBS + OVA as compared with those treated with either OVA or TNBS alone. Trinitrobenzenesulfonic Acid 183-187 serine (or cysteine) peptidase inhibitor, clade B, member 1, pseudogene Mus musculus 23-26 22814364-9 2013 Higher serum levels of OVA-specific immunoglobulin E, histamine expression and skewed antigen-specific Th2 polarization in the intestinal tissue were detected in mice sensitized with TNBS + OVA as compared with those treated with either OVA or TNBS alone. Trinitrobenzenesulfonic Acid 183-187 serine (or cysteine) peptidase inhibitor, clade B, member 1, pseudogene Mus musculus 190-193 22814364-9 2013 Higher serum levels of OVA-specific immunoglobulin E, histamine expression and skewed antigen-specific Th2 polarization in the intestinal tissue were detected in mice sensitized with TNBS + OVA as compared with those treated with either OVA or TNBS alone. Trinitrobenzenesulfonic Acid 183-187 serine (or cysteine) peptidase inhibitor, clade B, member 1, pseudogene Mus musculus 190-193 22814364-9 2013 Higher serum levels of OVA-specific immunoglobulin E, histamine expression and skewed antigen-specific Th2 polarization in the intestinal tissue were detected in mice sensitized with TNBS + OVA as compared with those treated with either OVA or TNBS alone. Trinitrobenzenesulfonic Acid 244-248 serine (or cysteine) peptidase inhibitor, clade B, member 1, pseudogene Mus musculus 23-26 22814364-9 2013 Higher serum levels of OVA-specific immunoglobulin E, histamine expression and skewed antigen-specific Th2 polarization in the intestinal tissue were detected in mice sensitized with TNBS + OVA as compared with those treated with either OVA or TNBS alone. Trinitrobenzenesulfonic Acid 244-248 serine (or cysteine) peptidase inhibitor, clade B, member 1, pseudogene Mus musculus 190-193 22814364-9 2013 Higher serum levels of OVA-specific immunoglobulin E, histamine expression and skewed antigen-specific Th2 polarization in the intestinal tissue were detected in mice sensitized with TNBS + OVA as compared with those treated with either OVA or TNBS alone. Trinitrobenzenesulfonic Acid 244-248 serine (or cysteine) peptidase inhibitor, clade B, member 1, pseudogene Mus musculus 190-193 22814364-10 2013 In addition, the TNBS-OVA-treated mice also showed an increased number of inflammatory cells, high levels of interleukin-4 and a decreased expression of interferon-gamma in the lamina propria mononuclear cells. Trinitrobenzenesulfonic Acid 17-21 serine (or cysteine) peptidase inhibitor, clade B, member 1, pseudogene Mus musculus 22-25 22814364-10 2013 In addition, the TNBS-OVA-treated mice also showed an increased number of inflammatory cells, high levels of interleukin-4 and a decreased expression of interferon-gamma in the lamina propria mononuclear cells. Trinitrobenzenesulfonic Acid 17-21 interleukin 4 Mus musculus 109-122 22814364-10 2013 In addition, the TNBS-OVA-treated mice also showed an increased number of inflammatory cells, high levels of interleukin-4 and a decreased expression of interferon-gamma in the lamina propria mononuclear cells. Trinitrobenzenesulfonic Acid 17-21 interferon gamma Mus musculus 153-169 23282580-3 2013 In this study, we assess the effects of genetic knockout of PI3Kgamma on the induction and resolution of colitis induced by the hapten trinitrobenzene sulfonic acid (TNBS). Trinitrobenzenesulfonic Acid 135-164 phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit gamma Mus musculus 60-69 23282580-3 2013 In this study, we assess the effects of genetic knockout of PI3Kgamma on the induction and resolution of colitis induced by the hapten trinitrobenzene sulfonic acid (TNBS). Trinitrobenzenesulfonic Acid 166-170 phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit gamma Mus musculus 60-69 23282580-7 2013 However, PI3Kgamma-/- mice have difficulty resolving acute inflammation because they failed to restore lost weight and had significantly elevated histologic damage scores and tissue myeloperoxidase levels at days 7 and 14 after TNBS administration compared with wild-type controls. Trinitrobenzenesulfonic Acid 228-232 phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit gamma Mus musculus 9-18 23375938-9 2013 Arctigenin also inhibited colon shortening, macroscopic scores and myeloperoxidase activity in TNBS-induced colitic mice. Trinitrobenzenesulfonic Acid 95-99 myeloperoxidase Mus musculus 67-82 23375938-10 2013 Arctigenin inhibited TNBS-induced IL-1beta, TNF-alpha and IL-6 expression, as well as PI3K, AKT and IKKbeta phosphorylation and NF-kappaB activation in mice, but increased IL-10 and CD204 expression. Trinitrobenzenesulfonic Acid 21-25 interleukin 1 beta Mus musculus 34-42 23375938-10 2013 Arctigenin inhibited TNBS-induced IL-1beta, TNF-alpha and IL-6 expression, as well as PI3K, AKT and IKKbeta phosphorylation and NF-kappaB activation in mice, but increased IL-10 and CD204 expression. Trinitrobenzenesulfonic Acid 21-25 tumor necrosis factor Mus musculus 44-53 23375938-10 2013 Arctigenin inhibited TNBS-induced IL-1beta, TNF-alpha and IL-6 expression, as well as PI3K, AKT and IKKbeta phosphorylation and NF-kappaB activation in mice, but increased IL-10 and CD204 expression. Trinitrobenzenesulfonic Acid 21-25 interleukin 6 Mus musculus 58-62 23375938-10 2013 Arctigenin inhibited TNBS-induced IL-1beta, TNF-alpha and IL-6 expression, as well as PI3K, AKT and IKKbeta phosphorylation and NF-kappaB activation in mice, but increased IL-10 and CD204 expression. Trinitrobenzenesulfonic Acid 21-25 interleukin 10 Mus musculus 172-177 23275612-6 2013 Using quantitative real-time PCR, we demonstrated that expression of Kir6.1, SUR2B, and inducible NO synthase (iNOS) mRNAs was significantly upregulated in TNBS-treated animals. Trinitrobenzenesulfonic Acid 156-160 nitric oxide synthase, inducible Cavia porcellus 88-109 23275612-6 2013 Using quantitative real-time PCR, we demonstrated that expression of Kir6.1, SUR2B, and inducible NO synthase (iNOS) mRNAs was significantly upregulated in TNBS-treated animals. Trinitrobenzenesulfonic Acid 156-160 nitric oxide synthase, inducible Cavia porcellus 111-115 23446334-10 2013 RESULTS: TNBS-induced colitis was inhibited in Bach1-deficient mice. Trinitrobenzenesulfonic Acid 9-13 BTB and CNC homology 1, basic leucine zipper transcription factor 1 Mus musculus 47-52 23446334-11 2013 TNBS administration increased the expression of HO-1 messenger RNA and protein in colonic mucosa in Bach1-deficient mice. Trinitrobenzenesulfonic Acid 0-4 heme oxygenase 1 Mus musculus 48-52 23434856-7 2013 Enhanced colonic mucosal injury, inflammatory response and oxidative stress were observed in the animals clystered with TNBS, which was manifested as the significant increase in colon mucosal damage index, MPO activity, levels of MDA, NO and PGE2, as well as the expressions of iNOS, COX-2 and NF-kappaB p65 proteins in the colonic mucosa, and the significant decrease in expressions of IkappaBalpha proteins in the colonic mucosa. Trinitrobenzenesulfonic Acid 120-124 myeloperoxidase Rattus norvegicus 206-209 23434856-7 2013 Enhanced colonic mucosal injury, inflammatory response and oxidative stress were observed in the animals clystered with TNBS, which was manifested as the significant increase in colon mucosal damage index, MPO activity, levels of MDA, NO and PGE2, as well as the expressions of iNOS, COX-2 and NF-kappaB p65 proteins in the colonic mucosa, and the significant decrease in expressions of IkappaBalpha proteins in the colonic mucosa. Trinitrobenzenesulfonic Acid 120-124 nitric oxide synthase 2 Rattus norvegicus 278-282 23434856-7 2013 Enhanced colonic mucosal injury, inflammatory response and oxidative stress were observed in the animals clystered with TNBS, which was manifested as the significant increase in colon mucosal damage index, MPO activity, levels of MDA, NO and PGE2, as well as the expressions of iNOS, COX-2 and NF-kappaB p65 proteins in the colonic mucosa, and the significant decrease in expressions of IkappaBalpha proteins in the colonic mucosa. Trinitrobenzenesulfonic Acid 120-124 NFKB inhibitor alpha Rattus norvegicus 387-399 24348533-3 2013 We previously reported that a traditional Japanese medicine, daikenchuto (TU-100), ameliorated a trinitrobenzenesulfonic acid- (TNBS-) induced type-1 model colitis exhibiting histopathological features of CD through adrenomedullin (ADM) enhancement. Trinitrobenzenesulfonic Acid 97-125 adrenomedullin Mus musculus 216-230 23305398-11 2013 TRPV1-/- mice demonstrated blunted effects of TNBS-induced colitis on expression and function of voltage-gated sodium channels in bladder sensory neurons, and delayed development of abdominal hypersensitivity upon colon-bladder cross-talk in genetically modified animals. Trinitrobenzenesulfonic Acid 46-50 transient receptor potential cation channel, subfamily V, member 1 Mus musculus 0-5 23291633-0 2013 Disturbance of hepatic and intestinal UDP-glucuronosyltransferase in rats with trinitrobenzene sulfonic acid-induced colitis. Trinitrobenzenesulfonic Acid 79-108 UDP glycosyltransferase 2 family, polypeptide B Rattus norvegicus 38-65 23840258-7 2013 TNBS decreased occludin, RhoA, and ROCK-I, while increasing Rac-1, PAK-1, and phosphorylated myosin light chain. Trinitrobenzenesulfonic Acid 0-4 occludin Rattus norvegicus 15-23 23840258-7 2013 TNBS decreased occludin, RhoA, and ROCK-I, while increasing Rac-1, PAK-1, and phosphorylated myosin light chain. Trinitrobenzenesulfonic Acid 0-4 ras homolog family member A Rattus norvegicus 25-29 23840258-7 2013 TNBS decreased occludin, RhoA, and ROCK-I, while increasing Rac-1, PAK-1, and phosphorylated myosin light chain. Trinitrobenzenesulfonic Acid 0-4 Rho-associated coiled-coil containing protein kinase 1 Rattus norvegicus 35-41 23840258-7 2013 TNBS decreased occludin, RhoA, and ROCK-I, while increasing Rac-1, PAK-1, and phosphorylated myosin light chain. Trinitrobenzenesulfonic Acid 0-4 Rac family small GTPase 1 Rattus norvegicus 60-65 23840258-7 2013 TNBS decreased occludin, RhoA, and ROCK-I, while increasing Rac-1, PAK-1, and phosphorylated myosin light chain. Trinitrobenzenesulfonic Acid 0-4 p21 (RAC1) activated kinase 1 Rattus norvegicus 67-72 23840258-8 2013 In addition, ATP content and ATP5D expression in colonic mucosa decreased after TNBS challenge. Trinitrobenzenesulfonic Acid 80-84 ATP synthase F1 subunit delta Rattus norvegicus 29-34 22819866-10 2012 TIMP-3-KO mice developed severe colitis after administration of TNBS, whereas TIMP-3-Tg mice were resistant to TNBS-induced colitis. Trinitrobenzenesulfonic Acid 64-68 tissue inhibitor of metalloproteinase 3 Mus musculus 0-6 23250811-0 2013 Curcumin improves TNBS-induced colitis in rats by inhibiting IL-27 expression via the TLR4/NF-kappaB signaling pathway. Trinitrobenzenesulfonic Acid 18-22 interleukin 27 Rattus norvegicus 61-66 23250811-0 2013 Curcumin improves TNBS-induced colitis in rats by inhibiting IL-27 expression via the TLR4/NF-kappaB signaling pathway. Trinitrobenzenesulfonic Acid 18-22 toll-like receptor 4 Rattus norvegicus 86-90 23027085-5 2012 The Th17 cytokine, IL-17, and the Th1 cytokine, IFN-gamma, were expressed at high levels in the TNBS-induced colitic mice. Trinitrobenzenesulfonic Acid 96-100 interleukin 17A Mus musculus 19-24 23027085-5 2012 The Th17 cytokine, IL-17, and the Th1 cytokine, IFN-gamma, were expressed at high levels in the TNBS-induced colitic mice. Trinitrobenzenesulfonic Acid 96-100 negative elongation factor complex member C/D, Th1l Mus musculus 4-7 23027085-5 2012 The Th17 cytokine, IL-17, and the Th1 cytokine, IFN-gamma, were expressed at high levels in the TNBS-induced colitic mice. Trinitrobenzenesulfonic Acid 96-100 interferon gamma Mus musculus 48-57 23027085-9 2012 In conclusion, Th17 and Th1 cells are involved in TNBS-induced IBD and the effect of the Th17 cells may be mediated through the induction of the secretion of pro-inflammatory cytokines. Trinitrobenzenesulfonic Acid 50-54 negative elongation factor complex member C/D, Th1l Mus musculus 15-18 23171464-2 2012 Previously, we revealed the reactive oxygen species generation by 2, 4, 6-trinitrobenzene sulphonic acid (TNBS) in vivo, followed by heat shock protein 70 (Hsp70) carbonylation and the exogenous antioxidant role of cell-permeable Hsp70. Trinitrobenzenesulfonic Acid 106-110 heat shock protein 1B Mus musculus 230-235 23030668-1 2012 Colonic administration of 2,4,6-trinitrobenzene sulfonic acid (TNBS) induced acute colitis in mice and elicited a Th1 immune response. Trinitrobenzenesulfonic Acid 26-61 negative elongation factor complex member C/D, Th1l Mus musculus 114-117 23030668-1 2012 Colonic administration of 2,4,6-trinitrobenzene sulfonic acid (TNBS) induced acute colitis in mice and elicited a Th1 immune response. Trinitrobenzenesulfonic Acid 63-67 negative elongation factor complex member C/D, Th1l Mus musculus 114-117 23030668-4 2012 We assessed the inflammation scores of TNBS-induced acute colitis in wild-type (WT), IL-17 knockout (KO), and IFN-gamma KO mice and measured the levels of inflammatory cytokines using real-time PCR and ELISAs. Trinitrobenzenesulfonic Acid 39-43 interleukin 17A Mus musculus 85-90 23030668-6 2012 Intraperitoneal injection of anti-IL-17 monoclonal antibody confirmed a specific role for IL-17 in TNBS-induced acute colitis in the 3 strains of mice. Trinitrobenzenesulfonic Acid 99-103 interleukin 17A Mus musculus 34-39 23030668-6 2012 Intraperitoneal injection of anti-IL-17 monoclonal antibody confirmed a specific role for IL-17 in TNBS-induced acute colitis in the 3 strains of mice. Trinitrobenzenesulfonic Acid 99-103 interleukin 17A Mus musculus 90-95 22942432-5 2012 The interaction of tyrosine phosphorylated SHP-2 (pY-SHP-2) with cytosolic STAT1 prevented the recruitment of STAT1 to IFN-gammaR and specifically inhibited STAT1 signaling, resulting in a reduction in Th1 cytokine production and an improvement in 2, 4, 6-trinitrobenzene sulfonic acid-induced colitis in mice. Trinitrobenzenesulfonic Acid 248-285 protein tyrosine phosphatase, non-receptor type 11 Mus musculus 43-48 22882778-3 2012 Furthermore, selective blockade of TRPV4 in the 2,4,6-trinitrobenzenesulfonic acid animal model alleviates colitis and pain associated with the intestinal inflammation. Trinitrobenzenesulfonic Acid 48-82 transient receptor potential cation channel subfamily V member 4 Homo sapiens 35-40 23092159-14 2012 Western blot analysis showed that compared with that of naive group, phosphorylated NR1 (pNR1) and pNR2B in TNBS rats were significantly increased in the spinal cord (pNR1: 3.87+-0.31 folds of naive control, pNR2B: 4.17 +- 0.24 folds of naive control). Trinitrobenzenesulfonic Acid 108-112 glutamate ionotropic receptor NMDA type subunit 1 Rattus norvegicus 84-87 22942432-5 2012 The interaction of tyrosine phosphorylated SHP-2 (pY-SHP-2) with cytosolic STAT1 prevented the recruitment of STAT1 to IFN-gammaR and specifically inhibited STAT1 signaling, resulting in a reduction in Th1 cytokine production and an improvement in 2, 4, 6-trinitrobenzene sulfonic acid-induced colitis in mice. Trinitrobenzenesulfonic Acid 248-285 protein tyrosine phosphatase, non-receptor type 11 Mus musculus 53-58 22942432-5 2012 The interaction of tyrosine phosphorylated SHP-2 (pY-SHP-2) with cytosolic STAT1 prevented the recruitment of STAT1 to IFN-gammaR and specifically inhibited STAT1 signaling, resulting in a reduction in Th1 cytokine production and an improvement in 2, 4, 6-trinitrobenzene sulfonic acid-induced colitis in mice. Trinitrobenzenesulfonic Acid 248-285 signal transducer and activator of transcription 1 Mus musculus 75-80 22942432-5 2012 The interaction of tyrosine phosphorylated SHP-2 (pY-SHP-2) with cytosolic STAT1 prevented the recruitment of STAT1 to IFN-gammaR and specifically inhibited STAT1 signaling, resulting in a reduction in Th1 cytokine production and an improvement in 2, 4, 6-trinitrobenzene sulfonic acid-induced colitis in mice. Trinitrobenzenesulfonic Acid 248-285 signal transducer and activator of transcription 1 Mus musculus 110-115 22942432-5 2012 The interaction of tyrosine phosphorylated SHP-2 (pY-SHP-2) with cytosolic STAT1 prevented the recruitment of STAT1 to IFN-gammaR and specifically inhibited STAT1 signaling, resulting in a reduction in Th1 cytokine production and an improvement in 2, 4, 6-trinitrobenzene sulfonic acid-induced colitis in mice. Trinitrobenzenesulfonic Acid 248-285 signal transducer and activator of transcription 1 Mus musculus 110-115 22776248-0 2012 Antioxidant sulforaphane and sensitizer trinitrobenzene sulfonate induce carboxylesterase-1 through a novel element transactivated by nuclear factor-E2 related factor-2. Trinitrobenzenesulfonic Acid 40-65 carboxylesterase 1 Homo sapiens 73-91 22849695-12 2012 Ginsenoside Re (20 mg/kg) inhibited the activation of NF-kappaB in TNBS-treated mice. Trinitrobenzenesulfonic Acid 67-71 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 54-63 22776248-4 2012 The aims of this study were to determine whether antioxidant sulforaphane (SFN) and sensitizer trinitrobenzene sulfonate (TNBS) target Keap1 similarly and whether they use the same element for CES1 induction. Trinitrobenzenesulfonic Acid 95-120 kelch like ECH associated protein 1 Homo sapiens 135-140 22426954-3 2012 Here, we assess the effects and mechanisms of IL-33 on the trinitrobenzene sulfonic acid (TNBS)-induced experimental colitis that mimics human CD. Trinitrobenzenesulfonic Acid 59-88 interleukin 33 Homo sapiens 46-51 22677088-7 2012 MPO activity and the TNF-alpha levels were significantly reduced in dietary fed rats when compared with TNBS group. Trinitrobenzenesulfonic Acid 104-108 myeloperoxidase Rattus norvegicus 0-3 22426954-3 2012 Here, we assess the effects and mechanisms of IL-33 on the trinitrobenzene sulfonic acid (TNBS)-induced experimental colitis that mimics human CD. Trinitrobenzenesulfonic Acid 90-94 interleukin 33 Homo sapiens 46-51 22426954-4 2012 We found that IL-33 levels were increased in the TNBS-treated mice, whereas recombinant IL-33 (rIL-33) administration substantially ameliorated TNBS-mediated colonic tissue injury and clinical symptoms of colitis. Trinitrobenzenesulfonic Acid 49-53 interleukin 33 Mus musculus 14-19 22426954-4 2012 We found that IL-33 levels were increased in the TNBS-treated mice, whereas recombinant IL-33 (rIL-33) administration substantially ameliorated TNBS-mediated colonic tissue injury and clinical symptoms of colitis. Trinitrobenzenesulfonic Acid 144-148 interleukin 33 Mus musculus 88-93 22426954-4 2012 We found that IL-33 levels were increased in the TNBS-treated mice, whereas recombinant IL-33 (rIL-33) administration substantially ameliorated TNBS-mediated colonic tissue injury and clinical symptoms of colitis. Trinitrobenzenesulfonic Acid 144-148 interleukin 33 Rattus norvegicus 95-101 22426954-6 2012 Importantly, rIL-33 treatment resulted in prominently upregulated Foxp3 expression in the TNBS-treated mice, and depletion of Tregs significantly abrogated the impact of IL-33 on reducing the development of colitis. Trinitrobenzenesulfonic Acid 90-94 interleukin 33 Rattus norvegicus 13-19 22426954-6 2012 Importantly, rIL-33 treatment resulted in prominently upregulated Foxp3 expression in the TNBS-treated mice, and depletion of Tregs significantly abrogated the impact of IL-33 on reducing the development of colitis. Trinitrobenzenesulfonic Acid 90-94 forkhead box P3 Mus musculus 66-71 22426954-6 2012 Importantly, rIL-33 treatment resulted in prominently upregulated Foxp3 expression in the TNBS-treated mice, and depletion of Tregs significantly abrogated the impact of IL-33 on reducing the development of colitis. Trinitrobenzenesulfonic Acid 90-94 interleukin 33 Mus musculus 14-19 22445727-4 2012 In murine experimental colitis in-vivo, myeloperoxidase activity decreased significantly in 2,4,6-trinitrobenzenesulfonic acid (TNBS)-colitis and oxazolone (OXA)-colitis models after treatment with ClNP while free clodronate did not show a mitigating effect. Trinitrobenzenesulfonic Acid 92-126 myeloperoxidase Mus musculus 40-55 22595989-0 2012 Expression of TNFAIP3 in intestinal epithelial cells protects from DSS- but not TNBS-induced colitis. Trinitrobenzenesulfonic Acid 80-84 tumor necrosis factor, alpha-induced protein 3 Mus musculus 14-21 22864746-6 2012 The myeloperoxidase and inducible nitric oxide synthase activities with malonyldialdehyde and nitric oxide levels in colonic tissues were significantly decreased in the GRd group compared with those in the TNBS group (p < 0.01). Trinitrobenzenesulfonic Acid 206-210 myeloperoxidase Rattus norvegicus 4-19 22736915-4 2012 RESULTS: TNBS group showed significantly elevated colonic MPO activity and increased TNF-alpha level. Trinitrobenzenesulfonic Acid 9-13 myeloperoxidase Rattus norvegicus 58-61 22736915-4 2012 RESULTS: TNBS group showed significantly elevated colonic MPO activity and increased TNF-alpha level. Trinitrobenzenesulfonic Acid 9-13 tumor necrosis factor Rattus norvegicus 85-94 22426941-10 2012 Our results suggest that down-regulation of TNF-alpha and COX-2 resulted in a decrease in inflammation caused by TNBS and thus provided some protection from the colonic damage caused by TNBS. Trinitrobenzenesulfonic Acid 113-117 tumor necrosis factor Rattus norvegicus 44-53 22173746-0 2012 Osteopontin ablation attenuates progression of colitis in TNBS model. Trinitrobenzenesulfonic Acid 58-62 secreted phosphoprotein 1 Mus musculus 0-11 22559170-5 2012 The number of functional groups on the HBP-modified HA surface, determined by a 2,4,6-trinitrobenzenesulfonic acid (TNBS) assay, was found to be 2.8 x 10(-5) mol/mg of HA and unaffected by the length of HBPs. Trinitrobenzenesulfonic Acid 80-114 heme binding protein 1 Homo sapiens 39-42 22559170-5 2012 The number of functional groups on the HBP-modified HA surface, determined by a 2,4,6-trinitrobenzenesulfonic acid (TNBS) assay, was found to be 2.8 x 10(-5) mol/mg of HA and unaffected by the length of HBPs. Trinitrobenzenesulfonic Acid 116-120 heme binding protein 1 Homo sapiens 39-42 22690070-14 2012 We confirmed that ferric iron limited the TNBS-induced increase of MPO activity in both the rodent species. Trinitrobenzenesulfonic Acid 42-46 myeloperoxidase Mus musculus 67-70 22426941-10 2012 Our results suggest that down-regulation of TNF-alpha and COX-2 resulted in a decrease in inflammation caused by TNBS and thus provided some protection from the colonic damage caused by TNBS. Trinitrobenzenesulfonic Acid 186-190 tumor necrosis factor Rattus norvegicus 44-53 22361727-11 2012 We suggest that BMP signaling was altered during TNBS-induced colitis and was recovered with BMP7 administration, suggesting that IBD is a reversible process. Trinitrobenzenesulfonic Acid 49-53 bone morphogenetic protein 2 Rattus norvegicus 16-19 21768202-6 2012 On the other hand, intestinal Mphi from 2,4,6-trinitrobenzene sulfonic acid-treated mice had decreased CRIg expression but increased CD11b expression, implying some contribution to the removal of immune complexes. Trinitrobenzenesulfonic Acid 40-75 V-set and immunoglobulin domain containing 4 Mus musculus 103-107 22654445-6 2012 At 5 d post TNBS, the pathological score and myeloperoxidase (MPO) activity in all TNBS treated rats were significantly elevated compared to that of the control (9.48 +- 1.86, 8.18 +- 0.67, 5.78 +- 0.77 vs 0, and 3.55 +- 1.11, 1.80 +- 0.82, 0.97 +- 0.08 unit/mg vs 0.14 +- 0.01 unit/mg, P < 0.05). Trinitrobenzenesulfonic Acid 83-87 myeloperoxidase Rattus norvegicus 45-60 22654445-6 2012 At 5 d post TNBS, the pathological score and myeloperoxidase (MPO) activity in all TNBS treated rats were significantly elevated compared to that of the control (9.48 +- 1.86, 8.18 +- 0.67, 5.78 +- 0.77 vs 0, and 3.55 +- 1.11, 1.80 +- 0.82, 0.97 +- 0.08 unit/mg vs 0.14 +- 0.01 unit/mg, P < 0.05). Trinitrobenzenesulfonic Acid 83-87 myeloperoxidase Rattus norvegicus 62-65 22300734-9 2012 EP4-MS pretreatment, but not unloaded ONO-AE2-724, significantly attenuated TNBS-induced colitis and diminished colonic mRNA expression levels of proinflammatory cytokines. Trinitrobenzenesulfonic Acid 76-80 prostaglandin E receptor 4 (subtype EP4) Mus musculus 0-3 22333949-8 2012 RESULTS: Colitis induction by dextran sodium sulfate or trinitrobenzene sulfonic acid was significantly reduced in B4galt1(+/-) mice, which had galactose deficiency in IgG oligosaccharides (similar to patients with Crohn"s disease) compared with B4galt1(+/+) mice. Trinitrobenzenesulfonic Acid 56-85 UDP-Gal:betaGlcNAc beta 1,4- galactosyltransferase, polypeptide 1 Mus musculus 115-122 21768202-6 2012 On the other hand, intestinal Mphi from 2,4,6-trinitrobenzene sulfonic acid-treated mice had decreased CRIg expression but increased CD11b expression, implying some contribution to the removal of immune complexes. Trinitrobenzenesulfonic Acid 40-75 integrin alpha M Mus musculus 133-138 22365194-9 2012 The mice that received beta-casein hydrolysate previously to TNBS showed decreased mortality rates, faster recovery of initial body weight loss, less microbial translocation to the liver, decreased beta-glucuronidase and myeloperoxidase activities in the gut, and decreased colonic macroscopic and microscopic damage compared with the animals that did not receive this hydrolysate. Trinitrobenzenesulfonic Acid 61-65 myeloperoxidase Mus musculus 221-236 22235147-0 2012 Selective glucocorticoid receptor agonists for the treatment of inflammatory bowel disease: studies in mice with acute trinitrobenzene sulfonic acid colitis. Trinitrobenzenesulfonic Acid 119-148 nuclear receptor subfamily 3, group C, member 1 Mus musculus 10-33 21887805-1 2012 The purpose of this study was to investigate whether baicalin, a Chinese herbal extract, down-regulates the expression of macrophage migration inhibitory factor (MIF), an inflammatory factor that regulates the function of macrophages (MPhi), in rats with trinitrobenzene sulphonic acid (TNBS)-induced ulcerative colitis (UC). Trinitrobenzenesulfonic Acid 287-291 macrophage migration inhibitory factor Rattus norvegicus 122-160 21887805-1 2012 The purpose of this study was to investigate whether baicalin, a Chinese herbal extract, down-regulates the expression of macrophage migration inhibitory factor (MIF), an inflammatory factor that regulates the function of macrophages (MPhi), in rats with trinitrobenzene sulphonic acid (TNBS)-induced ulcerative colitis (UC). Trinitrobenzenesulfonic Acid 287-291 macrophage migration inhibitory factor Rattus norvegicus 162-165 22410118-0 2012 1,3-Diphenylpropenone ameliorates TNBS-induced rat colitis through suppression of NF-kappaB activation and IL-8 induction. Trinitrobenzenesulfonic Acid 34-38 C-X-C motif chemokine ligand 8 Homo sapiens 107-111 22410118-6 2012 In the colon tissue, DPhP inhibited TNBS-induced NF-kappaB nuclear translocation, IL-8 and TNF-alpha expressions, and abnormal angiogenesis. Trinitrobenzenesulfonic Acid 36-40 C-X-C motif chemokine ligand 8 Homo sapiens 82-86 22410118-6 2012 In the colon tissue, DPhP inhibited TNBS-induced NF-kappaB nuclear translocation, IL-8 and TNF-alpha expressions, and abnormal angiogenesis. Trinitrobenzenesulfonic Acid 36-40 tumor necrosis factor Homo sapiens 91-100 22200667-9 2012 In vivo, intrarectal treatment with wild-type MFG-E8, but not its mutant counterpart, significantly inhibited body weight loss, colon shortening and histological inflammation induced by TNBS administration. Trinitrobenzenesulfonic Acid 186-190 milk fat globule EGF and factor V/VIII domain containing Mus musculus 46-52 22227208-6 2012 The results showed that GRd markedly attenuates the inflammatory response to TNBS-induced relapsing colitis, as evidenced by improved signs, increased body weight, decreased colonic weight/length ratio, reduced colonic macroscopic and microscopic damage scores, inhibited the activity of MPO, lowered proinflammatory cytokine levels and suppressed phosphorylation of p38 and JNK. Trinitrobenzenesulfonic Acid 77-81 myeloperoxidase Rattus norvegicus 288-291 22335898-8 2012 RESULTS: At 3 days post TNBS treatment, the protein level of TRPV1 was increased by 2-fold (p < 0.05) in the inflamed distal colon when examined with western blot. Trinitrobenzenesulfonic Acid 24-28 transient receptor potential cation channel, subfamily V, member 1 Rattus norvegicus 61-66 22227208-6 2012 The results showed that GRd markedly attenuates the inflammatory response to TNBS-induced relapsing colitis, as evidenced by improved signs, increased body weight, decreased colonic weight/length ratio, reduced colonic macroscopic and microscopic damage scores, inhibited the activity of MPO, lowered proinflammatory cytokine levels and suppressed phosphorylation of p38 and JNK. Trinitrobenzenesulfonic Acid 77-81 mitogen activated protein kinase 14 Rattus norvegicus 367-370 22227208-6 2012 The results showed that GRd markedly attenuates the inflammatory response to TNBS-induced relapsing colitis, as evidenced by improved signs, increased body weight, decreased colonic weight/length ratio, reduced colonic macroscopic and microscopic damage scores, inhibited the activity of MPO, lowered proinflammatory cytokine levels and suppressed phosphorylation of p38 and JNK. Trinitrobenzenesulfonic Acid 77-81 mitogen-activated protein kinase 8 Rattus norvegicus 375-378 22460462-2 2012 Here, we investigated whether sensory nerves and Ca(v)3.2 are involved in the H(2)S-induced mucosal cytoprotection against 2,4,6-trinitrobenzenesulfonic acid (TNBS)-induced colitis in rats. Trinitrobenzenesulfonic Acid 159-163 caveolin 3 Rattus norvegicus 49-55 23075874-8 2012 RESULTS: Nlrp3(-/-) mice treated with either DSS or TNBS exhibited attenuated colitis and lower mortality. Trinitrobenzenesulfonic Acid 52-56 NLR family, pyrin domain containing 3 Mus musculus 9-14 22159435-6 2012 TNBS-induced colitis significantly increased the colonic MDA levels and caspase-3 activities in group 2 in comparison to the control group. Trinitrobenzenesulfonic Acid 0-4 caspase 3 Rattus norvegicus 72-81 22056689-4 2012 In vivo binding specificity of MB(P-selectin) to P-selectin was tested in mice with trinitrobenzenesulfonic acid-induced colitis (n = 22) and control mice (n = 10). Trinitrobenzenesulfonic Acid 84-112 selectin, platelet Mus musculus 31-44 21484968-6 2012 METHODS: Here we investigated the role of lumican in the development of colitis mediated by intrarectal administration of the hapten 2-4-5, trinitrobenzene sulfonic acid (TNBS) in Lum(+/+) and Lum(-/-) mice. Trinitrobenzenesulfonic Acid 171-175 lumican Mus musculus 180-183 21484968-7 2012 RESULTS: The TNBS treated Lum(+/+) mouse colons showed marked increases in CXCL1, tumor necrosis factor alpha (TNF-alpha), and neutrophil infiltration, whereas these responses were significantly dampened in the Lum(-/-) mice. Trinitrobenzenesulfonic Acid 13-17 lumican Mus musculus 26-29 21484968-7 2012 RESULTS: The TNBS treated Lum(+/+) mouse colons showed marked increases in CXCL1, tumor necrosis factor alpha (TNF-alpha), and neutrophil infiltration, whereas these responses were significantly dampened in the Lum(-/-) mice. Trinitrobenzenesulfonic Acid 13-17 chemokine (C-X-C motif) ligand 1 Mus musculus 75-80 21484968-7 2012 RESULTS: The TNBS treated Lum(+/+) mouse colons showed marked increases in CXCL1, tumor necrosis factor alpha (TNF-alpha), and neutrophil infiltration, whereas these responses were significantly dampened in the Lum(-/-) mice. Trinitrobenzenesulfonic Acid 13-17 tumor necrosis factor Mus musculus 82-109 21484968-7 2012 RESULTS: The TNBS treated Lum(+/+) mouse colons showed marked increases in CXCL1, tumor necrosis factor alpha (TNF-alpha), and neutrophil infiltration, whereas these responses were significantly dampened in the Lum(-/-) mice. Trinitrobenzenesulfonic Acid 13-17 tumor necrosis factor Mus musculus 111-120 21484968-7 2012 RESULTS: The TNBS treated Lum(+/+) mouse colons showed marked increases in CXCL1, tumor necrosis factor alpha (TNF-alpha), and neutrophil infiltration, whereas these responses were significantly dampened in the Lum(-/-) mice. Trinitrobenzenesulfonic Acid 13-17 lumican Mus musculus 211-214 21484968-8 2012 The nuclear factor kappa B (NF-kappaB) transcription factor, known to regulate inflammatory genes, showed a robust increase after TNBS treatment in Lum(+/+) but not in Lum(-/-) colons. Trinitrobenzenesulfonic Acid 130-134 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 4-26 21484968-8 2012 The nuclear factor kappa B (NF-kappaB) transcription factor, known to regulate inflammatory genes, showed a robust increase after TNBS treatment in Lum(+/+) but not in Lum(-/-) colons. Trinitrobenzenesulfonic Acid 130-134 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 28-37 21484968-8 2012 The nuclear factor kappa B (NF-kappaB) transcription factor, known to regulate inflammatory genes, showed a robust increase after TNBS treatment in Lum(+/+) but not in Lum(-/-) colons. Trinitrobenzenesulfonic Acid 130-134 lumican Mus musculus 148-151 22044612-11 2012 The PAR-4-antagonist significantly increased the TNBS, but not the WAS-induced colonic hyperalgesia. Trinitrobenzenesulfonic Acid 49-53 coagulation factor II (thrombin) receptor-like 3 Mus musculus 4-9 22414698-4 2012 METHODS: Colitis was induced in CD1 mice by trinitrobenzene sulfonic acid. Trinitrobenzenesulfonic Acid 44-73 CD1 antigen complex Mus musculus 32-35 23209735-10 2012 Phospho-JNK and PARP-1 expression was also significantly higher in TNBS-treated rats, and treatment with glutamine significantly decreased JNK phosphorylation and PARP-1 proteolysis. Trinitrobenzenesulfonic Acid 67-71 mitogen-activated protein kinase 8 Rattus norvegicus 8-11 23209735-10 2012 Phospho-JNK and PARP-1 expression was also significantly higher in TNBS-treated rats, and treatment with glutamine significantly decreased JNK phosphorylation and PARP-1 proteolysis. Trinitrobenzenesulfonic Acid 67-71 poly (ADP-ribose) polymerase 1 Rattus norvegicus 16-22 23209735-10 2012 Phospho-JNK and PARP-1 expression was also significantly higher in TNBS-treated rats, and treatment with glutamine significantly decreased JNK phosphorylation and PARP-1 proteolysis. Trinitrobenzenesulfonic Acid 67-71 mitogen-activated protein kinase 8 Rattus norvegicus 139-142 23209735-10 2012 Phospho-JNK and PARP-1 expression was also significantly higher in TNBS-treated rats, and treatment with glutamine significantly decreased JNK phosphorylation and PARP-1 proteolysis. Trinitrobenzenesulfonic Acid 67-71 poly (ADP-ribose) polymerase 1 Rattus norvegicus 163-169 23166707-8 2012 FSG treatment improved the severity of colitis, by decreasing the TNBS-induced rise in gut permeability, visceral sensitivity, faecal proteolytic activity and PAR-2 expression at all post-TNBS points. Trinitrobenzenesulfonic Acid 66-70 F2R like trypsin receptor 1 Rattus norvegicus 159-164 22427801-7 2012 A single application of subcutaneous XG-102 was at least as effective or even better depending on the outcome parameter as the daily oral application of sulfasalazine used for treatment of IBD.The successful and substantial reduction of the severe, TNBS-evoked intestinal damages and clinical symptoms render the JNK-inhibiting peptide XG-102 a powerful therapeutic principle of IBD. Trinitrobenzenesulfonic Acid 249-253 mitogen-activated protein kinase 8 Mus musculus 313-316 21958875-6 2011 TNBS instillation induced COX-2 and iNOS expressions in colon and small mesenteric arteries; AM treatment decreased COX-2 expression only in microvessels from rats with colitis. Trinitrobenzenesulfonic Acid 0-4 prostaglandin-endoperoxide synthase 2 Rattus norvegicus 26-31 21922185-8 2011 PIR-A/B(med) cDCs actually migrated to the inflamed colon, and ameliorated the colitis induced by TNBS when transferred to colitis-induced recipients. Trinitrobenzenesulfonic Acid 98-102 paired Ig-like receptor B Mus musculus 0-7 21958875-8 2011 COX and NOS inhibitors altered the contractile ability of phenylephrine in small mesenteric arteries from TNBS rats, suggesting the involvement of COX-2 and iNOS derived factors in the deleterious effect of TNBS on vascular reactivity; AM administration was able to reduce such alteration. Trinitrobenzenesulfonic Acid 207-211 prostaglandin-endoperoxide synthase 2 Rattus norvegicus 147-152 21958875-8 2011 COX and NOS inhibitors altered the contractile ability of phenylephrine in small mesenteric arteries from TNBS rats, suggesting the involvement of COX-2 and iNOS derived factors in the deleterious effect of TNBS on vascular reactivity; AM administration was able to reduce such alteration. Trinitrobenzenesulfonic Acid 207-211 nitric oxide synthase 2 Rattus norvegicus 157-161 21958875-6 2011 TNBS instillation induced COX-2 and iNOS expressions in colon and small mesenteric arteries; AM treatment decreased COX-2 expression only in microvessels from rats with colitis. Trinitrobenzenesulfonic Acid 0-4 nitric oxide synthase 2 Rattus norvegicus 36-40 21802389-10 2011 Cat-S deletion attenuated colonic inflammatory pain induced with trinitrobenzene sulfonic acid. Trinitrobenzenesulfonic Acid 65-94 cathepsin S Mus musculus 0-5 21763243-5 2011 RESULTS: TNBS induced TRPA1-dependent release of colonic substance P and CGRP, influx of Ca2+, and sustained ionic inward currents in colonic sensory neurons and transfected HEK293t cells. Trinitrobenzenesulfonic Acid 9-13 calcitonin related polypeptide alpha Homo sapiens 73-77 21751235-4 2011 Trinitrobenzenesulfonic acid-induced (TNBS) colitis was induced in CD26-deficient (CD26(-/-) ) and wild-type (C57BL/6) mice. Trinitrobenzenesulfonic Acid 0-28 dipeptidylpeptidase 4 Mus musculus 67-71 21973321-4 2011 In this study, we investigated the water-soluble, polysaccharide components of Reishi (designated as MAK) in murine colitis induced by trinitrobenzene sulphonic acid (TNBS). Trinitrobenzenesulfonic Acid 167-171 male germ cell-associated kinase Mus musculus 101-104 21973321-10 2011 Intestinal inflammation by TNBS was improved by feeding with MAK. Trinitrobenzenesulfonic Acid 27-31 male germ cell-associated kinase Mus musculus 61-64 21973321-11 2011 MLNs of mice treated with TNBS produced IFN-gamma, which was inhibited by feeding with MAK. Trinitrobenzenesulfonic Acid 26-30 interferon gamma Mus musculus 40-49 21973321-11 2011 MLNs of mice treated with TNBS produced IFN-gamma, which was inhibited by feeding with MAK. Trinitrobenzenesulfonic Acid 26-30 male germ cell-associated kinase Mus musculus 87-90 21973321-12 2011 In contrast, MLNs of mice treated with TNBS inhibited GM-CSF production, which was induced by feeding with MAK. Trinitrobenzenesulfonic Acid 39-43 colony stimulating factor 2 (granulocyte-macrophage) Mus musculus 54-60 21973321-12 2011 In contrast, MLNs of mice treated with TNBS inhibited GM-CSF production, which was induced by feeding with MAK. Trinitrobenzenesulfonic Acid 39-43 male germ cell-associated kinase Mus musculus 107-110 21762661-5 2011 RESULTS: TNBS and DSS induced more severe levels of inflammation in beta-actin-hPepT1 transgenic mice than wild-type littermates. Trinitrobenzenesulfonic Acid 9-13 actin, beta Mus musculus 68-78 22039891-7 2011 Only DQ124298:g.344A>G MUC4 polymorphism was significantly associated with both NBA and TNB (P-value < 0.05) with favourable effects coming from the Meishan origin. Trinitrobenzenesulfonic Acid 91-94 mucin-4 Sus scrofa 26-30 21762661-5 2011 RESULTS: TNBS and DSS induced more severe levels of inflammation in beta-actin-hPepT1 transgenic mice than wild-type littermates. Trinitrobenzenesulfonic Acid 9-13 solute carrier family 15 member 1 Homo sapiens 79-85 21763243-6 2011 Analysis of mutant forms of TRPA1 revealed that TNBS bound covalently to cysteine (and lysine) residues in the cytoplasmic N-terminus. Trinitrobenzenesulfonic Acid 48-52 transient receptor potential cation channel, subfamily A, member 1 Mus musculus 28-33 21763243-10 2011 Colitis induction by TNBS or dextran-sulfate-sodium-salt was inhibited or reduced in TRPA1-/- mice and by 2-(1,3-dimethyl-2,6-dioxo-1,2,3,6-tetrahydro-7H-purin-7-yl)-N-(4-isopro-pylphenyl)-acetamide, a pharmacologic inhibitor of TRPA1. Trinitrobenzenesulfonic Acid 21-25 transient receptor potential cation channel, subfamily A, member 1 Mus musculus 85-90 21763243-5 2011 RESULTS: TNBS induced TRPA1-dependent release of colonic substance P and CGRP, influx of Ca2+, and sustained ionic inward currents in colonic sensory neurons and transfected HEK293t cells. Trinitrobenzenesulfonic Acid 9-13 transient receptor potential cation channel subfamily A member 1 Homo sapiens 22-27 21763243-10 2011 Colitis induction by TNBS or dextran-sulfate-sodium-salt was inhibited or reduced in TRPA1-/- mice and by 2-(1,3-dimethyl-2,6-dioxo-1,2,3,6-tetrahydro-7H-purin-7-yl)-N-(4-isopro-pylphenyl)-acetamide, a pharmacologic inhibitor of TRPA1. Trinitrobenzenesulfonic Acid 21-25 transient receptor potential cation channel, subfamily A, member 1 Mus musculus 229-234 22400335-6 2011 Sn2+ is easily crystallized to form SnO2 nanoparticles on the surface of TNBs and being considered as unfavorable metal dopant for the present intercalation purpose. Trinitrobenzenesulfonic Acid 73-77 solute carrier family 38 member 5 Homo sapiens 0-3 21153768-3 2011 In this study, we observed the effects of combined treatment with 5-aminosalicylic acid (5-ASA) and recombinant human ITF (rhITF) on the expression of Myeloperoxidase (MPO), nuclear factor-kappaB (NF-kappaB) and epidermal growth factor (EGF) in trinitrobenzene sulphonic acid (TNBS) induced colitis in rats. Trinitrobenzenesulfonic Acid 277-281 trefoil factor 3 Homo sapiens 118-121 21863329-4 2011 Thus, this study aimed to evaluate the effect of Etanercept (ETC), a tumour necrosis factor alpha (TNF-alpha) antagonist on the 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced experimental colitis. Trinitrobenzenesulfonic Acid 128-163 tumor necrosis factor Rattus norvegicus 99-108 21863329-4 2011 Thus, this study aimed to evaluate the effect of Etanercept (ETC), a tumour necrosis factor alpha (TNF-alpha) antagonist on the 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced experimental colitis. Trinitrobenzenesulfonic Acid 165-169 tumor necrosis factor Rattus norvegicus 99-108 21863329-7 2011 The gene expression of TNF-alpha mRNA, decreased significantly in this group compared to the TNBS non-treated group. Trinitrobenzenesulfonic Acid 93-97 tumor necrosis factor Rattus norvegicus 23-32 21863329-9 2011 Taken together, our results suggest that ETC attenuates intestinal colitis induced by TNBS in Wistar rats by TNF-alpha downregulation. Trinitrobenzenesulfonic Acid 86-90 tumor necrosis factor Rattus norvegicus 109-118 22234755-5 2011 The relief of trinitrobenzene sulfonic acid-induced colitis was accompanied by significantly decreased production of tumor necrosis factor-alpha in both serum and intra-colon (p<0.05) and by significantly increased production of interleukin-10 in both serum and intra-colon (p<0.05). Trinitrobenzenesulfonic Acid 14-43 tumor necrosis factor Rattus norvegicus 117-144 21898680-5 2011 To this end, we pretreated MSCs with IFN-gamma and assessed their therapeutic effects in dextran sodium sulfate (DSS)- and trinitrobenzene sulfonate (TNBS)-induced colitis in mice. Trinitrobenzenesulfonic Acid 123-148 interferon gamma Mus musculus 37-46 22234755-5 2011 The relief of trinitrobenzene sulfonic acid-induced colitis was accompanied by significantly decreased production of tumor necrosis factor-alpha in both serum and intra-colon (p<0.05) and by significantly increased production of interleukin-10 in both serum and intra-colon (p<0.05). Trinitrobenzenesulfonic Acid 14-43 interleukin 10 Rattus norvegicus 232-246 22234755-6 2011 CONCLUSIONS: Peifeikang can effectively ameliorate trinitrobenzene sulfonic acid-induced colitis in rats, the underlying mechanism of which may be attributed to the modulatory effects of Peifeikang on the production of tumor necrosis factor-alpha and interleukin-10. Trinitrobenzenesulfonic Acid 51-80 tumor necrosis factor Rattus norvegicus 219-246 21554873-7 2011 When administered to TNBS-treated mice, CSY0073 effectively attenuated influx of neutrophils and macrophages into the colonic mucosa and reduced the intestinal expression pro-inflammatory cytokines TNFalpha, IL-2 and IFNgamma. Trinitrobenzenesulfonic Acid 21-25 tumor necrosis factor Mus musculus 198-206 21668898-3 2011 In this study, trinitrobenzene sulphonic acid (TNBS) was used to induce colitis in TNF-receptor single or double knock-out (DKO) BALB/c mice and in wild-type counterparts. Trinitrobenzenesulfonic Acid 47-51 tumor necrosis factor Mus musculus 83-86 21668898-6 2011 Strikingly, systemic inflammatory response (including splenomegaly and monocyte expansion) was found in WT and TNF-R1(-/-) mice after TNBS, instead of TNF-R2(-/-) and TNF-R DKO mice. Trinitrobenzenesulfonic Acid 134-138 tumor necrosis factor receptor superfamily, member 1b Mus musculus 111-117 21668898-6 2011 Strikingly, systemic inflammatory response (including splenomegaly and monocyte expansion) was found in WT and TNF-R1(-/-) mice after TNBS, instead of TNF-R2(-/-) and TNF-R DKO mice. Trinitrobenzenesulfonic Acid 134-138 tumor necrosis factor Mus musculus 111-114 21887846-0 2011 Hyaluronic acid as a rescue therapy for trinitrobenzene sulfonic acid-induced colitis through Cox-2 and PGE2 in a Toll-like receptor 4-dependent way. Trinitrobenzenesulfonic Acid 40-69 prostaglandin-endoperoxide synthase 2 Mus musculus 94-99 21887846-0 2011 Hyaluronic acid as a rescue therapy for trinitrobenzene sulfonic acid-induced colitis through Cox-2 and PGE2 in a Toll-like receptor 4-dependent way. Trinitrobenzenesulfonic Acid 40-69 toll-like receptor 4 Mus musculus 114-134 21887846-1 2011 We hypothesized whether systemic administration of high-molecular-weight hyaluronic acid (HMW HA) could rescue trinitrobenzene sulfonic acid (TNBS)-induced colitis through Toll-like receptor 4 (TLR4) signal. Trinitrobenzenesulfonic Acid 111-140 toll-like receptor 4 Mus musculus 172-192 21887846-1 2011 We hypothesized whether systemic administration of high-molecular-weight hyaluronic acid (HMW HA) could rescue trinitrobenzene sulfonic acid (TNBS)-induced colitis through Toll-like receptor 4 (TLR4) signal. Trinitrobenzenesulfonic Acid 111-140 toll-like receptor 4 Mus musculus 194-198 21887846-1 2011 We hypothesized whether systemic administration of high-molecular-weight hyaluronic acid (HMW HA) could rescue trinitrobenzene sulfonic acid (TNBS)-induced colitis through Toll-like receptor 4 (TLR4) signal. Trinitrobenzenesulfonic Acid 142-146 toll-like receptor 4 Mus musculus 172-192 21887846-1 2011 We hypothesized whether systemic administration of high-molecular-weight hyaluronic acid (HMW HA) could rescue trinitrobenzene sulfonic acid (TNBS)-induced colitis through Toll-like receptor 4 (TLR4) signal. Trinitrobenzenesulfonic Acid 142-146 toll-like receptor 4 Mus musculus 194-198 21512155-6 2011 After trinitrobenzene sulfonic acid-induced colon inflammation, we observed significant decreases in the amount of TREK-1 mRNA, in the response of TREK-2-like channels to membrane stretch, and in the whole cell outward current during osmotic stretch in LS colon DRG neurons. Trinitrobenzenesulfonic Acid 6-35 potassium channel, subfamily K, member 2 Mus musculus 115-121 21600888-2 2011 When ginsenoside Rb1 or compound K were orally administered to 2,4,6-trinitrobenzene sulfuric acid (TNBS)-induced colitic mice, these agents inhibited colon shortening, macroscopic score, and colonic thickening. Trinitrobenzenesulfonic Acid 100-104 RB transcriptional corepressor 1 Mus musculus 17-20 21600888-3 2011 Furthermore, treatment with ginsenoside Rb1 or compound K at 20mg/kg inhibited colonic myeloperoxidase activity by 84% and 88%, respectively, as compared with TNBS alone (p<0.05), and also potently inhibited the expression of tumor necrosis factor-alpha, interleukin (IL)-1beta and IL-6, but increased the expression of IL-10. Trinitrobenzenesulfonic Acid 159-163 RB transcriptional corepressor 1 Mus musculus 40-43 21600888-4 2011 Both ginsenoside Rb1 and compound K blocked the TNBS-induced expressions of COX-2 and iNOS and the activation of NF-kappaB in mice. Trinitrobenzenesulfonic Acid 48-52 RB transcriptional corepressor 1 Mus musculus 17-20 21600888-4 2011 Both ginsenoside Rb1 and compound K blocked the TNBS-induced expressions of COX-2 and iNOS and the activation of NF-kappaB in mice. Trinitrobenzenesulfonic Acid 48-52 cytochrome c oxidase II, mitochondrial Mus musculus 76-81 21600888-4 2011 Both ginsenoside Rb1 and compound K blocked the TNBS-induced expressions of COX-2 and iNOS and the activation of NF-kappaB in mice. Trinitrobenzenesulfonic Acid 48-52 nitric oxide synthase 2, inducible Mus musculus 86-90 21600888-4 2011 Both ginsenoside Rb1 and compound K blocked the TNBS-induced expressions of COX-2 and iNOS and the activation of NF-kappaB in mice. Trinitrobenzenesulfonic Acid 48-52 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 113-122 20693187-0 2011 Arsenic trioxide reduces 2,4,6-trinitrobenzene sulfonic acid-induced murine colitis via nuclear factor-kappaB down-regulation and caspase-3 activation. Trinitrobenzenesulfonic Acid 25-60 caspase 3 Mus musculus 130-139 21551239-4 2011 2-Arachidonoylglycerol levels were raised in the trinitrobenzene sulfonic acid (TNBS)-induced colitis mouse model by inhibiting monoacylglycerol lipase (MAGL), the primary enzyme responsible for hydrolysis of 2-arachidonoylglycerol, using the selective inhibitor JZL184. Trinitrobenzenesulfonic Acid 49-78 monoglyceride lipase Mus musculus 128-151 21551239-4 2011 2-Arachidonoylglycerol levels were raised in the trinitrobenzene sulfonic acid (TNBS)-induced colitis mouse model by inhibiting monoacylglycerol lipase (MAGL), the primary enzyme responsible for hydrolysis of 2-arachidonoylglycerol, using the selective inhibitor JZL184. Trinitrobenzenesulfonic Acid 49-78 monoglyceride lipase Mus musculus 153-157 21551239-4 2011 2-Arachidonoylglycerol levels were raised in the trinitrobenzene sulfonic acid (TNBS)-induced colitis mouse model by inhibiting monoacylglycerol lipase (MAGL), the primary enzyme responsible for hydrolysis of 2-arachidonoylglycerol, using the selective inhibitor JZL184. Trinitrobenzenesulfonic Acid 80-84 monoglyceride lipase Mus musculus 128-151 21551239-4 2011 2-Arachidonoylglycerol levels were raised in the trinitrobenzene sulfonic acid (TNBS)-induced colitis mouse model by inhibiting monoacylglycerol lipase (MAGL), the primary enzyme responsible for hydrolysis of 2-arachidonoylglycerol, using the selective inhibitor JZL184. Trinitrobenzenesulfonic Acid 80-84 monoglyceride lipase Mus musculus 153-157 21551239-7 2011 Coadministration of either CB(1) (SR141716A) or CB(2) (AM630) selective antagonists with JZL184 completely abolished the protective effect of MAGL inhibition on TNBS-induced colon alterations, thus demonstrating the involvement of both cannabinoid receptors. Trinitrobenzenesulfonic Acid 161-165 monoglyceride lipase Mus musculus 142-146 21605284-7 2011 At 7 days following TNBS treatment, the number of DRG neurons surrounded by TH-immunoreactive fibers and the protein levels of TH were significantly increased in T13, L1, and L2 DRGs (two- to threefold, P < 0.05). Trinitrobenzenesulfonic Acid 20-24 tyrosine hydroxylase Rattus norvegicus 76-78 21605284-7 2011 At 7 days following TNBS treatment, the number of DRG neurons surrounded by TH-immunoreactive fibers and the protein levels of TH were significantly increased in T13, L1, and L2 DRGs (two- to threefold, P < 0.05). Trinitrobenzenesulfonic Acid 20-24 tyrosine hydroxylase Rattus norvegicus 127-129 21605284-10 2011 Comparison of the level of TH and the severity of colonic inflammation showed that following TNBS treatment, the degree of colonic inflammation was most severe at day 3, subsided at day 7, and significantly recovered by day 21. Trinitrobenzenesulfonic Acid 93-97 tyrosine hydroxylase Rattus norvegicus 27-29 21605284-11 2011 However, the levels of TH in T13-L2 DRGs were increased at both 3 days and 7 days post TNBS treatment and persisted up to 21 days (two- to fivefold increase, P < 0.05) as examined. Trinitrobenzenesulfonic Acid 87-91 tyrosine hydroxylase Rattus norvegicus 23-25 21512155-6 2011 After trinitrobenzene sulfonic acid-induced colon inflammation, we observed significant decreases in the amount of TREK-1 mRNA, in the response of TREK-2-like channels to membrane stretch, and in the whole cell outward current during osmotic stretch in LS colon DRG neurons. Trinitrobenzenesulfonic Acid 6-35 potassium channel, subfamily K, member 10 Mus musculus 147-153 21373265-6 2011 Recent studies suggest that the induction of HO-1 expression plays a critical protective role in intestinal damage models induced by ischemia-reperfusion, indomethacin, lipopolysaccharide-associated sepsis, trinitrobenzene sulfonic acid, and dextran sulfate sodium, indicating that activation of HO-1 may act as an endogenous defensive mechanism to reduce inflammation and tissue injury in the gastrointestinal tract. Trinitrobenzenesulfonic Acid 207-236 heme oxygenase 1 Homo sapiens 45-49 21490394-8 2011 Furthermore, treating mice with infliximab (Remicade), a clinically used TNF-specific antibody, suppressed DSS- and TNBS-induced PUMA expression and colitis. Trinitrobenzenesulfonic Acid 116-120 tumor necrosis factor Mus musculus 73-76 21198552-11 2011 Kalopanaxsaponin A inhibited NF-kappaB and mitogen-activated protein kinase activation induced by TNBS by suppressing IRAK-1 activation. Trinitrobenzenesulfonic Acid 98-102 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 29-38 21198552-11 2011 Kalopanaxsaponin A inhibited NF-kappaB and mitogen-activated protein kinase activation induced by TNBS by suppressing IRAK-1 activation. Trinitrobenzenesulfonic Acid 98-102 interleukin-1 receptor-associated kinase 1 Mus musculus 118-124 21199654-8 2011 In mice given TNBS or DSS, transgenic expression of elafin or disruption of NE and PR-3 protected against the development of colitis. Trinitrobenzenesulfonic Acid 14-18 peptidase inhibitor 3 Homo sapiens 52-58 21455100-10 2011 Rosiglitazone alone decreased expression of IL-6; used with TNBS it decreased expression of MPO in intestinal tissue, yet did not increase the expression of IL-10. Trinitrobenzenesulfonic Acid 60-64 myeloperoxidase Rattus norvegicus 92-95 21321105-2 2011 Previous work indicated that a region on chromosome 11 encoding the IL-12p40 subunit regulates strain differences in susceptibility to murine trinitrobenzene sulfonic acid-induced colitis. Trinitrobenzenesulfonic Acid 142-171 interleukin 12b Mus musculus 68-76 21193524-6 2011 Relative to intracolonic saline treatment, TNBS significantly enhanced the VMR to colorectal distension in C57BL/6 mice 2, 7, 10, and 14 days posttreatment, whereas TNBS-induced visceral hypersensitivity was significantly suppressed in GFRalpha3 KO mice. Trinitrobenzenesulfonic Acid 43-47 glial cell line derived neurotrophic factor family receptor alpha 3 Mus musculus 236-245 21193524-6 2011 Relative to intracolonic saline treatment, TNBS significantly enhanced the VMR to colorectal distension in C57BL/6 mice 2, 7, 10, and 14 days posttreatment, whereas TNBS-induced visceral hypersensitivity was significantly suppressed in GFRalpha3 KO mice. Trinitrobenzenesulfonic Acid 165-169 glial cell line derived neurotrophic factor family receptor alpha 3 Mus musculus 236-245 21193524-7 2011 The proportion of GFRalpha3 immunopositive thoracolumbar and lumbosacral colorectal dorsal root ganglion neurons was significantly elevated 2 days after TNBS treatment. Trinitrobenzenesulfonic Acid 153-157 glial cell line derived neurotrophic factor family receptor alpha 3 Mus musculus 18-27 21600206-13 2011 Neutralization of endogenous IL-22 disrupted the protective effect of Ficz on TNBS-induced colitis. Trinitrobenzenesulfonic Acid 78-82 interleukin 22 Mus musculus 29-34 21244371-0 2011 Inhibitor of PI3Kgamma ameliorates TNBS-induced colitis in mice by affecting the functional activity of CD4+CD25+FoxP3+ regulatory T cells. Trinitrobenzenesulfonic Acid 35-39 phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit gamma Mus musculus 13-22 21244371-0 2011 Inhibitor of PI3Kgamma ameliorates TNBS-induced colitis in mice by affecting the functional activity of CD4+CD25+FoxP3+ regulatory T cells. Trinitrobenzenesulfonic Acid 35-39 CD4 antigen Mus musculus 104-107 21244371-0 2011 Inhibitor of PI3Kgamma ameliorates TNBS-induced colitis in mice by affecting the functional activity of CD4+CD25+FoxP3+ regulatory T cells. Trinitrobenzenesulfonic Acid 35-39 interleukin 2 receptor, alpha chain Mus musculus 108-112 21244371-0 2011 Inhibitor of PI3Kgamma ameliorates TNBS-induced colitis in mice by affecting the functional activity of CD4+CD25+FoxP3+ regulatory T cells. Trinitrobenzenesulfonic Acid 35-39 forkhead box P3 Mus musculus 113-118 21499209-5 2011 RESULTS: Levels of BDNF in DRGs and spinal cords (T9-13) were significantly higher in trinitrobenzene sulfonic acid rats compared with controls, accompanied by an increase in the number of pancreas-specific neurons expressing BDNF immunoreactivity. Trinitrobenzenesulfonic Acid 86-115 brain-derived neurotrophic factor Rattus norvegicus 19-23 21042292-9 2011 TNBS-CysN group developed a less severe colitis compared with the TNBS group (macroscopic score 0.43+-0.78 vs 3.28+-0.95, microscopic score 6.62+-12.01 vs 19.25+-6.04, P<0.05, respectively) associated with a decrease of TG activity, TG2 and isopeptide bond immunohistochemical expression, TNF-alpha and IL-6 levels. Trinitrobenzenesulfonic Acid 0-4 tumor necrosis factor Rattus norvegicus 292-301 20722057-2 2011 Insulin-like growth factor-I (IGF-I) expression is increased in smooth muscle cells of the muscularis propria in CD and in animal models of CD, including trinitrobenzene sulfonic acid (TNBS)-induced colitis. Trinitrobenzenesulfonic Acid 154-183 insulin-like growth factor 1 Mus musculus 0-28 20722057-2 2011 Insulin-like growth factor-I (IGF-I) expression is increased in smooth muscle cells of the muscularis propria in CD and in animal models of CD, including trinitrobenzene sulfonic acid (TNBS)-induced colitis. Trinitrobenzenesulfonic Acid 154-183 insulin-like growth factor 1 Mus musculus 30-35 20722057-2 2011 Insulin-like growth factor-I (IGF-I) expression is increased in smooth muscle cells of the muscularis propria in CD and in animal models of CD, including trinitrobenzene sulfonic acid (TNBS)-induced colitis. Trinitrobenzenesulfonic Acid 185-189 insulin-like growth factor 1 Mus musculus 0-28 20722057-2 2011 Insulin-like growth factor-I (IGF-I) expression is increased in smooth muscle cells of the muscularis propria in CD and in animal models of CD, including trinitrobenzene sulfonic acid (TNBS)-induced colitis. Trinitrobenzenesulfonic Acid 185-189 insulin-like growth factor 1 Mus musculus 30-35 21042292-9 2011 TNBS-CysN group developed a less severe colitis compared with the TNBS group (macroscopic score 0.43+-0.78 vs 3.28+-0.95, microscopic score 6.62+-12.01 vs 19.25+-6.04, P<0.05, respectively) associated with a decrease of TG activity, TG2 and isopeptide bond immunohistochemical expression, TNF-alpha and IL-6 levels. Trinitrobenzenesulfonic Acid 0-4 interleukin 6 Rattus norvegicus 306-310 21102504-0 2011 Blockade of complement activation product C5a activity using specific antibody attenuates intestinal damage in trinitrobenzene sulfonic acid induced model of colitis. Trinitrobenzenesulfonic Acid 111-140 complement C5a receptor 1 Homo sapiens 42-45 21102504-6 2011 Strikingly, treatment with anti-C5a at 24 h after TNBS instillation showed remarkable therapeutic effects, whereas prednisolone did not. Trinitrobenzenesulfonic Acid 50-54 complement C5a receptor 1 Homo sapiens 32-35 20718942-7 2010 KEY RESULTS: Glucagon-like peptide 2 treatment was associated with a significant amelioration of weight loss, and reduced neutrophil infiltration and microscopic colitis scores in the TNBS animals. Trinitrobenzenesulfonic Acid 184-188 mast cell protease 10 Rattus norvegicus 13-36 20980995-7 2011 Finally, blocking TL1A-DR3 interactions abrogates 2,4,6 trinitrobenzenesulfonic acid (TNBS) colitis, indicating that these interactions influence other causes of intestinal inflammation as well. Trinitrobenzenesulfonic Acid 50-84 tumor necrosis factor (ligand) superfamily, member 15 Mus musculus 18-22 20980995-7 2011 Finally, blocking TL1A-DR3 interactions abrogates 2,4,6 trinitrobenzenesulfonic acid (TNBS) colitis, indicating that these interactions influence other causes of intestinal inflammation as well. Trinitrobenzenesulfonic Acid 50-84 tumor necrosis factor receptor superfamily, member 25 Mus musculus 23-26 22040876-13 2011 The expression levels of mRNA and proteins for TGF-beta1, HSP47, and collagen I were elevated in colonic mucosa treated with TNBS. Trinitrobenzenesulfonic Acid 125-129 transforming growth factor, beta 1 Rattus norvegicus 47-56 22286041-3 2011 The aim of this paper was to evaluate the anti-inflammatory effect of the administration of milks fermented by Lactococcus lactis strains that produce IL-10 under the control of the xylose-inducible expression system using a trinitrobenzenesulfonic acid-induced colitis murine model. Trinitrobenzenesulfonic Acid 225-253 interleukin 10 Mus musculus 151-156 20828550-4 2010 Its oral administration inhibited macroscopic score, body weight gain, colon shortening, myeloperoxidase activity, and lipid peroxidation in the colons of TNBS-treated C3H/HeN and C3H/HeJ mice. Trinitrobenzenesulfonic Acid 155-159 myeloperoxidase Mus musculus 89-104 20828550-5 2010 Berberine inhibited colonic expression of iNOS, COX-2, IL-1beta, IL-6, and TNF-alpha, but increased IL-10 expression in the colons of TNBS-treated C3H/HeN and C3H/HeJ mice. Trinitrobenzenesulfonic Acid 134-138 tumor necrosis factor Mus musculus 75-84 20828550-5 2010 Berberine inhibited colonic expression of iNOS, COX-2, IL-1beta, IL-6, and TNF-alpha, but increased IL-10 expression in the colons of TNBS-treated C3H/HeN and C3H/HeJ mice. Trinitrobenzenesulfonic Acid 134-138 interleukin 10 Mus musculus 100-105 21131560-10 2011 Forkhead box P3 (Foxp3)(egfp) mice revealed that TCDD increased the Foxp3+ Treg population in gut immune tissue following TNBS exposure. Trinitrobenzenesulfonic Acid 122-126 forkhead box P3 Mus musculus 0-15 21131560-10 2011 Forkhead box P3 (Foxp3)(egfp) mice revealed that TCDD increased the Foxp3+ Treg population in gut immune tissue following TNBS exposure. Trinitrobenzenesulfonic Acid 122-126 forkhead box P3 Mus musculus 17-22 21131560-10 2011 Forkhead box P3 (Foxp3)(egfp) mice revealed that TCDD increased the Foxp3+ Treg population in gut immune tissue following TNBS exposure. Trinitrobenzenesulfonic Acid 122-126 forkhead box P3 Mus musculus 68-73 21342497-5 2011 RESULTS: To test our hypothesis, we first investigated the changes of TLR2-4 in the rat CP model induced by intrapancreatic infusion of trinitrobenzene sulfonic acid (TNBS). Trinitrobenzenesulfonic Acid 136-165 toll-like receptor 2 Rattus norvegicus 70-76 21342497-5 2011 RESULTS: To test our hypothesis, we first investigated the changes of TLR2-4 in the rat CP model induced by intrapancreatic infusion of trinitrobenzene sulfonic acid (TNBS). Trinitrobenzenesulfonic Acid 167-171 toll-like receptor 2 Rattus norvegicus 70-76 21342497-6 2011 Western blot showed that after TNBS infusion, TLR3, but not TLR2 or TLR4, was increased gradually and maintained at a very high level for up to 5 w, which correlated with the changing course of mechanical allodynia. Trinitrobenzenesulfonic Acid 31-35 toll-like receptor 3 Rattus norvegicus 46-50 21167883-0 2011 Use of superoxide dismutase and catalase producing lactic acid bacteria in TNBS induced Crohn"s disease in mice. Trinitrobenzenesulfonic Acid 75-79 catalase Mus musculus 32-40 21424108-0 2011 Targeting IL-12/IL-23 by employing a p40 peptide-based vaccine ameliorates TNBS-induced acute and chronic murine colitis. Trinitrobenzenesulfonic Acid 75-79 interleukin 23, alpha subunit p19 Mus musculus 16-21 21424108-0 2011 Targeting IL-12/IL-23 by employing a p40 peptide-based vaccine ameliorates TNBS-induced acute and chronic murine colitis. Trinitrobenzenesulfonic Acid 75-79 interleukin 12b Mus musculus 37-40 21424108-8 2011 After administrations of TNBS, vaccinated mice had significantly less body weight loss and a significant decrease of inflammatory scores, collagen deposition and expression of p40, IL-12, IL-23, IL-17, TNF, iNOS and Bcl-2 in colon tissues, compared with carrier and saline groups. Trinitrobenzenesulfonic Acid 25-29 interleukin 12b Mus musculus 176-179 21424108-8 2011 After administrations of TNBS, vaccinated mice had significantly less body weight loss and a significant decrease of inflammatory scores, collagen deposition and expression of p40, IL-12, IL-23, IL-17, TNF, iNOS and Bcl-2 in colon tissues, compared with carrier and saline groups. Trinitrobenzenesulfonic Acid 25-29 interleukin 23, alpha subunit p19 Mus musculus 188-193 21424108-8 2011 After administrations of TNBS, vaccinated mice had significantly less body weight loss and a significant decrease of inflammatory scores, collagen deposition and expression of p40, IL-12, IL-23, IL-17, TNF, iNOS and Bcl-2 in colon tissues, compared with carrier and saline groups. Trinitrobenzenesulfonic Acid 25-29 interleukin 17A Mus musculus 195-200 21424108-8 2011 After administrations of TNBS, vaccinated mice had significantly less body weight loss and a significant decrease of inflammatory scores, collagen deposition and expression of p40, IL-12, IL-23, IL-17, TNF, iNOS and Bcl-2 in colon tissues, compared with carrier and saline groups. Trinitrobenzenesulfonic Acid 25-29 tumor necrosis factor Mus musculus 202-205 21424108-8 2011 After administrations of TNBS, vaccinated mice had significantly less body weight loss and a significant decrease of inflammatory scores, collagen deposition and expression of p40, IL-12, IL-23, IL-17, TNF, iNOS and Bcl-2 in colon tissues, compared with carrier and saline groups. Trinitrobenzenesulfonic Acid 25-29 nitric oxide synthase 2, inducible Mus musculus 207-211 21424108-8 2011 After administrations of TNBS, vaccinated mice had significantly less body weight loss and a significant decrease of inflammatory scores, collagen deposition and expression of p40, IL-12, IL-23, IL-17, TNF, iNOS and Bcl-2 in colon tissues, compared with carrier and saline groups. Trinitrobenzenesulfonic Acid 25-29 B cell leukemia/lymphoma 2 Mus musculus 216-221 21984950-5 2011 LPM from TNBS-treated mice secreted significantly more TNF-alpha at basal state and in response to LPS than LPM from untreated mice (p<0.05). Trinitrobenzenesulfonic Acid 9-13 tumor necrosis factor Mus musculus 55-64 21984950-6 2011 LITAF mRNA and protein levels were elevated in LPM from TNBS compared with untreated animals and LPS further increased LITAF protein levels in LPM from inflamed tissue (P<0.05). Trinitrobenzenesulfonic Acid 56-60 LPS-induced TN factor Mus musculus 0-5 21984950-8 2011 Twenty four hours following TNBS administration, colonic tissue from LITAF mac -/- mice had less MPO activity and reduced colonic TNF-alpha mRNA then WT C57BL/6 mice (p<0.05). Trinitrobenzenesulfonic Acid 28-32 LPS-induced TN factor Mus musculus 69-74 21853095-8 2011 Furthermore BTZO-15 reduced the ulcerated area and rectal MPO activity in 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis rats without affecting rectal TNF-alpha levels. Trinitrobenzenesulfonic Acid 74-109 myeloperoxidase Rattus norvegicus 58-61 21853095-8 2011 Furthermore BTZO-15 reduced the ulcerated area and rectal MPO activity in 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis rats without affecting rectal TNF-alpha levels. Trinitrobenzenesulfonic Acid 111-115 myeloperoxidase Rattus norvegicus 58-61 20718942-9 2010 In control, non-inflamed animals, GLP-2 treatment increased the number of VIP expressing neurons per ganglion; in TNBS-treated animals, GLP-2 prevented an inflammation-induced reduction in the numbers of VIP expressing neurons per ganglion. Trinitrobenzenesulfonic Acid 114-118 mast cell protease 10 Rattus norvegicus 136-141 20889569-3 2010 We found increased mRNA expression levels of collagen, vimentin, and the fibrogenic factors transforming growth factor beta1 and insulin-like growth factor 1 in the chronically inflamed colons of WT mice treated with repeated intracolonic TNBS administrations. Trinitrobenzenesulfonic Acid 239-243 insulin-like growth factor 1 Mus musculus 73-157 20889569-5 2010 Treatment of TNBS-exposed WT mice with the NK-1R antagonist CJ-12255 reduced colonic inflammation, colonic fibrosis, fibroblast accumulation, and expression levels of the fibrogenic factors. Trinitrobenzenesulfonic Acid 13-17 tachykinin receptor 1 Mus musculus 43-48 20889569-6 2010 NK-1R knockout mice chronically exposed to TNBS had similar colonic inflammation compared with WT, but reduced colonic fibrosis, fibroblast accumulation, and expression levels of fibrogenic factors. Trinitrobenzenesulfonic Acid 43-47 tachykinin receptor 1 Mus musculus 0-5 19932037-3 2010 In the present study, 2,4,6-trinitrobenzene sulfonic acid (TNBS) was administered to heterozygous (BDNF(+/-)) knock-out and wild-type (BDNF(+/+)) mice to induce colitis. Trinitrobenzenesulfonic Acid 22-57 brain derived neurotrophic factor Mus musculus 99-103 20094779-0 2010 Inhalation of carbon monoxide ameliorates TNBS-induced colitis in mice through the inhibition of TNF-alpha expression. Trinitrobenzenesulfonic Acid 42-46 tumor necrosis factor Mus musculus 97-106 20501335-6 2010 Likewise, TNBS colitis triggered 15.8-fold up-regulation of SP mRNA 1 month after TNBS (n=5, p <= 0.05). Trinitrobenzenesulfonic Acid 10-14 tachykinin precursor 1 Homo sapiens 60-62 20501335-7 2010 Desensitization of colonic TRPV1 receptors prior to TNBS abolished SP increase in the urinary bladder. Trinitrobenzenesulfonic Acid 52-56 tachykinin precursor 1 Homo sapiens 67-69 20627999-6 2010 Results demonstrated that preadministration of rifaximin ameliorated the clinical hallmarks of colitis in DSS- and TNBS-treated hPXR mice as determined by body weight loss and assessment of diarrhea, rectal bleeding, colon length, and histology. Trinitrobenzenesulfonic Acid 115-119 nuclear receptor subfamily 1 group I member 2 Homo sapiens 128-132 20339899-5 2010 RESULTS: Total deficiency of PAR(2) resulted in a marked reduction in severity of both TNBS and DSS induced colitis as assessed by MPO activity, macroscopic damage, bowel thickness, and leukocyte adherence. Trinitrobenzenesulfonic Acid 87-91 coagulation factor II (thrombin) receptor-like 1 Mus musculus 29-35 20647696-6 2010 A randomized phase II trial comparing gemcitabine and carboplatin(GC)to GC plus BSI-201(PARP inhibitor)in patients with metastatic TNB cancer showed significantly longer progression-free survival and overall survival. Trinitrobenzenesulfonic Acid 131-134 collagen type XI alpha 2 chain Homo sapiens 88-92 20546811-8 2010 The tumor necrosis factor-alpha, interleukin-6, and nitric oxide synthase 2 mRNA content of both liver and skeletal muscle was increased in TNBS-treated mice; and plasma tumor necrosis factor-alpha and interleukin-6 concentrations were also elevated. Trinitrobenzenesulfonic Acid 140-144 tumor necrosis factor Mus musculus 4-31 20546811-8 2010 The tumor necrosis factor-alpha, interleukin-6, and nitric oxide synthase 2 mRNA content of both liver and skeletal muscle was increased in TNBS-treated mice; and plasma tumor necrosis factor-alpha and interleukin-6 concentrations were also elevated. Trinitrobenzenesulfonic Acid 140-144 interleukin 6 Mus musculus 33-46 20546811-8 2010 The tumor necrosis factor-alpha, interleukin-6, and nitric oxide synthase 2 mRNA content of both liver and skeletal muscle was increased in TNBS-treated mice; and plasma tumor necrosis factor-alpha and interleukin-6 concentrations were also elevated. Trinitrobenzenesulfonic Acid 140-144 tumor necrosis factor Mus musculus 170-197 20546811-8 2010 The tumor necrosis factor-alpha, interleukin-6, and nitric oxide synthase 2 mRNA content of both liver and skeletal muscle was increased in TNBS-treated mice; and plasma tumor necrosis factor-alpha and interleukin-6 concentrations were also elevated. Trinitrobenzenesulfonic Acid 140-144 interleukin 6 Mus musculus 202-215 20546811-9 2010 These data suggest that TNBS-induced colitis is independent of a change in muscle protein synthesis but dependent on stimulation of protein degradation via increased expression of muscle-specific atrogenes, which may be mediated in part by the reduction in circulating concentration of IGF-I and the concomitant increase in inflammatory mediators observed in the blood and muscle per se. Trinitrobenzenesulfonic Acid 24-28 insulin-like growth factor 1 Mus musculus 286-291 20469967-0 2010 Exosomes derived from interleukin-10-treated dendritic cells can inhibit trinitrobenzene sulfonic acid-induced rat colitis. Trinitrobenzenesulfonic Acid 73-102 interleukin 10 Rattus norvegicus 22-36 20469967-3 2010 Based on the essential role of IL-10 in the development of normal mucosal immunity, we investigated whether exosomes derived from DCs treated with IL-10 (known as IL-10-exosomes) can suppress the trinitrobenzene sulfonic acid (TNBS)-induced colitis. Trinitrobenzenesulfonic Acid 196-225 interleukin 10 Rattus norvegicus 163-177 20469967-3 2010 Based on the essential role of IL-10 in the development of normal mucosal immunity, we investigated whether exosomes derived from DCs treated with IL-10 (known as IL-10-exosomes) can suppress the trinitrobenzene sulfonic acid (TNBS)-induced colitis. Trinitrobenzenesulfonic Acid 227-231 interleukin 10 Rattus norvegicus 163-177 19932037-3 2010 In the present study, 2,4,6-trinitrobenzene sulfonic acid (TNBS) was administered to heterozygous (BDNF(+/-)) knock-out and wild-type (BDNF(+/+)) mice to induce colitis. Trinitrobenzenesulfonic Acid 59-63 brain derived neurotrophic factor Mus musculus 99-103 19932037-6 2010 In inflammatory state of colitis, TNBS induced upregulation of BDNF in dorsal root ganglia of both genotypes while BDNF(+/-) mice showing significantly lower sensitivity in the colon at 30 mm Hg and lower sensitivity in bladder than BDNF(+/+) mice. Trinitrobenzenesulfonic Acid 34-38 brain derived neurotrophic factor Mus musculus 63-67 20210978-4 2010 METHODS: Three daily enemas containing 2,4,6-trinitrobenzene sulfonic acid (TNBS), which were given to rats produced chronic colitis and ongoing activation of Fos in brain neurons. Trinitrobenzenesulfonic Acid 39-74 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 159-162 20338922-9 2010 In vivo, nNOS axon number was reduced threefold by day 1 of trinitrobenzene sulfonic acid-induced rat colitis, preceding the hyperplasia of ISMC described earlier in this model. Trinitrobenzenesulfonic Acid 60-89 nitric oxide synthase 1 Rattus norvegicus 9-13 19924805-2 2010 We sought to investigate whether targeting transforming growth factor-beta1 (TGF-beta1), a key profibrotic mediator, with a peptide-based virus-like particle vaccine would be effective in suppressing intestinal fibrosis by using a mouse model of 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced chronic colitis. Trinitrobenzenesulfonic Acid 283-287 transforming growth factor, beta 1 Mus musculus 77-86 20187766-0 2010 All-trans retinoic acid ameliorates trinitrobenzene sulfonic acid-induced colitis by shifting Th1 to Th2 profile. Trinitrobenzenesulfonic Acid 36-65 negative elongation factor complex member C/D, Th1l Mus musculus 94-97 20187766-0 2010 All-trans retinoic acid ameliorates trinitrobenzene sulfonic acid-induced colitis by shifting Th1 to Th2 profile. Trinitrobenzenesulfonic Acid 36-65 heart and neural crest derivatives expressed 2 Mus musculus 101-104 20361960-0 2010 Cyclooxygenase-2 inhibitors prevent trinitrobenzene sulfonic acid-induced P-glycoprotein up-regulation in vitro and in vivo. Trinitrobenzenesulfonic Acid 36-65 prostaglandin-endoperoxide synthase 2 Homo sapiens 0-16 20361960-0 2010 Cyclooxygenase-2 inhibitors prevent trinitrobenzene sulfonic acid-induced P-glycoprotein up-regulation in vitro and in vivo. Trinitrobenzenesulfonic Acid 36-65 ATP binding cassette subfamily B member 1 Homo sapiens 74-88 20361960-4 2010 Since COX-2 isoform is overexpressed in colic inflammatory states, we examined the inhibitory effect of COX-2-inhibitors on P-gp expression and function under COX-2 stimulated conditions mediated by trinitrobenzene sulfonic acid (TNBS) in vitro, in Caco-2 cells, and in TNBS-induced colitis in mice. Trinitrobenzenesulfonic Acid 199-228 mitochondrially encoded cytochrome c oxidase II Homo sapiens 104-109 20361960-4 2010 Since COX-2 isoform is overexpressed in colic inflammatory states, we examined the inhibitory effect of COX-2-inhibitors on P-gp expression and function under COX-2 stimulated conditions mediated by trinitrobenzene sulfonic acid (TNBS) in vitro, in Caco-2 cells, and in TNBS-induced colitis in mice. Trinitrobenzenesulfonic Acid 199-228 ATP binding cassette subfamily B member 1 Homo sapiens 124-128 20361960-4 2010 Since COX-2 isoform is overexpressed in colic inflammatory states, we examined the inhibitory effect of COX-2-inhibitors on P-gp expression and function under COX-2 stimulated conditions mediated by trinitrobenzene sulfonic acid (TNBS) in vitro, in Caco-2 cells, and in TNBS-induced colitis in mice. Trinitrobenzenesulfonic Acid 199-228 mitochondrially encoded cytochrome c oxidase II Homo sapiens 104-109 20361960-7 2010 We showed that COX-2 stimulation in Caco-2 cells by 0.1mM TNBS exposure for 24h induced P-gp protein expression and activity. Trinitrobenzenesulfonic Acid 58-62 mitochondrially encoded cytochrome c oxidase II Homo sapiens 15-20 20361960-7 2010 We showed that COX-2 stimulation in Caco-2 cells by 0.1mM TNBS exposure for 24h induced P-gp protein expression and activity. Trinitrobenzenesulfonic Acid 58-62 ATP binding cassette subfamily B member 1 Homo sapiens 88-92 20363741-9 2010 Transforming growth factor (TGF)-beta1, a known inducer of EMT in epithelial cells, induces EMT in rat intestinal epithelial cells in vitro, and bone morphogenic protein-7, an antagonist of TGF-beta1, inhibits EMT and fibrosis both in vitro and in the TNBS-treated mice. Trinitrobenzenesulfonic Acid 252-256 transforming growth factor, beta 1 Rattus norvegicus 0-38 20701071-6 2010 On the third day, all the blood values increased in MT1 (1 and 2 mg/kg) and MT2 (1 and 2 mg/kg) in the TNBS-administered groups. Trinitrobenzenesulfonic Acid 103-107 metallothionein 2A Rattus norvegicus 52-64 20701071-6 2010 On the third day, all the blood values increased in MT1 (1 and 2 mg/kg) and MT2 (1 and 2 mg/kg) in the TNBS-administered groups. Trinitrobenzenesulfonic Acid 103-107 metallothionein 2A Rattus norvegicus 76-88 20628432-8 2010 Thus, endothelins contribute importantly to abdominal and hind paw referred mechanical hyperalgesia during TNBS-induced colitis mainly through ETA receptor-signaled mechanisms. Trinitrobenzenesulfonic Acid 107-111 endothelin receptor type A Mus musculus 143-146 20210978-4 2010 METHODS: Three daily enemas containing 2,4,6-trinitrobenzene sulfonic acid (TNBS), which were given to rats produced chronic colitis and ongoing activation of Fos in brain neurons. Trinitrobenzenesulfonic Acid 76-80 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 159-162 19924809-8 2010 Serum LBP increased in WT mice following TNBS administration, in conjunction with increased serum TNF-alpha, IL-6, and IL-10, and expansion of regulatory T-cell numbers. Trinitrobenzenesulfonic Acid 41-45 lipopolysaccharide binding protein Mus musculus 6-9 20149842-10 2010 Real-time RT-PCR indicated that GFAP expression was significantly increased in TNBS treated rats compared to the sham group. Trinitrobenzenesulfonic Acid 79-83 glial fibrillary acidic protein Rattus norvegicus 32-36 19924809-8 2010 Serum LBP increased in WT mice following TNBS administration, in conjunction with increased serum TNF-alpha, IL-6, and IL-10, and expansion of regulatory T-cell numbers. Trinitrobenzenesulfonic Acid 41-45 tumor necrosis factor Mus musculus 98-107 19882302-2 2010 METHODS: We measured the ability of lactic acid bacteria (LAB) to inhibit lipid peroxidation in vitro and to inhibit colitis outcomes, colon shortening, and myeloperoxidase activity in TNBS-induced colitis in C3H/HeN and C3H/HeJ mice. Trinitrobenzenesulfonic Acid 185-189 myeloperoxidase Mus musculus 157-172 19924809-8 2010 Serum LBP increased in WT mice following TNBS administration, in conjunction with increased serum TNF-alpha, IL-6, and IL-10, and expansion of regulatory T-cell numbers. Trinitrobenzenesulfonic Acid 41-45 interleukin 6 Mus musculus 109-113 19924809-8 2010 Serum LBP increased in WT mice following TNBS administration, in conjunction with increased serum TNF-alpha, IL-6, and IL-10, and expansion of regulatory T-cell numbers. Trinitrobenzenesulfonic Acid 41-45 interleukin 10 Mus musculus 119-124 19956958-5 2010 RESULT: Intrarectal treatment of TNBS in mice caused colon shortening and also increased colonic expression of IL-1beta, IL-6, and TNF-alpha expression. Trinitrobenzenesulfonic Acid 33-37 interleukin 1 beta Mus musculus 111-119 19956958-5 2010 RESULT: Intrarectal treatment of TNBS in mice caused colon shortening and also increased colonic expression of IL-1beta, IL-6, and TNF-alpha expression. Trinitrobenzenesulfonic Acid 33-37 interleukin 6 Mus musculus 121-125 19956958-5 2010 RESULT: Intrarectal treatment of TNBS in mice caused colon shortening and also increased colonic expression of IL-1beta, IL-6, and TNF-alpha expression. Trinitrobenzenesulfonic Acid 33-37 tumor necrosis factor Mus musculus 131-140 20118800-11 2010 In contrast, IL-13 and IL-17 were consistently elevated after administration of TNBS to the colon of young rats. Trinitrobenzenesulfonic Acid 80-84 interleukin 13 Rattus norvegicus 13-18 20181893-4 2010 In the murine trinitrobenzene sulfonic acid model of colitis, inhibition of this enzyme leads to worsened disease severity, suggesting that IDO acts as a natural break in limiting colitis. Trinitrobenzenesulfonic Acid 14-43 indoleamine 2,3-dioxygenase 1 Mus musculus 140-143 20181893-9 2010 Using both the trinitrobenzene sulfonic acid and dextran sodium sulfate models of colitis, we show the importance of IDO-1s induction in limiting colitis severity. Trinitrobenzenesulfonic Acid 15-44 indoleamine 2,3-dioxygenase 1 Homo sapiens 117-122 20118800-11 2010 In contrast, IL-13 and IL-17 were consistently elevated after administration of TNBS to the colon of young rats. Trinitrobenzenesulfonic Acid 80-84 interleukin 17A Rattus norvegicus 23-28 20228420-0 2010 Mice lacking cannabinoid CB1-, CB2-receptors or both receptors show increased susceptibility to trinitrobenzene sulfonic acid (TNBS)-induced colitis. Trinitrobenzenesulfonic Acid 96-125 cannabinoid receptor 1 (brain) Mus musculus 25-28 19706070-8 2010 In wild type (wt) and GC-C null mice, the instillation of TNBS induced similar hyperalgesia and allodynia. Trinitrobenzenesulfonic Acid 58-62 guanylate cyclase 2c Mus musculus 22-26 20143464-1 2010 AIM: To investigate the expression of microRNA155 (miRNA155) in trinitrobenzene sulphonic acid (TNBS)-induced colitis and the relationship between miRNA155 and tumor necrosis factor (TNF) expressions. Trinitrobenzenesulfonic Acid 96-100 microRNA 155 Mus musculus 38-49 20143464-1 2010 AIM: To investigate the expression of microRNA155 (miRNA155) in trinitrobenzene sulphonic acid (TNBS)-induced colitis and the relationship between miRNA155 and tumor necrosis factor (TNF) expressions. Trinitrobenzenesulfonic Acid 96-100 microRNA 155 Mus musculus 51-59 20228420-0 2010 Mice lacking cannabinoid CB1-, CB2-receptors or both receptors show increased susceptibility to trinitrobenzene sulfonic acid (TNBS)-induced colitis. Trinitrobenzenesulfonic Acid 96-125 cannabinoid receptor 2 (macrophage) Mus musculus 31-34 20228420-0 2010 Mice lacking cannabinoid CB1-, CB2-receptors or both receptors show increased susceptibility to trinitrobenzene sulfonic acid (TNBS)-induced colitis. Trinitrobenzenesulfonic Acid 127-131 cannabinoid receptor 1 (brain) Mus musculus 25-28 20228420-0 2010 Mice lacking cannabinoid CB1-, CB2-receptors or both receptors show increased susceptibility to trinitrobenzene sulfonic acid (TNBS)-induced colitis. Trinitrobenzenesulfonic Acid 127-131 cannabinoid receptor 2 (macrophage) Mus musculus 31-34 20080610-5 2010 We found that inhibition of KCa3.1(-/-) protected mice from developing severe colitis in two mouse models of inflammatory bowel disease, which were induced by (i) the adoptive transfer of mouse naive CD4 T cells into rag2(-/-) recipients and (ii) trinitrobenzene sulfonic acid. Trinitrobenzenesulfonic Acid 247-276 potassium intermediate/small conductance calcium-activated channel, subfamily N, member 4 Mus musculus 28-34 20181058-4 2010 RESULTS: DSS and TNBS induced the protein expression of TLR-4 and activated transcription factor NF-kappaB. Trinitrobenzenesulfonic Acid 17-21 toll-like receptor 4 Mus musculus 56-61 20181058-4 2010 RESULTS: DSS and TNBS induced the protein expression of TLR-4 and activated transcription factor NF-kappaB. Trinitrobenzenesulfonic Acid 17-21 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 97-106 20181058-8 2010 DSS and TNBS increased lipid peroxide (malondialdehyde) and 4-hydroxy-2-nonenal content in the colon, but reduced glutathione content and superoxide dismutase and catalase activities. Trinitrobenzenesulfonic Acid 8-12 catalase Mus musculus 163-171 20181058-12 2010 DISCUSSION: These findings suggest that DSS and TNBS may cause colitis by inducing lipid peroxidation and enterobacterial proliferation, which may deteriorate the colitis by regulating proinflammatory cytokines via TLR-4-linked NF-kappaB activation pathway. Trinitrobenzenesulfonic Acid 48-52 toll-like receptor 4 Mus musculus 215-220 20181058-12 2010 DISCUSSION: These findings suggest that DSS and TNBS may cause colitis by inducing lipid peroxidation and enterobacterial proliferation, which may deteriorate the colitis by regulating proinflammatory cytokines via TLR-4-linked NF-kappaB activation pathway. Trinitrobenzenesulfonic Acid 48-52 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 228-237 19875705-8 2010 TNBS-induced colitis increased in VMR to CRD and induced c-fos in spinal neurons in trpa1(+/+) but not in trpa1(-/-) mice. Trinitrobenzenesulfonic Acid 0-4 FBJ osteosarcoma oncogene Mus musculus 57-62 19875705-8 2010 TNBS-induced colitis increased in VMR to CRD and induced c-fos in spinal neurons in trpa1(+/+) but not in trpa1(-/-) mice. Trinitrobenzenesulfonic Acid 0-4 transient receptor potential cation channel, subfamily A, member 1 Mus musculus 84-89 19051017-1 2009 Anti-inflammatory effects of short-chain inulin-like fructans (SCF) on trinitrobenzene sulfonic acid (TNBS)-induced colitis were investigated in rats, focusing specifically on endotoxin and bacterial translocations. Trinitrobenzenesulfonic Acid 71-100 KIT ligand Rattus norvegicus 29-61 19733696-7 2009 In conclusion, Si-Ni-San and glycyrrhizin significantly ameliorated TNBS-induced colitis in mice through regulating pro- and anti-inflammatory cytokine production. Trinitrobenzenesulfonic Acid 68-72 N(alpha)-acetyltransferase 50, NatE catalytic subunit Mus musculus 21-24 20136961-8 2009 A highly significant elevation of IFN-gamma and TNF-alpha were observed in the TNBS-induced colitis group. Trinitrobenzenesulfonic Acid 79-83 interferon gamma Mus musculus 34-43 20136961-8 2009 A highly significant elevation of IFN-gamma and TNF-alpha were observed in the TNBS-induced colitis group. Trinitrobenzenesulfonic Acid 79-83 tumor necrosis factor Mus musculus 48-57 20136961-12 2009 TLR4 expression was elevated after injected with TNBS and was downregulated in the eggs group. Trinitrobenzenesulfonic Acid 49-53 toll-like receptor 4 Mus musculus 0-4 21062534-4 2010 In fact, it has been demonstrated that the activation of HO-1 may act as an endogenous defensive mechanism to reduce inflammation and tissue injury in various animal intestinal injury models induced by ischemia-reperfusion, indomethacin, lipopolysaccharide-associated sepsis, trinitrobenzene sulfonic acid or dextran sulfate sodium. Trinitrobenzenesulfonic Acid 276-305 heme oxygenase 1 Homo sapiens 57-61 20090409-6 2010 Betamethasone and, to a lesser extent, tacrolimus led to a marked reduction of chemical-induced IL-8 expression by TNBS and CAld. Trinitrobenzenesulfonic Acid 115-119 C-X-C motif chemokine ligand 8 Homo sapiens 96-100 19661154-6 2009 Induction of inflammation by a subthreshold dose of 17 mg/kg trinitrobenzene sulfonic acid (TNBS) in rats moderately decreased muscularis externa concentration of VIP, and it had little effect on the contractile response of circular smooth muscle strips to ACh. Trinitrobenzenesulfonic Acid 61-90 vasoactive intestinal peptide Rattus norvegicus 163-166 19661154-6 2009 Induction of inflammation by a subthreshold dose of 17 mg/kg trinitrobenzene sulfonic acid (TNBS) in rats moderately decreased muscularis externa concentration of VIP, and it had little effect on the contractile response of circular smooth muscle strips to ACh. Trinitrobenzenesulfonic Acid 92-96 vasoactive intestinal peptide Rattus norvegicus 163-166 19661154-8 2009 The induction of more severe inflammation by 68 mg/kg TNBS induced marked suppression of colonic circular muscle contractility and decrease in serum VIP. Trinitrobenzenesulfonic Acid 54-58 vasoactive intestinal peptide Homo sapiens 149-152 19560465-4 2009 METHODS: Foxo4-null mice were subjected to trinitrobenzene sulfonic acid (TNBS) treatment. Trinitrobenzenesulfonic Acid 43-72 forkhead box O4 Mus musculus 9-14 19560465-4 2009 METHODS: Foxo4-null mice were subjected to trinitrobenzene sulfonic acid (TNBS) treatment. Trinitrobenzenesulfonic Acid 74-78 forkhead box O4 Mus musculus 9-14 19560465-13 2009 FoxO4 transcription is transiently repressed in response to TNBS treatment and in patients with IBD. Trinitrobenzenesulfonic Acid 60-64 forkhead box O4 Homo sapiens 0-5 19051017-1 2009 Anti-inflammatory effects of short-chain inulin-like fructans (SCF) on trinitrobenzene sulfonic acid (TNBS)-induced colitis were investigated in rats, focusing specifically on endotoxin and bacterial translocations. Trinitrobenzenesulfonic Acid 71-100 KIT ligand Rattus norvegicus 63-66 19051017-1 2009 Anti-inflammatory effects of short-chain inulin-like fructans (SCF) on trinitrobenzene sulfonic acid (TNBS)-induced colitis were investigated in rats, focusing specifically on endotoxin and bacterial translocations. Trinitrobenzenesulfonic Acid 102-106 KIT ligand Rattus norvegicus 63-66 19693649-5 2009 Upon treatment with hyper-IL-6, IRF4(-/-) mice lost their protective properties towards TNBS application. Trinitrobenzenesulfonic Acid 88-92 interleukin 6 Mus musculus 26-30 19693649-5 2009 Upon treatment with hyper-IL-6, IRF4(-/-) mice lost their protective properties towards TNBS application. Trinitrobenzenesulfonic Acid 88-92 interferon regulatory factor 4 Mus musculus 32-36 19703989-4 2009 We first show that mucosal CD103(-) DCs selectively express SIRPalpha and that their frequency was augmented in the lamina propria and mLNs of mice that developed Th17-biased colitis in response to trinitrobenzene sulfonic acid. Trinitrobenzenesulfonic Acid 198-227 integrin alpha E, epithelial-associated Mus musculus 27-32 19703989-4 2009 We first show that mucosal CD103(-) DCs selectively express SIRPalpha and that their frequency was augmented in the lamina propria and mLNs of mice that developed Th17-biased colitis in response to trinitrobenzene sulfonic acid. Trinitrobenzenesulfonic Acid 198-227 signal-regulatory protein alpha Mus musculus 60-69 19505427-12 2009 IL-25 ameliorated TNBS- and oxazolone-colitis. Trinitrobenzenesulfonic Acid 18-22 interleukin 25 Homo sapiens 0-5 19597321-5 2009 LAB also blocked activation of the transcription factor, NF-kappaB, and expression of TLR-4 induced by TNBS. Trinitrobenzenesulfonic Acid 103-107 toll-like receptor 4 Mus musculus 86-91 19239624-10 2009 These findings suggest that the TNBS evoked increase in Na(v) 1.8 currents is associated with increased numbers of channels. Trinitrobenzenesulfonic Acid 32-36 sodium channel, voltage-gated, type X, alpha Mus musculus 56-65 19492815-6 2009 AChE inhibitors, including paraoxon and aflatoxin B1, were detected successfully using this sensor by measuring the residual activity of AChE on paper, using Ellman"s colorimetric assay, with capture of the 5-thio-2-nitrobenzoate (TNB(-)) product on the PVAm layer. Trinitrobenzenesulfonic Acid 231-234 acetylcholinesterase (Cartwright blood group) Homo sapiens 0-4 19492815-6 2009 AChE inhibitors, including paraoxon and aflatoxin B1, were detected successfully using this sensor by measuring the residual activity of AChE on paper, using Ellman"s colorimetric assay, with capture of the 5-thio-2-nitrobenzoate (TNB(-)) product on the PVAm layer. Trinitrobenzenesulfonic Acid 231-234 acetylcholinesterase (Cartwright blood group) Homo sapiens 137-141 19525396-7 2009 Anti-CD70 Ab treatment also suppressed trinitrobenzene sulfonic acid-induced colitis in SJL/J mice. Trinitrobenzenesulfonic Acid 39-68 CD70 antigen Mus musculus 5-9 19696546-12 2009 But, the number of myofibroblasts stained with vimentin and SMA in both control and TNBS group was smaller than that in BMT group. Trinitrobenzenesulfonic Acid 84-88 vimentin Mus musculus 47-55 19696546-12 2009 But, the number of myofibroblasts stained with vimentin and SMA in both control and TNBS group was smaller than that in BMT group. Trinitrobenzenesulfonic Acid 84-88 immunoglobulin mu binding protein 2 Mus musculus 60-63 19359426-7 2009 Basal IGF-I receptor phosphorylation in inflamed muscle from TNBS-treated rats was increased by 86 +/- 8% over vehicle-treated controls. Trinitrobenzenesulfonic Acid 61-65 insulin-like growth factor 1 receptor Rattus norvegicus 6-20 19359426-8 2009 Basal ERK1/2, p70S6 kinase, and GSK-3beta phosphorylation in muscle cells of TNBS-treated rats were also increased by 140-180%. Trinitrobenzenesulfonic Acid 77-81 mitogen activated protein kinase 3 Rattus norvegicus 6-12 19359426-8 2009 Basal ERK1/2, p70S6 kinase, and GSK-3beta phosphorylation in muscle cells of TNBS-treated rats were also increased by 140-180%. Trinitrobenzenesulfonic Acid 77-81 glycogen synthase kinase 3 beta Rattus norvegicus 32-41 19443690-4 2009 TNBS-induced inflammation in the colon increases NT and NTR1 expression in mesenteric adipose tissues, including mesenteric preadipocytes. Trinitrobenzenesulfonic Acid 0-4 neurotensin receptor 1 Mus musculus 56-60 19617644-12 2009 The protein expression for PPARgamma, which was down-regulated in rat colonic mucosa after exposure to TNBS as compared to that in intact colonic mucosa, was not significantly influenced by ghrelin treatment. Trinitrobenzenesulfonic Acid 103-107 peroxisome proliferator-activated receptor gamma Rattus norvegicus 27-36 19443690-10 2009 We also found that supernatants from NT-exposed 3T3-L1-NTR1 preadipocytes and mesenteric fat obtained from wild-type mice 2 days after TNBS administration stimulate an IL-6-dependent macrophage migration measured by a macrophage migration assay, whereas this response is reduced when mesenteric fat from NT KO mice is used. Trinitrobenzenesulfonic Acid 135-139 neurotensin Mus musculus 37-39 19443690-10 2009 We also found that supernatants from NT-exposed 3T3-L1-NTR1 preadipocytes and mesenteric fat obtained from wild-type mice 2 days after TNBS administration stimulate an IL-6-dependent macrophage migration measured by a macrophage migration assay, whereas this response is reduced when mesenteric fat from NT KO mice is used. Trinitrobenzenesulfonic Acid 135-139 interleukin 6 Mus musculus 168-172 19193812-9 2009 Ileal mucosa was sampled for mucin fractional synthesis rate measurement, which was greater in the TNBS-treated group (114 +/- 15%/d) than in the control group (61 +/- 8%/d) (P = 0.021). Trinitrobenzenesulfonic Acid 99-103 LOC100508689 Homo sapiens 29-34 19220658-8 2009 Trinitrobenzene sulfonic acid-induced expression of TNF-alpha and IL-1beta was reduced by muscovite and 5-ASA treatment. Trinitrobenzenesulfonic Acid 0-29 tumor necrosis factor Rattus norvegicus 52-61 19220658-8 2009 Trinitrobenzene sulfonic acid-induced expression of TNF-alpha and IL-1beta was reduced by muscovite and 5-ASA treatment. Trinitrobenzenesulfonic Acid 0-29 interleukin 1 beta Rattus norvegicus 66-74 19109523-8 2009 Results from Western blot and real-time PCR indicated that NHE8 protein and mRNA were significantly reduced in TNBS rats and LPS rats. Trinitrobenzenesulfonic Acid 111-115 solute carrier family 9 member A8 Rattus norvegicus 59-63 19238344-5 2009 The upregulation of WISP-1 was positively correlated with iNOS expression in two models of colitis, induced by intrarectal trinitrobenzenesulfonic acid (TNBS) or occurring spontaneously in IL-10 deficient mice. Trinitrobenzenesulfonic Acid 123-151 cellular communication network factor 4 Mus musculus 20-26 19238344-5 2009 The upregulation of WISP-1 was positively correlated with iNOS expression in two models of colitis, induced by intrarectal trinitrobenzenesulfonic acid (TNBS) or occurring spontaneously in IL-10 deficient mice. Trinitrobenzenesulfonic Acid 123-151 nitric oxide synthase 2, inducible Mus musculus 58-62 19238344-5 2009 The upregulation of WISP-1 was positively correlated with iNOS expression in two models of colitis, induced by intrarectal trinitrobenzenesulfonic acid (TNBS) or occurring spontaneously in IL-10 deficient mice. Trinitrobenzenesulfonic Acid 153-157 cellular communication network factor 4 Mus musculus 20-26 19238344-5 2009 The upregulation of WISP-1 was positively correlated with iNOS expression in two models of colitis, induced by intrarectal trinitrobenzenesulfonic acid (TNBS) or occurring spontaneously in IL-10 deficient mice. Trinitrobenzenesulfonic Acid 153-157 nitric oxide synthase 2, inducible Mus musculus 58-62 19238344-6 2009 Loss of iNOS, studied using iNOS(-/-) mice in both TNBS-induced and IL-10(-/-) colitis models, significantly attenuated the colitis-related WISP-1 increase. Trinitrobenzenesulfonic Acid 51-55 nitric oxide synthase 2, inducible Mus musculus 8-12 19238529-3 2009 The main aims of this study is to evaluate effects of intraperitoneal injection recombinant human TFF3 on the expression of tumour necrosis factor alpha (TNF-alpha), toll-like receptor 4(TLR4), and nuclear factor kappaB (NF-kappaB) in trinitrobenzene sulphonic acid (TNBS) induced colitis mice. Trinitrobenzenesulfonic Acid 267-271 trefoil factor 3 Homo sapiens 98-102 19238529-7 2009 Once daily application of hTFF3 for 5 days after TNBS/ethanol had been injected, both microscopic and macroscopic injury and inflammatory index had been reduced compared with controls. Trinitrobenzenesulfonic Acid 49-53 trefoil factor 3 Homo sapiens 26-31 19095763-6 2009 Intestinal myeloperoxidase and histamine levels were significantly increased, whereas the survival rate and state of health were significantly decreased in TNBS-treated mice that lacked SERT. Trinitrobenzenesulfonic Acid 156-160 solute carrier family 6 (neurotransmitter transporter, serotonin), member 4 Mus musculus 186-190 19109523-12 2009 In conclusion, our studies suggest that TNF-alpha decreases NHE8 expression in inflammation induced by TNBS and LPS, which may contribute to the diarrhea associated with inflammation. Trinitrobenzenesulfonic Acid 103-107 tumor necrosis factor Homo sapiens 40-49 19109523-12 2009 In conclusion, our studies suggest that TNF-alpha decreases NHE8 expression in inflammation induced by TNBS and LPS, which may contribute to the diarrhea associated with inflammation. Trinitrobenzenesulfonic Acid 103-107 solute carrier family 9 member A8 Homo sapiens 60-64 19050899-6 2009 Intrarectal treatment of TNBS in mice caused colon shortening and also increased colonic expression of IL-1beta, IL-6, and TNF-alpha expression. Trinitrobenzenesulfonic Acid 25-29 interleukin 1 beta Mus musculus 103-111 19109961-4 2009 METHODS: The 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis model was conducted in TWEAK- or Fn14-deficient mice or in normal mice treated with a TWEAK-blocking monoclonal antibody, and clinical severity, histopathology, immunohistochemistry for cell infiltrates, TWEAK and Fn14, gene expression profiling in the colon, and systemic adaptive immunity were assessed. Trinitrobenzenesulfonic Acid 13-48 tumor necrosis factor (ligand) superfamily, member 12 Mus musculus 95-100 19109961-4 2009 METHODS: The 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis model was conducted in TWEAK- or Fn14-deficient mice or in normal mice treated with a TWEAK-blocking monoclonal antibody, and clinical severity, histopathology, immunohistochemistry for cell infiltrates, TWEAK and Fn14, gene expression profiling in the colon, and systemic adaptive immunity were assessed. Trinitrobenzenesulfonic Acid 13-48 tumor necrosis factor receptor superfamily, member 12a Mus musculus 105-109 19109961-4 2009 METHODS: The 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis model was conducted in TWEAK- or Fn14-deficient mice or in normal mice treated with a TWEAK-blocking monoclonal antibody, and clinical severity, histopathology, immunohistochemistry for cell infiltrates, TWEAK and Fn14, gene expression profiling in the colon, and systemic adaptive immunity were assessed. Trinitrobenzenesulfonic Acid 50-54 tumor necrosis factor (ligand) superfamily, member 12 Mus musculus 95-100 19109961-4 2009 METHODS: The 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis model was conducted in TWEAK- or Fn14-deficient mice or in normal mice treated with a TWEAK-blocking monoclonal antibody, and clinical severity, histopathology, immunohistochemistry for cell infiltrates, TWEAK and Fn14, gene expression profiling in the colon, and systemic adaptive immunity were assessed. Trinitrobenzenesulfonic Acid 50-54 tumor necrosis factor receptor superfamily, member 12a Mus musculus 105-109 19109961-8 2009 Neutrophil and macrophage infiltrates, chemokines, cytokines, and matrix metalloproteinase expression were reduced in the TWEAK-deficient colon after TNBS administration; however, systemic adaptive immune responses to trinitrophenyl were not altered. Trinitrobenzenesulfonic Acid 150-154 tumor necrosis factor (ligand) superfamily, member 12 Mus musculus 122-127 19196500-10 2009 The TNBS-induced increase in the TNFalpha-mRNA expression was suppressed by STW 5 but not by STW 6. Trinitrobenzenesulfonic Acid 4-8 tumor necrosis factor Rattus norvegicus 33-41 19200168-0 2009 Smad3 loss confers resistance to the development of trinitrobenzene sulfonic acid-induced colorectal fibrosis. Trinitrobenzenesulfonic Acid 52-81 SMAD family member 3 Mus musculus 0-5 19200168-2 2009 The aim of this study was to evaluate the potential role of Smad3 in the pathogenesis of colonic fibrosis induced by trinitrobenzene sulfonic acid (TNBS) in Smad3 null mice. Trinitrobenzenesulfonic Acid 117-146 SMAD family member 3 Mus musculus 60-65 19200168-2 2009 The aim of this study was to evaluate the potential role of Smad3 in the pathogenesis of colonic fibrosis induced by trinitrobenzene sulfonic acid (TNBS) in Smad3 null mice. Trinitrobenzenesulfonic Acid 117-146 SMAD family member 3 Mus musculus 157-162 19200168-2 2009 The aim of this study was to evaluate the potential role of Smad3 in the pathogenesis of colonic fibrosis induced by trinitrobenzene sulfonic acid (TNBS) in Smad3 null mice. Trinitrobenzenesulfonic Acid 148-152 SMAD family member 3 Mus musculus 60-65 19200168-2 2009 The aim of this study was to evaluate the potential role of Smad3 in the pathogenesis of colonic fibrosis induced by trinitrobenzene sulfonic acid (TNBS) in Smad3 null mice. Trinitrobenzenesulfonic Acid 148-152 SMAD family member 3 Mus musculus 157-162 19200168-3 2009 MATERIALS AND METHODS: Chronic colitis-associated fibrosis was induced in 15 Smad3 null and 13 wild-type mice by intra-rectal administration of TNBS. Trinitrobenzenesulfonic Acid 144-148 SMAD family member 3 Mus musculus 77-82 19171847-9 2009 Our data demonstrate that MMP-2 and MMP-9 activities were highly upregulated in wild-type (WT) mice treated with DSS, S.T., or TNBS whereas dKO mice were resistant to the development of colitis. Trinitrobenzenesulfonic Acid 127-131 matrix metallopeptidase 2 Mus musculus 26-31 19171847-9 2009 Our data demonstrate that MMP-2 and MMP-9 activities were highly upregulated in wild-type (WT) mice treated with DSS, S.T., or TNBS whereas dKO mice were resistant to the development of colitis. Trinitrobenzenesulfonic Acid 127-131 matrix metallopeptidase 9 Mus musculus 36-41 19002562-3 2009 In this study, we investigated the effects of curcumin on the expression of TLR-4 and MyD88, the upstream signaling pathway in experimental colitis induced in the Sprague-Dawley male rats by intra-rectal administration of trinitrobenzenesulfonic acid (TNBS). Trinitrobenzenesulfonic Acid 222-250 toll-like receptor 4 Rattus norvegicus 76-81 19002562-3 2009 In this study, we investigated the effects of curcumin on the expression of TLR-4 and MyD88, the upstream signaling pathway in experimental colitis induced in the Sprague-Dawley male rats by intra-rectal administration of trinitrobenzenesulfonic acid (TNBS). Trinitrobenzenesulfonic Acid 222-250 MYD88, innate immune signal transduction adaptor Rattus norvegicus 86-91 19002562-9 2009 TNBS-induced increase in the level of MPO activity and MDA concentrations was reversed by curcumin treatment, whereas the same dose of curcumin did not affect their levels in the non-colitis animals. Trinitrobenzenesulfonic Acid 0-4 myeloperoxidase Rattus norvegicus 38-41 19050899-6 2009 Intrarectal treatment of TNBS in mice caused colon shortening and also increased colonic expression of IL-1beta, IL-6, and TNF-alpha expression. Trinitrobenzenesulfonic Acid 25-29 interleukin 6 Mus musculus 113-117 19050899-6 2009 Intrarectal treatment of TNBS in mice caused colon shortening and also increased colonic expression of IL-1beta, IL-6, and TNF-alpha expression. Trinitrobenzenesulfonic Acid 25-29 tumor necrosis factor Mus musculus 123-132 19050899-8 2009 Lactobacillus HY7801 inhibited the NF-kappaB activation and TLR-4 expression induced by TNBS, as well as the expression of cyclooxygenase 2. Trinitrobenzenesulfonic Acid 88-92 toll-like receptor 4 Mus musculus 60-65 19067146-5 2009 The TNBS treatment caused colon shortening, increased myeloperoxidase activity, induced IL-1beta, TNF-alpha, and IL-6 expression in the colon, activated NF-kappaB, and potentiated the GAG-degrading activities of intestinal microflora. Trinitrobenzenesulfonic Acid 4-8 interleukin 1 beta Mus musculus 88-96 19067146-5 2009 The TNBS treatment caused colon shortening, increased myeloperoxidase activity, induced IL-1beta, TNF-alpha, and IL-6 expression in the colon, activated NF-kappaB, and potentiated the GAG-degrading activities of intestinal microflora. Trinitrobenzenesulfonic Acid 4-8 tumor necrosis factor Mus musculus 98-107 19067146-5 2009 The TNBS treatment caused colon shortening, increased myeloperoxidase activity, induced IL-1beta, TNF-alpha, and IL-6 expression in the colon, activated NF-kappaB, and potentiated the GAG-degrading activities of intestinal microflora. Trinitrobenzenesulfonic Acid 4-8 interleukin 6 Mus musculus 113-117 19028925-7 2009 In the presence of amiloride and PSA (picrylsulfonic acid), pHi recovery was also significantly affected. Trinitrobenzenesulfonic Acid 33-36 glucose-6-phosphate isomerase Homo sapiens 60-63 19028925-7 2009 In the presence of amiloride and PSA (picrylsulfonic acid), pHi recovery was also significantly affected. Trinitrobenzenesulfonic Acid 38-57 glucose-6-phosphate isomerase Homo sapiens 60-63 18831034-1 2008 BACKGROUND: We previously identified a major quantitative trait locus (qtl) on mouse chromosome 9 (Tnbs1) that confers resistance/susceptibility to trinitrobenzene sulfonic acid (TNBS) induced colitis. Trinitrobenzenesulfonic Acid 148-177 tri-nitrobenzene sulfonic acid susceptible 1 Mus musculus 99-104 18687707-3 2009 METHODS: The GH effect upon mucosal injury due to 2,4,6-trinitro-benzenesulfonic acid (TNBS) administration was determined in STAT5b-deficient mice and wild-type (WT) controls. Trinitrobenzenesulfonic Acid 50-85 growth hormone Mus musculus 13-15 18687707-3 2009 METHODS: The GH effect upon mucosal injury due to 2,4,6-trinitro-benzenesulfonic acid (TNBS) administration was determined in STAT5b-deficient mice and wild-type (WT) controls. Trinitrobenzenesulfonic Acid 87-91 growth hormone Mus musculus 13-15 18831034-1 2008 BACKGROUND: We previously identified a major quantitative trait locus (qtl) on mouse chromosome 9 (Tnbs1) that confers resistance/susceptibility to trinitrobenzene sulfonic acid (TNBS) induced colitis. Trinitrobenzenesulfonic Acid 179-183 tri-nitrobenzene sulfonic acid susceptible 1 Mus musculus 99-104 18649083-9 2008 Further, the preventive transfer of wt or IL-10tg gammadelta T cells ameliorated TNBS-induced colitis resulting in prolonged survival and reduced histological damage (1.5+/-0.4 and 1.3+/-0.2, respectively vs. 3.8+/-0.3 in untransferred mice, p<0.05). Trinitrobenzenesulfonic Acid 81-85 interleukin 10 Mus musculus 42-47 18623154-5 2008 TNBS administration induced a marked increase of vascular cell adhesion molecule (VCAM-1), inducible nitric oxide synthase (iNOS), and cyclooxygenase-2 (COX-2) protein levels. Trinitrobenzenesulfonic Acid 0-4 vascular cell adhesion molecule 1 Rattus norvegicus 82-88 18623154-5 2008 TNBS administration induced a marked increase of vascular cell adhesion molecule (VCAM-1), inducible nitric oxide synthase (iNOS), and cyclooxygenase-2 (COX-2) protein levels. Trinitrobenzenesulfonic Acid 0-4 nitric oxide synthase 2 Rattus norvegicus 91-122 18623154-5 2008 TNBS administration induced a marked increase of vascular cell adhesion molecule (VCAM-1), inducible nitric oxide synthase (iNOS), and cyclooxygenase-2 (COX-2) protein levels. Trinitrobenzenesulfonic Acid 0-4 nitric oxide synthase 2 Rattus norvegicus 124-128 18623154-5 2008 TNBS administration induced a marked increase of vascular cell adhesion molecule (VCAM-1), inducible nitric oxide synthase (iNOS), and cyclooxygenase-2 (COX-2) protein levels. Trinitrobenzenesulfonic Acid 0-4 prostaglandin-endoperoxide synthase 2 Rattus norvegicus 135-151 18623154-5 2008 TNBS administration induced a marked increase of vascular cell adhesion molecule (VCAM-1), inducible nitric oxide synthase (iNOS), and cyclooxygenase-2 (COX-2) protein levels. Trinitrobenzenesulfonic Acid 0-4 prostaglandin-endoperoxide synthase 2 Rattus norvegicus 153-158 18623154-10 2008 CONCLUSIONS: Inhibition of the expression of proinflammatory mediators that are regulated by the NF-kappaB and STAT signaling pathways contribute to the therapeutical effect of glutamine in the TNBS model of experimental colitis. Trinitrobenzenesulfonic Acid 194-198 signal transducer and activator of transcription 1 Rattus norvegicus 111-115 19079231-5 2008 In inflamed tissues of mice with colitis induced by either the trinitrobenzene sulfonic acid or oxazolone, p-Smad3 was low despite active TGF-beta1 being produced in excess. Trinitrobenzenesulfonic Acid 63-92 SMAD family member 3 Mus musculus 109-114 18703751-9 2008 MPO activity was decreased significantly in response to monotherapy with 5-ASA and each of the antioxidants plus 5-ASA when compared to TNBS. Trinitrobenzenesulfonic Acid 136-140 myeloperoxidase Rattus norvegicus 0-3 18955701-8 2008 The TNBS-treated rats exhibited a marked, reversible inflammatory response within the hippocampus, characterized by microglial activation and increases in tumor necrosis factor alpha (TNFalpha) levels. Trinitrobenzenesulfonic Acid 4-8 tumor necrosis factor Rattus norvegicus 155-182 18955701-8 2008 The TNBS-treated rats exhibited a marked, reversible inflammatory response within the hippocampus, characterized by microglial activation and increases in tumor necrosis factor alpha (TNFalpha) levels. Trinitrobenzenesulfonic Acid 4-8 tumor necrosis factor Rattus norvegicus 184-192 18837084-14 2008 CONCLUSION: Ilomastat improves TNB-induced UC in rats by inhibiting the MMP-1 activity. Trinitrobenzenesulfonic Acid 31-34 matrix metallopeptidase 1 Rattus norvegicus 72-77 18583045-3 2008 The present study was aimed to investigate the role of TRPA1 in visceral hyperalgesia after trinitrobenzene sulfonic acid (TNBS)-induced colitis. Trinitrobenzenesulfonic Acid 92-121 transient receptor potential cation channel subfamily A member 1 Homo sapiens 55-60 18827968-0 2008 Treatment with bindarit, an inhibitor of MCP-1 synthesis, protects mice against trinitrobenzene sulfonic acid-induced colitis. Trinitrobenzenesulfonic Acid 80-109 chemokine (C-C motif) ligand 2 Mus musculus 41-46 18653784-3 2008 As CXCR2 is involved in neutrophil migration, this study aimed to evaluate whether the systemic therapeutic treatment with selective CXCR2 antagonist SB225002 ameliorates experimental colitis, which was induced in mice by 2,4,6-trinitrobenzene sulfonic acid (TNBS). Trinitrobenzenesulfonic Acid 222-257 chemokine (C-X-C motif) receptor 2 Mus musculus 133-138 18653784-3 2008 As CXCR2 is involved in neutrophil migration, this study aimed to evaluate whether the systemic therapeutic treatment with selective CXCR2 antagonist SB225002 ameliorates experimental colitis, which was induced in mice by 2,4,6-trinitrobenzene sulfonic acid (TNBS). Trinitrobenzenesulfonic Acid 259-263 chemokine (C-X-C motif) receptor 2 Mus musculus 133-138 18460552-3 2008 METHODS: Colonic inflammation in wild-type and PAR(2)(-/-) mice was induced by dextran sodium sulfate, trinitrobenzene sulfonic acid (TNBS), a T helper-1 predominant model, or oxazolone, a T helper-2 predominant model. Trinitrobenzenesulfonic Acid 103-132 coagulation factor II (thrombin) receptor-like 1 Mus musculus 47-53 18460552-3 2008 METHODS: Colonic inflammation in wild-type and PAR(2)(-/-) mice was induced by dextran sodium sulfate, trinitrobenzene sulfonic acid (TNBS), a T helper-1 predominant model, or oxazolone, a T helper-2 predominant model. Trinitrobenzenesulfonic Acid 134-138 coagulation factor II (thrombin) receptor-like 1 Mus musculus 47-53 18583045-3 2008 The present study was aimed to investigate the role of TRPA1 in visceral hyperalgesia after trinitrobenzene sulfonic acid (TNBS)-induced colitis. Trinitrobenzenesulfonic Acid 123-127 transient receptor potential cation channel subfamily A member 1 Homo sapiens 55-60 18583045-4 2008 Results indicate that TNBS induced a significant increase in visceral sensitivity to colonic distension and chemical irritation accompanied by up-regulation of TRPA1 in colonic afferent dorsal root ganglia (DRG). Trinitrobenzenesulfonic Acid 22-26 transient receptor potential cation channel subfamily A member 1 Homo sapiens 160-165 18704302-0 2008 Oxymatrine improves TNBS-induced colitis in rats by inhibiting the expression of NF-kappaB p65. Trinitrobenzenesulfonic Acid 20-24 synaptotagmin 1 Rattus norvegicus 91-94 18690297-7 2008 RESULTS: Trinitrobenzene sulfonic acid enema resulted in pronounced pathological changes of colonic mucosa in model rats, which were in accordance with the significantly elevated myeloperoxidase activity. Trinitrobenzenesulfonic Acid 9-38 myeloperoxidase Rattus norvegicus 179-194 18547706-6 2008 DCrc showed a dose-dependent upregulation of CD86 after treatment with the contact allergens 2,4,6-trinitrobenzenesulfonic acid, the prohapten isoeugenol, and alpha-hexyl cinnamic aldehyde. Trinitrobenzenesulfonic Acid 93-127 CD86 molecule Homo sapiens 45-49 18650383-3 2008 We demonstrate that, compared to wild type, mice genetically deficient in MCH had substantially reduced local inflammatory responses in a mouse model of experimental colitis induced by intracolonic administration of 2,4,6 trinitrobenzene sulfonic acid (TNBS). Trinitrobenzenesulfonic Acid 216-251 pro-melanin concentrating hormone Homo sapiens 74-77 18650383-3 2008 We demonstrate that, compared to wild type, mice genetically deficient in MCH had substantially reduced local inflammatory responses in a mouse model of experimental colitis induced by intracolonic administration of 2,4,6 trinitrobenzene sulfonic acid (TNBS). Trinitrobenzenesulfonic Acid 253-257 pro-melanin concentrating hormone Homo sapiens 74-77 18650383-4 2008 Likewise, mice receiving treatments with an anti-MCH antibody, either prophylactically or after the establishment of colitis, developed attenuated TNBS-associated colonic inflammation and survived longer. Trinitrobenzenesulfonic Acid 147-151 pro-melanin concentrating hormone Homo sapiens 49-52 18359536-7 2008 Besides, VIP treatment restored in vivo the numbers of TLR2 and TLR4 positive CD4+CD25+ T lymphocytes, augmented by TNBS administration, and increased the expression of molecules involved in regulatory T cell function, such as Foxp3 and TGF-beta. Trinitrobenzenesulfonic Acid 116-120 vasoactive intestinal polypeptide Mus musculus 9-12 18403481-4 2008 In a mouse model of acute, trinitrobenzene sulfonic acid-induced experimental colitis, we demonstrate that, despite low glucocorticoid levels, CRH-deficient mice develop substantially reduced local inflammatory responses. Trinitrobenzenesulfonic Acid 27-56 corticotropin releasing hormone Mus musculus 143-146 18300276-11 2008 An intracolonic RELMbeta challenge was performed in the trinitrobenzene sulfonic acid (TNBS)-murine model of colitis and macroscopic and histological scores were monitored. Trinitrobenzenesulfonic Acid 56-85 resistin like beta Mus musculus 16-24 18300276-11 2008 An intracolonic RELMbeta challenge was performed in the trinitrobenzene sulfonic acid (TNBS)-murine model of colitis and macroscopic and histological scores were monitored. Trinitrobenzenesulfonic Acid 87-91 resistin like beta Mus musculus 16-24 17994277-4 2008 Our aim was to determine the effects of indomethacin and RA and to evaluate their correlation to SPARC expression in the TNBS mouse model. Trinitrobenzenesulfonic Acid 121-125 secreted acidic cysteine rich glycoprotein Mus musculus 97-102 17994277-7 2008 The expression of SPARC was inversely related to fibrosis, but not to inflammation, in the TNBS-alone groups at 2 weeks; these differences were lost by 8 weeks. Trinitrobenzenesulfonic Acid 91-95 secreted acidic cysteine rich glycoprotein Mus musculus 18-23 18200517-2 2008 Trinitrobenzene sulfonic acid (TNBS) colitis in NKT-deficient SJL/J mice has been described as Th1-mediated inflammation, whereas BALB/c mice are believed to exhibit a mixed Th1/Th2 response. Trinitrobenzenesulfonic Acid 0-29 negative elongation factor complex member C/D, Th1l Mus musculus 95-98 18200517-2 2008 Trinitrobenzene sulfonic acid (TNBS) colitis in NKT-deficient SJL/J mice has been described as Th1-mediated inflammation, whereas BALB/c mice are believed to exhibit a mixed Th1/Th2 response. Trinitrobenzenesulfonic Acid 31-35 negative elongation factor complex member C/D, Th1l Mus musculus 95-98 18200517-2 2008 Trinitrobenzene sulfonic acid (TNBS) colitis in NKT-deficient SJL/J mice has been described as Th1-mediated inflammation, whereas BALB/c mice are believed to exhibit a mixed Th1/Th2 response. Trinitrobenzenesulfonic Acid 31-35 heart and neural crest derivatives expressed 2 Mus musculus 178-181 18535667-6 2008 Furthermore, IRF4-deficient mice were protected from T cell-dependent chronic intestinal inflammation in trinitrobenzene sulfonic acid- and oxazolone-induced colitis. Trinitrobenzenesulfonic Acid 105-134 interferon regulatory factor 4 Mus musculus 13-17 18359536-2 2008 We have recently demonstrated in TNBS-induced colitis, a murine model of CD, that VIP plays a homeostatic role, by reducing TNBS-induced TLR2 and TLR4 expression to control levels. Trinitrobenzenesulfonic Acid 33-37 vasoactive intestinal polypeptide Mus musculus 82-85 18458699-15 2008 CONCLUSION: Selective COX-2 inhibitor-celecoxib could decrease the expression of COX-2 in intestinal tissue, attenuate the inflammatory index of colon tissues of experimental colitis induced by TNBS. Trinitrobenzenesulfonic Acid 194-198 cytochrome c oxidase II, mitochondrial Rattus norvegicus 22-27 18563732-7 2008 We identified TNBS-induced ROS and myeloperoxidase (MPO) proteins and demonstrated that the increase in ROS resulted in IL-12 production. Trinitrobenzenesulfonic Acid 14-18 myeloperoxidase Homo sapiens 35-50 18563732-7 2008 We identified TNBS-induced ROS and myeloperoxidase (MPO) proteins and demonstrated that the increase in ROS resulted in IL-12 production. Trinitrobenzenesulfonic Acid 14-18 myeloperoxidase Homo sapiens 52-55 18419134-3 2008 Thiol specific reagents showed significant redox cycling between the reactive thiols and the TNB anion, and using NEM, four of the six reactive thiols are critical to the functionality of hBCATc. Trinitrobenzenesulfonic Acid 93-96 branched chain amino acid transaminase 1 Homo sapiens 188-194 18377896-7 2008 Semi-quantitative PCR showed minimal mRNA for NGF in control mucosa that increased sharply by 6 h post-TNBS. Trinitrobenzenesulfonic Acid 103-107 nerve growth factor Rattus norvegicus 46-49 18377896-8 2008 Laser-capture microdissection was used to collect colonic epithelial cells, where mRNA for NGF was markedly increased by 6 h post-TNBS. Trinitrobenzenesulfonic Acid 130-134 nerve growth factor Rattus norvegicus 91-94 18288370-5 2008 On day 7 after TNBS treatment, macroscopic damage of the mucosa could be easily detected and the percentage of colon-innervated DRG neurons expressing CGRP and VR1 increased nearly two folds respectively [(95.38+-9.45)% vs (42.86+-.02)% for CGRP, (89.23+-8.21)% vs (32.54+-4.58)% for VR1]. Trinitrobenzenesulfonic Acid 15-19 calcitonin-related polypeptide alpha Rattus norvegicus 151-155 18322307-7 2008 TNBS administration also significantly enhanced the serum and colonic mucosal cytokines (TNF-alpha and IL-6) and eicosanoids (LTB4 and PGE2) levels, which paralleled with the severity of colitis. Trinitrobenzenesulfonic Acid 0-4 tumor necrosis factor Rattus norvegicus 89-98 18322307-7 2008 TNBS administration also significantly enhanced the serum and colonic mucosal cytokines (TNF-alpha and IL-6) and eicosanoids (LTB4 and PGE2) levels, which paralleled with the severity of colitis. Trinitrobenzenesulfonic Acid 0-4 interleukin 6 Rattus norvegicus 103-107 18395085-3 2008 METHODS: Both dextran sulfate sodium colitis and trinitrobenzene sulfonic acid-relapsing colitis were induced in wild-type and IL-21-deficient mice. Trinitrobenzenesulfonic Acid 49-78 interleukin 21 Mus musculus 127-132 18395085-7 2008 RESULTS: High IL-21 was seen in wild-type mice with dextran sulfate sodium- and trinitrobenzene sulfonic acid-relapsing colitis. Trinitrobenzenesulfonic Acid 80-109 interleukin 21 Mus musculus 14-19 18322237-3 2008 Thus, we hypothesized that CD73 is protective in mucosal inflammation as modeled by trinitrobenzene sulfonate (TNBS) colitis. Trinitrobenzenesulfonic Acid 84-109 5' nucleotidase, ecto Mus musculus 27-31 18288370-5 2008 On day 7 after TNBS treatment, macroscopic damage of the mucosa could be easily detected and the percentage of colon-innervated DRG neurons expressing CGRP and VR1 increased nearly two folds respectively [(95.38+-9.45)% vs (42.86+-.02)% for CGRP, (89.23+-8.21)% vs (32.54+-4.58)% for VR1]. Trinitrobenzenesulfonic Acid 15-19 transient receptor potential cation channel, subfamily V, member 1 Rattus norvegicus 160-163 18288370-5 2008 On day 7 after TNBS treatment, macroscopic damage of the mucosa could be easily detected and the percentage of colon-innervated DRG neurons expressing CGRP and VR1 increased nearly two folds respectively [(95.38+-9.45)% vs (42.86+-.02)% for CGRP, (89.23+-8.21)% vs (32.54+-4.58)% for VR1]. Trinitrobenzenesulfonic Acid 15-19 calcitonin-related polypeptide alpha Rattus norvegicus 241-245 18288370-5 2008 On day 7 after TNBS treatment, macroscopic damage of the mucosa could be easily detected and the percentage of colon-innervated DRG neurons expressing CGRP and VR1 increased nearly two folds respectively [(95.38+-9.45)% vs (42.86+-.02)% for CGRP, (89.23+-8.21)% vs (32.54+-4.58)% for VR1]. Trinitrobenzenesulfonic Acid 15-19 transient receptor potential cation channel, subfamily V, member 1 Rattus norvegicus 284-287 18288370-6 2008 When the colon inflammatory reaction was resolved on days 21 and 42 after TNBS treatment, the percentage of colon-innervated DRG neurons expressing CGRP and VR1 were still higher than that in the control group [(86.25+-8.21)%, (68.28+-7.12)% vs (42.86+-5.02)% for CGRP; (67.22+-6.52)%, (56.25+-4.86)% vs (32.54+-4.58)% for VR1]. Trinitrobenzenesulfonic Acid 74-78 calcitonin-related polypeptide alpha Rattus norvegicus 148-152 18288370-6 2008 When the colon inflammatory reaction was resolved on days 21 and 42 after TNBS treatment, the percentage of colon-innervated DRG neurons expressing CGRP and VR1 were still higher than that in the control group [(86.25+-8.21)%, (68.28+-7.12)% vs (42.86+-5.02)% for CGRP; (67.22+-6.52)%, (56.25+-4.86)% vs (32.54+-4.58)% for VR1]. Trinitrobenzenesulfonic Acid 74-78 transient receptor potential cation channel, subfamily V, member 1 Rattus norvegicus 157-160 18288370-6 2008 When the colon inflammatory reaction was resolved on days 21 and 42 after TNBS treatment, the percentage of colon-innervated DRG neurons expressing CGRP and VR1 were still higher than that in the control group [(86.25+-8.21)%, (68.28+-7.12)% vs (42.86+-5.02)% for CGRP; (67.22+-6.52)%, (56.25+-4.86)% vs (32.54+-4.58)% for VR1]. Trinitrobenzenesulfonic Acid 74-78 calcitonin-related polypeptide alpha Rattus norvegicus 264-268 18288370-6 2008 When the colon inflammatory reaction was resolved on days 21 and 42 after TNBS treatment, the percentage of colon-innervated DRG neurons expressing CGRP and VR1 were still higher than that in the control group [(86.25+-8.21)%, (68.28+-7.12)% vs (42.86+-5.02)% for CGRP; (67.22+-6.52)%, (56.25+-4.86)% vs (32.54+-4.58)% for VR1]. Trinitrobenzenesulfonic Acid 74-78 transient receptor potential cation channel, subfamily V, member 1 Rattus norvegicus 323-326 18242212-8 2008 The levels of T helper cell 2 type cytokines such as IL-4 and IL-13 in the LP T cells were significantly higher, but the levels of interferon gamma were lower in OXA- or TNBS-treated CD30LKO mice than in wild-type mice. Trinitrobenzenesulfonic Acid 170-174 interleukin 4 Mus musculus 53-57 17977946-2 2008 The present study aimed to clarify changes in population dynamics of intestinal muscularis macrophages during colonic inflammation and to test possible inhibitory actions of agents targeting monocyte chemoattractant protein-1 (MCP-1) on muscularis macrophage dynamics and motility disorder in the colonic inflammation elicited by 2,4,6-trinitrobenzene sulfonic acid. Trinitrobenzenesulfonic Acid 330-365 C-C motif chemokine ligand 2 Homo sapiens 227-232 17562175-0 2008 Tanshinone IIA ameliorates trinitrobenzene sulfonic acid (TNBS)-induced murine colitis. Trinitrobenzenesulfonic Acid 27-56 ATPase, class II, type 9A Mus musculus 11-14 17562175-0 2008 Tanshinone IIA ameliorates trinitrobenzene sulfonic acid (TNBS)-induced murine colitis. Trinitrobenzenesulfonic Acid 58-62 ATPase, class II, type 9A Mus musculus 11-14 18242212-8 2008 The levels of T helper cell 2 type cytokines such as IL-4 and IL-13 in the LP T cells were significantly higher, but the levels of interferon gamma were lower in OXA- or TNBS-treated CD30LKO mice than in wild-type mice. Trinitrobenzenesulfonic Acid 170-174 interleukin 13 Mus musculus 62-67 18242212-8 2008 The levels of T helper cell 2 type cytokines such as IL-4 and IL-13 in the LP T cells were significantly higher, but the levels of interferon gamma were lower in OXA- or TNBS-treated CD30LKO mice than in wild-type mice. Trinitrobenzenesulfonic Acid 170-174 tumor necrosis factor receptor superfamily, member 8 Mus musculus 183-187 18242212-9 2008 In vivo administration of agonistic anti-CD30 mAb ameliorated OXA-induced colitis but aggravated TNBS-induced colitis in CD30LKO mice. Trinitrobenzenesulfonic Acid 97-101 tumor necrosis factor receptor superfamily, member 8 Mus musculus 41-45 17991707-13 2008 TNBS-induced colitis increased TRPV1-like immunoreactivity and TRPV1 mRNA content in pelvic afferent neuronal cell bodies in DRG L6-S1. Trinitrobenzenesulfonic Acid 0-4 transient receptor potential cation channel, subfamily V, member 1 Rattus norvegicus 31-36 17991707-13 2008 TNBS-induced colitis increased TRPV1-like immunoreactivity and TRPV1 mRNA content in pelvic afferent neuronal cell bodies in DRG L6-S1. Trinitrobenzenesulfonic Acid 0-4 transient receptor potential cation channel, subfamily V, member 1 Rattus norvegicus 63-68 18166352-5 2008 RESULTS: Our results show that the FG-4497-mediated induction of HIF-1alpha provides an overall beneficial influence on clinical symptoms [weight loss, colon length, tissue tumor necrosis factor-alpha (TNFalpha)] in murine trinitrobenzene sulfonic acid (TNBS) colitis, most likely because of their barrier protective function and wound healing during severe tissue hypoxia at the site of inflammation. Trinitrobenzenesulfonic Acid 223-252 hypoxia inducible factor 1, alpha subunit Mus musculus 65-75 18166352-5 2008 RESULTS: Our results show that the FG-4497-mediated induction of HIF-1alpha provides an overall beneficial influence on clinical symptoms [weight loss, colon length, tissue tumor necrosis factor-alpha (TNFalpha)] in murine trinitrobenzene sulfonic acid (TNBS) colitis, most likely because of their barrier protective function and wound healing during severe tissue hypoxia at the site of inflammation. Trinitrobenzenesulfonic Acid 254-258 hypoxia inducible factor 1, alpha subunit Mus musculus 65-75 17911375-0 2008 Immune modulatory treatment of trinitrobenzene sulfonic acid colitis with calcitriol is associated with a change of a T helper (Th) 1/Th17 to a Th2 and regulatory T cell profile. Trinitrobenzenesulfonic Acid 31-60 negative elongation factor complex member C/D, Th1l Mus musculus 118-133 17911375-0 2008 Immune modulatory treatment of trinitrobenzene sulfonic acid colitis with calcitriol is associated with a change of a T helper (Th) 1/Th17 to a Th2 and regulatory T cell profile. Trinitrobenzenesulfonic Acid 31-60 heart and neural crest derivatives expressed 2 Mus musculus 144-147 17936198-7 2007 Biochemically, the HSD decreased tissue myeloperoxidase activity and protected the mitochondria in the colon of TNBS-treated animals as evaluated by preserving tissue oxygen consumption, mitochondrial DNA, and expression of cytochrome c. The HSD increased levels of nuclear respiratory factor-1 and mitochondrial transcription factor-A in normal colon tissue and under inflammatory conditions. Trinitrobenzenesulfonic Acid 112-116 nuclear respiratory factor 1 Rattus norvegicus 266-294 17595021-18 2007 This implies that the crosslink density of RDBC matrices after treatment with CDI/NHS is higher than expected on the basis of amide bond formation only, as determined by the TNBS assay. Trinitrobenzenesulfonic Acid 174-178 NHS actin remodeling regulator Bos taurus 78-85 17973636-6 2007 Myeloperoxidase levels in the colons were comparable to control levels 56 days after TNBS treatment. Trinitrobenzenesulfonic Acid 85-89 myeloperoxidase Cavia porcellus 0-15 17914959-0 2007 Effect of heme oxygenase-1 induction by octreotide on TNBS-induced colitis. Trinitrobenzenesulfonic Acid 54-58 heme oxygenase 1 Rattus norvegicus 10-26 18408386-4 2008 RESULTS: TNBS caused a significant reduction in body weight and an increase in MPO activity in colonic, but not in the ileal samples in animals with colitis. Trinitrobenzenesulfonic Acid 9-13 myeloperoxidase Rattus norvegicus 79-82 18667799-2 2008 We review the role of VIP in 2,4,6-trinitrobenzenesulfonic acid (TNBS)-induced colitis as a murine model of Crohn"s disease. Trinitrobenzenesulfonic Acid 29-63 vasoactive intestinal polypeptide Mus musculus 22-25 18667799-2 2008 We review the role of VIP in 2,4,6-trinitrobenzenesulfonic acid (TNBS)-induced colitis as a murine model of Crohn"s disease. Trinitrobenzenesulfonic Acid 65-69 vasoactive intestinal polypeptide Mus musculus 22-25 17947450-14 2007 TNBS- and DSS-induced colitis results in increased colonic mucosal blood flow, most probably due to increased eNOS activity. Trinitrobenzenesulfonic Acid 0-4 nitric oxide synthase 3 Rattus norvegicus 110-114 18176016-6 2007 In an organ culture, spontaneous release of a mucosal mast cell-specific protease (RMCP-2) from the distal colon tissue of TNBS-treated rats was significantly larger than that of sham animals. Trinitrobenzenesulfonic Acid 123-127 mast cell protease 2 Rattus norvegicus 83-89 17943250-4 2007 Simultaneous inhibition of iNOS and COX-2 was investigated in the current study in 2, 4, 6 trinitrobenzene sulphonic acid (TNBS)-induced colitis in rats. Trinitrobenzenesulfonic Acid 123-127 nitric oxide synthase 2 Rattus norvegicus 27-31 17943250-4 2007 Simultaneous inhibition of iNOS and COX-2 was investigated in the current study in 2, 4, 6 trinitrobenzene sulphonic acid (TNBS)-induced colitis in rats. Trinitrobenzenesulfonic Acid 123-127 prostaglandin-endoperoxide synthase 2 Rattus norvegicus 36-41 17719181-12 2007 TRPV1 immunoreactivity in the TL (69.1+/-4.6%) and LS (66.4+/-4.2%) DRG in vehicle-treated rats was increased following TNBS but significantly lower in the preemptive JYL1421-treated group (28.6+/-3.9 and 32.3+/-2.3 respectively, P<0.05). Trinitrobenzenesulfonic Acid 120-124 transient receptor potential cation channel, subfamily V, member 1 Rattus norvegicus 0-5 17363466-7 2007 In trinitrobenzene sulfonic acid-induced colitis, rats with knockdown of CLR displayed a significantly greater degree of edema and necrosis than saline- or control dsRNA-injected rats. Trinitrobenzenesulfonic Acid 3-32 calcitonin receptor like receptor Rattus norvegicus 73-76 17988539-6 2007 TLR4 expression of colon was up-regulated in mice of TNBS group and down-regulated in schistosome ova group which was still higher than that of normal controls (0.762 +/- 0.054 vs 0.325 +/- 0.029 vs 0.237 +/- 0.021, P < 0.01). Trinitrobenzenesulfonic Acid 53-57 toll-like receptor 4 Mus musculus 0-4 17678632-4 2007 Moreover, TMMC suppressed the expression of intercellular adhesion molecule-1, interleukin 1beta (IL-1beta) and tumor necrosis factor-alpha (TNF-alpha) in the mice treated with TNBS. Trinitrobenzenesulfonic Acid 177-181 intercellular adhesion molecule 1 Mus musculus 44-77 17678632-4 2007 Moreover, TMMC suppressed the expression of intercellular adhesion molecule-1, interleukin 1beta (IL-1beta) and tumor necrosis factor-alpha (TNF-alpha) in the mice treated with TNBS. Trinitrobenzenesulfonic Acid 177-181 interleukin 1 beta Mus musculus 79-96 17678632-4 2007 Moreover, TMMC suppressed the expression of intercellular adhesion molecule-1, interleukin 1beta (IL-1beta) and tumor necrosis factor-alpha (TNF-alpha) in the mice treated with TNBS. Trinitrobenzenesulfonic Acid 177-181 interleukin 1 beta Mus musculus 98-106 17678632-4 2007 Moreover, TMMC suppressed the expression of intercellular adhesion molecule-1, interleukin 1beta (IL-1beta) and tumor necrosis factor-alpha (TNF-alpha) in the mice treated with TNBS. Trinitrobenzenesulfonic Acid 177-181 tumor necrosis factor Mus musculus 112-139 17678632-4 2007 Moreover, TMMC suppressed the expression of intercellular adhesion molecule-1, interleukin 1beta (IL-1beta) and tumor necrosis factor-alpha (TNF-alpha) in the mice treated with TNBS. Trinitrobenzenesulfonic Acid 177-181 tumor necrosis factor Mus musculus 141-150 17670946-3 2007 Besides the increased inflammatory response, LRH-1 heterozygous mice exposed to 2,4,6-trinitrobenzene sulfonic acid show lower local corticosterone production as a result of an impaired intestinal expression of the enzymes CYP11A1 and CYP11B1, which control the local synthesis of corticosterone in the intestine. Trinitrobenzenesulfonic Acid 80-115 nuclear receptor subfamily 5, group A, member 2 Mus musculus 45-50 17670946-3 2007 Besides the increased inflammatory response, LRH-1 heterozygous mice exposed to 2,4,6-trinitrobenzene sulfonic acid show lower local corticosterone production as a result of an impaired intestinal expression of the enzymes CYP11A1 and CYP11B1, which control the local synthesis of corticosterone in the intestine. Trinitrobenzenesulfonic Acid 80-115 cytochrome P450, family 11, subfamily a, polypeptide 1 Mus musculus 223-230 17670946-3 2007 Besides the increased inflammatory response, LRH-1 heterozygous mice exposed to 2,4,6-trinitrobenzene sulfonic acid show lower local corticosterone production as a result of an impaired intestinal expression of the enzymes CYP11A1 and CYP11B1, which control the local synthesis of corticosterone in the intestine. Trinitrobenzenesulfonic Acid 80-115 cytochrome P450, family 11, subfamily b, polypeptide 1 Mus musculus 235-242 17363466-8 2007 Levels of the proinflammatory cytokines TNF-alpha and IL-6 were markedly upregulated by trinitrobenzene sulfonic acid treatment. Trinitrobenzenesulfonic Acid 88-117 tumor necrosis factor Rattus norvegicus 40-49 17363466-8 2007 Levels of the proinflammatory cytokines TNF-alpha and IL-6 were markedly upregulated by trinitrobenzene sulfonic acid treatment. Trinitrobenzenesulfonic Acid 88-117 interleukin 6 Rattus norvegicus 54-58 17343846-7 2007 Inflammation following TNBS induction was characterized by increased colonic wall thickness, edema, diffuse inflammatory cells infiltration, necrosis reaching an ulcer index (UI) of 9.66+/-0.66 cm(2) and increased MPO activity and TNF-alpha colonic levels. Trinitrobenzenesulfonic Acid 23-27 myeloperoxidase Rattus norvegicus 214-217 17089128-0 2007 Blockade of STAT3 by antisense oligonucleotide in TNBS-induced murine colitis. Trinitrobenzenesulfonic Acid 50-54 signal transducer and activator of transcription 3 Mus musculus 12-17 17089128-3 2007 This study was executed to investigate the role of STAT3 protein on the pathogenesis of trinitrobenzene sulfonic acid (TNBS)-induced colitis, the pathogenesis of which is CD-like. Trinitrobenzenesulfonic Acid 88-117 signal transducer and activator of transcription 3 Mus musculus 51-56 17089128-3 2007 This study was executed to investigate the role of STAT3 protein on the pathogenesis of trinitrobenzene sulfonic acid (TNBS)-induced colitis, the pathogenesis of which is CD-like. Trinitrobenzenesulfonic Acid 119-123 signal transducer and activator of transcription 3 Mus musculus 51-56 17089128-9 2007 The mice that were administered STAT3 antisense oligonucleotide showed less colonic tissue damage with decreased production of inflammatory cytokines such as TNF-alpha and INF-gamma in mucosa compared with that of those TNBS-induced colitis. Trinitrobenzenesulfonic Acid 220-224 signal transducer and activator of transcription 3 Mus musculus 32-37 17124609-0 2007 The effect of heme oxygenase-1 induction by glutamine on TNBS-induced colitis. Trinitrobenzenesulfonic Acid 57-61 heme oxygenase 1 Rattus norvegicus 14-30 17124609-8 2007 RESULT: TNBS-induced colitis significantly increased the colonic MDA levels, caspase-3 activities, and HO-1 expression in comparison to the control group. Trinitrobenzenesulfonic Acid 8-12 caspase 3 Rattus norvegicus 77-86 17124609-8 2007 RESULT: TNBS-induced colitis significantly increased the colonic MDA levels, caspase-3 activities, and HO-1 expression in comparison to the control group. Trinitrobenzenesulfonic Acid 8-12 heme oxygenase 1 Rattus norvegicus 103-107 17343846-7 2007 Inflammation following TNBS induction was characterized by increased colonic wall thickness, edema, diffuse inflammatory cells infiltration, necrosis reaching an ulcer index (UI) of 9.66+/-0.66 cm(2) and increased MPO activity and TNF-alpha colonic levels. Trinitrobenzenesulfonic Acid 23-27 tumor necrosis factor Rattus norvegicus 231-240 17343846-12 2007 The COX-2 expression was elevated in TNBS group; however rosiglitazone administration reduced the COX-2 overexpression. Trinitrobenzenesulfonic Acid 37-41 cytochrome c oxidase II, mitochondrial Rattus norvegicus 4-9 17343846-13 2007 A high expression of NF-kappaB p65 and p38 MAPK proteins appeared in colon mucosa from control TNBS-treated rats; nevertheless, PPARgamma agonist treatment drastically decreased them. Trinitrobenzenesulfonic Acid 95-99 synaptotagmin 1 Rattus norvegicus 31-34 17343846-13 2007 A high expression of NF-kappaB p65 and p38 MAPK proteins appeared in colon mucosa from control TNBS-treated rats; nevertheless, PPARgamma agonist treatment drastically decreased them. Trinitrobenzenesulfonic Acid 95-99 mitogen activated protein kinase 14 Rattus norvegicus 39-42 17343846-13 2007 A high expression of NF-kappaB p65 and p38 MAPK proteins appeared in colon mucosa from control TNBS-treated rats; nevertheless, PPARgamma agonist treatment drastically decreased them. Trinitrobenzenesulfonic Acid 95-99 peroxisome proliferator-activated receptor gamma Rattus norvegicus 128-137 17292349-5 2007 TNBS challenge led to an early and substantial induction of HO-1 protein expression and heme oxygenase activity in the colon that peaked after 48-72 h and declined over 10 days. Trinitrobenzenesulfonic Acid 0-4 heme oxygenase 1 Rattus norvegicus 60-64 17272517-8 2007 TNBS-mediated increases in the number of CCR6-bearing lamina propria T cells were also substantially reduced by anti-MIP-3alpha neutralizing monoclonal antibody treatment. Trinitrobenzenesulfonic Acid 0-4 chemokine (C-C motif) ligand 20 Mus musculus 117-127 17386408-6 2007 Moreover, treatments with sinomenine (100 mg/kg and 200 mg/kg) decreased the up-regulated mRNA and protein levels of tumour necrosis factor-alpha(TNF-alpha) and interferon-gamma (IFN-gamma) caused by TNBS. Trinitrobenzenesulfonic Acid 200-204 tumor necrosis factor Mus musculus 146-155 17386408-6 2007 Moreover, treatments with sinomenine (100 mg/kg and 200 mg/kg) decreased the up-regulated mRNA and protein levels of tumour necrosis factor-alpha(TNF-alpha) and interferon-gamma (IFN-gamma) caused by TNBS. Trinitrobenzenesulfonic Acid 200-204 interferon gamma Mus musculus 161-177 17386408-6 2007 Moreover, treatments with sinomenine (100 mg/kg and 200 mg/kg) decreased the up-regulated mRNA and protein levels of tumour necrosis factor-alpha(TNF-alpha) and interferon-gamma (IFN-gamma) caused by TNBS. Trinitrobenzenesulfonic Acid 200-204 interferon gamma Mus musculus 179-188 17386408-7 2007 Our findings suggest that sinomenine attenuates TNBS-induced colitis in mice and the therapeutic mechanism might be related to the reduction of up-regulated colonic TNF-alpha and IFN-gamma production caused by TNBS. Trinitrobenzenesulfonic Acid 210-214 tumor necrosis factor Mus musculus 165-174 17386408-7 2007 Our findings suggest that sinomenine attenuates TNBS-induced colitis in mice and the therapeutic mechanism might be related to the reduction of up-regulated colonic TNF-alpha and IFN-gamma production caused by TNBS. Trinitrobenzenesulfonic Acid 210-214 interferon gamma Mus musculus 179-188 17272517-4 2007 The aim of this study was to determine whether MIP-3alpha production is increased during murine 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis and to examine the effect of anti-MIP-3alpha neutralizing monoclonal antibody administration in this model. Trinitrobenzenesulfonic Acid 96-131 chemokine (C-C motif) ligand 20 Mus musculus 47-57 17272517-4 2007 The aim of this study was to determine whether MIP-3alpha production is increased during murine 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis and to examine the effect of anti-MIP-3alpha neutralizing monoclonal antibody administration in this model. Trinitrobenzenesulfonic Acid 133-137 chemokine (C-C motif) ligand 20 Mus musculus 47-57 17272517-5 2007 We found that the administration of TNBS significantly increased colonic MIP-3alpha protein levels in Balb/c mice. Trinitrobenzenesulfonic Acid 36-40 chemokine (C-C motif) ligand 20 Mus musculus 73-83 17272517-6 2007 Consistent with this, a marked increase in the number of CCR6-bearing lamina propria CD4(+) and CD8(+) T cells was also observed in TNBS-treated animals. Trinitrobenzenesulfonic Acid 132-136 chemokine (C-C motif) receptor 6 Mus musculus 57-61 17272517-7 2007 Treatment of mice with an anti-MIP-3alpha neutralizing monoclonal antibody significantly reduced TNBS-mediated increases in colonic weight-to-length ratio, mucosal ulceration, histological damage, and myeloperoxidase activity. Trinitrobenzenesulfonic Acid 97-101 chemokine (C-C motif) ligand 20 Mus musculus 31-41 17272517-7 2007 Treatment of mice with an anti-MIP-3alpha neutralizing monoclonal antibody significantly reduced TNBS-mediated increases in colonic weight-to-length ratio, mucosal ulceration, histological damage, and myeloperoxidase activity. Trinitrobenzenesulfonic Acid 97-101 myeloperoxidase Mus musculus 201-216 17272517-8 2007 TNBS-mediated increases in the number of CCR6-bearing lamina propria T cells were also substantially reduced by anti-MIP-3alpha neutralizing monoclonal antibody treatment. Trinitrobenzenesulfonic Acid 0-4 chemokine (C-C motif) receptor 6 Mus musculus 41-45 17442970-0 2007 Induction of IL-13 triggers TGF-beta1-dependent tissue fibrosis in chronic 2,4,6-trinitrobenzene sulfonic acid colitis. Trinitrobenzenesulfonic Acid 75-110 interleukin 13 Homo sapiens 13-18 17442970-0 2007 Induction of IL-13 triggers TGF-beta1-dependent tissue fibrosis in chronic 2,4,6-trinitrobenzene sulfonic acid colitis. Trinitrobenzenesulfonic Acid 75-110 transforming growth factor beta 1 Homo sapiens 28-37 17442970-7 2007 These studies show that in chronic 2,4,6-trinitrobenzene sulfonic acid colitis, fibrosis is dependent on the development of an IL-13 response that acts through a novel cell surface-expressed IL-13R to induce TGF-beta(1). Trinitrobenzenesulfonic Acid 35-70 interleukin 13 Homo sapiens 127-132 17442970-7 2007 These studies show that in chronic 2,4,6-trinitrobenzene sulfonic acid colitis, fibrosis is dependent on the development of an IL-13 response that acts through a novel cell surface-expressed IL-13R to induce TGF-beta(1). Trinitrobenzenesulfonic Acid 35-70 interleukin 13 receptor subunit alpha 2 Homo sapiens 191-197 17442970-7 2007 These studies show that in chronic 2,4,6-trinitrobenzene sulfonic acid colitis, fibrosis is dependent on the development of an IL-13 response that acts through a novel cell surface-expressed IL-13R to induce TGF-beta(1). Trinitrobenzenesulfonic Acid 35-70 transforming growth factor beta 1 Homo sapiens 208-219 17292349-2 2007 In the present work, HO-1 expression in trinitrobenzene sulphonic acid (TNBS)-induced colitis in the rat and the effects of HO-1 modulation, particularly by the HO-1 inducer, heme, were further evaluated. Trinitrobenzenesulfonic Acid 72-76 heme oxygenase 1 Rattus norvegicus 21-25 17465495-11 2007 Both TNF-alpha and IL-12 levels were significantly reduced among TNBS induced colitis animals treated with thalidomide compared with animals that did not receive thalidomide. Trinitrobenzenesulfonic Acid 65-69 tumor necrosis factor Homo sapiens 5-14 17465495-14 2007 CONCLUSION: Thalidomide significantly attenuates TNBS-induced colitis by inhibiting the intestinal production of TNF-alpha, IL-12, and VEGF. Trinitrobenzenesulfonic Acid 49-53 tumor necrosis factor Homo sapiens 113-122 17303123-3 2007 In the present study, we determined that the expression of CGRP was increased in bladder afferent neurons in lumbosacral DRG following tri-nitrobenzene sulfonic acid (TNBS)-induced colitis in rat. Trinitrobenzenesulfonic Acid 135-165 calcitonin-related polypeptide alpha Rattus norvegicus 59-63 17465495-14 2007 CONCLUSION: Thalidomide significantly attenuates TNBS-induced colitis by inhibiting the intestinal production of TNF-alpha, IL-12, and VEGF. Trinitrobenzenesulfonic Acid 49-53 vascular endothelial growth factor A Homo sapiens 135-139 17489361-6 2007 The block of HERG by maprotiline was examined after treatment of trinitrobenzene sulfonic acid (TNBS), an amino-group reagent that neutralizes the positively charged amino-groups of peptide N-terminal and lysine residues. Trinitrobenzenesulfonic Acid 96-100 potassium voltage-gated channel subfamily H member 2 Homo sapiens 13-17 17303123-3 2007 In the present study, we determined that the expression of CGRP was increased in bladder afferent neurons in lumbosacral DRG following tri-nitrobenzene sulfonic acid (TNBS)-induced colitis in rat. Trinitrobenzenesulfonic Acid 167-171 calcitonin-related polypeptide alpha Rattus norvegicus 59-63 17517520-2 2007 This study describes the changes in the expression of nerve growth factor (NGF) and interleukin-10 (IL-10) in the colon and in various segments of the small intestine in two rat models of experimental colitis induced by iodoacetamide or 2,4,6-trinitrobenzene sulfonic acid (TNBS). Trinitrobenzenesulfonic Acid 237-272 nerve growth factor Rattus norvegicus 54-73 17408649-2 2007 METHODS: We investigated the therapeutic potential of Rspo1 in ameliorating experimental colitis induced by dextran sulfate sodium (DSS) or trinitrobenzene sulfonic acid (TNBS) as well as nonsteroidal anti-inflammatory drug-induced colitis in interleukin (IL)-10-deficient mice. Trinitrobenzenesulfonic Acid 140-169 R-spondin 1 Mus musculus 54-59 17408649-6 2007 Likewise, Rspo1 therapy also alleviated TNBS-induced interstitial inflammation and mucosal erosion in the mouse colon. Trinitrobenzenesulfonic Acid 40-44 R-spondin 1 Mus musculus 10-15 17517520-2 2007 This study describes the changes in the expression of nerve growth factor (NGF) and interleukin-10 (IL-10) in the colon and in various segments of the small intestine in two rat models of experimental colitis induced by iodoacetamide or 2,4,6-trinitrobenzene sulfonic acid (TNBS). Trinitrobenzenesulfonic Acid 274-278 interleukin 10 Rattus norvegicus 100-105 17517520-4 2007 NGF and IL-10 increased significantly in homogenates of strips isolated from all small intestinal segments, 3-6h after iodoacetamide or TNBS administration and remained elevated until the colonic inflammation subsided. Trinitrobenzenesulfonic Acid 136-140 nerve growth factor Rattus norvegicus 0-3 17517520-2 2007 This study describes the changes in the expression of nerve growth factor (NGF) and interleukin-10 (IL-10) in the colon and in various segments of the small intestine in two rat models of experimental colitis induced by iodoacetamide or 2,4,6-trinitrobenzene sulfonic acid (TNBS). Trinitrobenzenesulfonic Acid 237-272 interleukin 10 Rattus norvegicus 100-105 17517520-4 2007 NGF and IL-10 increased significantly in homogenates of strips isolated from all small intestinal segments, 3-6h after iodoacetamide or TNBS administration and remained elevated until the colonic inflammation subsided. Trinitrobenzenesulfonic Acid 136-140 interleukin 10 Rattus norvegicus 8-13 17517520-2 2007 This study describes the changes in the expression of nerve growth factor (NGF) and interleukin-10 (IL-10) in the colon and in various segments of the small intestine in two rat models of experimental colitis induced by iodoacetamide or 2,4,6-trinitrobenzene sulfonic acid (TNBS). Trinitrobenzenesulfonic Acid 274-278 nerve growth factor Rattus norvegicus 54-73 17312139-4 2007 These findings correlate in vivo with enhanced susceptibility of tissue-specific PPAR-gamma null mice to trinitrobenzene sulfonic acid-induced colitis. Trinitrobenzenesulfonic Acid 105-134 peroxisome proliferator activated receptor gamma Mus musculus 81-91 18174677-6 2007 RESULTS: TNBS induced severe colitis as evidenced by increased colonic edema, mucosal lesion area, histopathological score, MPO activity, and TNF-alpha level. Trinitrobenzenesulfonic Acid 9-13 myeloperoxidase Rattus norvegicus 124-127 17116325-8 2007 Flow cytometric measurements of 15-LOX correlated negatively with TNB (r=-0.33; P<0.05) and adjusted TNB (r=-0.34; P<0.05). Trinitrobenzenesulfonic Acid 66-69 polyunsaturated fatty acid lipoxygenase ALOX15 Sus scrofa 32-38 17116325-8 2007 Flow cytometric measurements of 15-LOX correlated negatively with TNB (r=-0.33; P<0.05) and adjusted TNB (r=-0.34; P<0.05). Trinitrobenzenesulfonic Acid 104-107 polyunsaturated fatty acid lipoxygenase ALOX15 Sus scrofa 32-38 16545971-10 2007 TNBS and/or WAS caused significant inflammatory changes at day 5, while only TNBS+WAS also showed signs of mucosal inflammation on day 14 and significantly elevated IL-2 levels on day 28. Trinitrobenzenesulfonic Acid 77-81 interleukin 2 Homo sapiens 165-169 16973935-8 2007 Four days after TNBS treatment, plasma corticosterone was unaltered in all groups; however, TNF-alpha was significantly increased in adult TNBS-treated rats that had LPS as neonates compared with all other groups. Trinitrobenzenesulfonic Acid 139-143 tumor necrosis factor Rattus norvegicus 92-101 17306201-8 2007 However, the ESR1: c.1227T allele was significantly associated with TNB. Trinitrobenzenesulfonic Acid 68-71 estrogen receptor 1 Sus scrofa 13-17 17324399-11 2007 Progesterone enhanced TNBS-induced MIF (P < .001) and TNF-alpha (P < .01) production, while EB decreased MIF (P < .01) and IL-beta levels (P < .01). Trinitrobenzenesulfonic Acid 22-26 macrophage migration inhibitory factor Rattus norvegicus 35-38 17324399-11 2007 Progesterone enhanced TNBS-induced MIF (P < .001) and TNF-alpha (P < .01) production, while EB decreased MIF (P < .01) and IL-beta levels (P < .01). Trinitrobenzenesulfonic Acid 22-26 tumor necrosis factor Rattus norvegicus 57-66 17575720-10 2007 The TNBS-induced increases in the activities of myeloperoxidase in the colonic tissue were blunted significantly in hyperthermia-treated animals. Trinitrobenzenesulfonic Acid 4-8 myeloperoxidase Rattus norvegicus 48-63 18174677-6 2007 RESULTS: TNBS induced severe colitis as evidenced by increased colonic edema, mucosal lesion area, histopathological score, MPO activity, and TNF-alpha level. Trinitrobenzenesulfonic Acid 9-13 tumor necrosis factor Rattus norvegicus 142-151 17145956-3 2006 Using the 2,4,6-trinitrobenzene sulfonic acid (TNBS)-colitis model we show here that Vanin-1 deficiency protects from colitis. Trinitrobenzenesulfonic Acid 10-45 vanin 1 Homo sapiens 85-92 16763055-8 2007 Blocking the GITR/ligand for GITR (GITRL) signal by giving soluble GITR prevented TNBS-induced colitis in normal GITR(+/+) and also in lymphocyte-deficient SCID mice. Trinitrobenzenesulfonic Acid 82-86 tumor necrosis factor (ligand) superfamily, member 18 Mus musculus 35-40 16763055-8 2007 Blocking the GITR/ligand for GITR (GITRL) signal by giving soluble GITR prevented TNBS-induced colitis in normal GITR(+/+) and also in lymphocyte-deficient SCID mice. Trinitrobenzenesulfonic Acid 82-86 tumor necrosis factor (ligand) superfamily, member 18 Mus musculus 29-33 16763055-8 2007 Blocking the GITR/ligand for GITR (GITRL) signal by giving soluble GITR prevented TNBS-induced colitis in normal GITR(+/+) and also in lymphocyte-deficient SCID mice. Trinitrobenzenesulfonic Acid 82-86 tumor necrosis factor (ligand) superfamily, member 18 Mus musculus 29-33 16763055-6 2007 RESULTS: Using GITR(-/-) mice, GITR deletion protected against 2,4,6-trinitrobenzene sulphonic acid (TNBS)-induced colitis by reducing innate immune responses and effector T cell activity. Trinitrobenzenesulfonic Acid 101-105 tumor necrosis factor (ligand) superfamily, member 18 Mus musculus 31-35 16763055-8 2007 Blocking the GITR/ligand for GITR (GITRL) signal by giving soluble GITR prevented TNBS-induced colitis in normal GITR(+/+) and also in lymphocyte-deficient SCID mice. Trinitrobenzenesulfonic Acid 82-86 tumor necrosis factor (ligand) superfamily, member 18 Mus musculus 13-24 16763055-8 2007 Blocking the GITR/ligand for GITR (GITRL) signal by giving soluble GITR prevented TNBS-induced colitis in normal GITR(+/+) and also in lymphocyte-deficient SCID mice. Trinitrobenzenesulfonic Acid 82-86 tumor necrosis factor (ligand) superfamily, member 18 Mus musculus 13-17 17145956-3 2006 Using the 2,4,6-trinitrobenzene sulfonic acid (TNBS)-colitis model we show here that Vanin-1 deficiency protects from colitis. Trinitrobenzenesulfonic Acid 47-51 vanin 1 Homo sapiens 85-92 17148664-5 2006 Trinitrobenzene sulfonic acid (TNBS) administration was used to induce colitis in STAT5b-deficient mice and wild-type controls, with and without rosiglitazone pretreatment. Trinitrobenzenesulfonic Acid 0-29 signal transducer and activator of transcription 5B Mus musculus 82-88 17148664-5 2006 Trinitrobenzene sulfonic acid (TNBS) administration was used to induce colitis in STAT5b-deficient mice and wild-type controls, with and without rosiglitazone pretreatment. Trinitrobenzenesulfonic Acid 31-35 signal transducer and activator of transcription 5B Mus musculus 82-88 17148664-8 2006 STAT5b-deficient mice exhibited reduced basal PPARgamma nuclear abundance and developed more severe proximal colitis after TNBS administration. Trinitrobenzenesulfonic Acid 123-127 signal transducer and activator of transcription 5B Mus musculus 0-6 17177830-5 2006 Typically, death occurred within 4 days after the TNBS injection when the mice were treated with anti-GITR. Trinitrobenzenesulfonic Acid 50-54 tumor necrosis factor receptor superfamily, member 18 Mus musculus 102-106 17087939-5 2006 RESULTS: TGF-beta1 levels were increased in the inflamed tissues of mice with colitis induced by either TNBS or oxazolone. Trinitrobenzenesulfonic Acid 104-108 transforming growth factor, beta 1 Mus musculus 9-18 17087939-8 2006 In addition, Smad7 antisense oligonucleotide had a therapeutic effect on relapsing TNBS-induced colitis but not on cell-transfer colitis. Trinitrobenzenesulfonic Acid 83-87 SMAD family member 7 Mus musculus 13-18 17087944-5 2006 METHODS: We examined the therapeutic action of DC(VIP) in the colitis induced by intracolonic administration of trinitrobenzene sulfonic acid, evaluating diverse clinical signs of the disease including weight loss, diarrhea, colitis, and histopathology. Trinitrobenzenesulfonic Acid 112-141 vasoactive intestinal peptide Homo sapiens 50-53 17082612-3 2006 Systemic administration of anti-CR3 significantly ameliorated established intestinal inflammation following the intrarectal administration of trinitrobenzene sulfonic acid (TNBS-colitis), as well as colitis and skin inflammation in C57BL/10 RAG-2(-/-) mice reconstituted with CD4+CD45RBhigh T cells. Trinitrobenzenesulfonic Acid 142-171 integrin alpha M Mus musculus 32-35 17109694-5 2006 Ethanol/TNBS induced a transient inflammation, with normalization of MPO and histological signs of an early phase of recovery after 1 week. Trinitrobenzenesulfonic Acid 8-12 myeloperoxidase Rattus norvegicus 69-72 17109694-6 2006 The number of cholinergic neurones was not altered, but myenteric neuronal nitric oxide synthase (nNOS)-immunoreactivity was significantly lower in the early phase of recovery after TNBS compared with water (1.8 +/- 0.2 vs 3.5 +/- 0.2 neurones ganglion(-1), P < 0.001). Trinitrobenzenesulfonic Acid 182-186 nitric oxide synthase 1 Rattus norvegicus 66-96 17109694-6 2006 The number of cholinergic neurones was not altered, but myenteric neuronal nitric oxide synthase (nNOS)-immunoreactivity was significantly lower in the early phase of recovery after TNBS compared with water (1.8 +/- 0.2 vs 3.5 +/- 0.2 neurones ganglion(-1), P < 0.001). Trinitrobenzenesulfonic Acid 182-186 nitric oxide synthase 1 Rattus norvegicus 98-102 17109694-9 2006 In the early phase of recovery after ethanol/TNBS-induced jejunal inflammation, a loss of motor inhibition occurs due to a decrease of myenteric nNOS activity. Trinitrobenzenesulfonic Acid 45-49 nitric oxide synthase 1 Rattus norvegicus 145-149 16942839-0 2006 Phosphorylation of NMDA NR1 subunits in the myenteric plexus during TNBS induced colitis. Trinitrobenzenesulfonic Acid 68-72 glutamate ionotropic receptor NMDA type subunit 1 Rattus norvegicus 24-27 17075345-7 2006 TNBS induced macroscopic and microscopic damages, an increase in MPO activity, and intense immunostaining for nitrotyrosine. Trinitrobenzenesulfonic Acid 0-4 myeloperoxidase Bos taurus 65-68 16928387-0 2006 Paeonol attenuates TNBS-induced colitis by inhibiting NF-kappaB and STAT1 transactivation. Trinitrobenzenesulfonic Acid 19-23 signal transducer and activator of transcription 1 Homo sapiens 68-73 16942839-4 2006 We examined the levels of NMDA NR1 phosphorylation in trinitrobenzene sulfonic acid (TNBS) induced colitis in rats and compared it to protein translation and the development of visceral hypersensitivity. Trinitrobenzenesulfonic Acid 54-83 glutamate ionotropic receptor NMDA type subunit 1 Rattus norvegicus 31-34 16942839-4 2006 We examined the levels of NMDA NR1 phosphorylation in trinitrobenzene sulfonic acid (TNBS) induced colitis in rats and compared it to protein translation and the development of visceral hypersensitivity. Trinitrobenzenesulfonic Acid 85-89 glutamate ionotropic receptor NMDA type subunit 1 Rattus norvegicus 31-34 16942839-5 2006 We have previously, demonstrated an increase in the C1 cassette of NR1 mRNA expression at 14, 21, and 28 days following TNBS administration. Trinitrobenzenesulfonic Acid 120-124 glutamate ionotropic receptor NMDA type subunit 1 Rattus norvegicus 67-70 16942839-6 2006 In this study, we examined the NR1 serine phosphorylation at 14 days following TNBS injection. Trinitrobenzenesulfonic Acid 79-83 glutamate ionotropic receptor NMDA type subunit 1 Rattus norvegicus 31-34 16942839-10 2006 Serine phosphorylation of the NR1 subunit with C1 cassette appears at 14 days after TNBS injection. Trinitrobenzenesulfonic Acid 84-88 glutamate ionotropic receptor NMDA type subunit 1 Rattus norvegicus 30-33 16880762-8 2006 DNA binding and Western blotting revealed increase in NF-kappaB activation and IkappaBalpha depletion in TNBS-treated mice from Day 2 through Day 8 with a maximum at Day 4, which resulted from increased phosphorylation of IkappaBalpha and higher activity of IkappaB kinase (IKK). Trinitrobenzenesulfonic Acid 105-109 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 54-63 16964428-13 2006 Sucrase isomaltase expression and activity decreased in the ileum of TNBS-induced rats, while aminopeptidase activity was lower in the jejunum. Trinitrobenzenesulfonic Acid 69-73 sucrase-isomaltase Rattus norvegicus 0-18 16880762-8 2006 DNA binding and Western blotting revealed increase in NF-kappaB activation and IkappaBalpha depletion in TNBS-treated mice from Day 2 through Day 8 with a maximum at Day 4, which resulted from increased phosphorylation of IkappaBalpha and higher activity of IkappaB kinase (IKK). Trinitrobenzenesulfonic Acid 105-109 nuclear factor of kappa light polypeptide gene enhancer in B cells inhibitor, alpha Mus musculus 79-91 16880762-8 2006 DNA binding and Western blotting revealed increase in NF-kappaB activation and IkappaBalpha depletion in TNBS-treated mice from Day 2 through Day 8 with a maximum at Day 4, which resulted from increased phosphorylation of IkappaBalpha and higher activity of IkappaB kinase (IKK). Trinitrobenzenesulfonic Acid 105-109 nuclear factor of kappa light polypeptide gene enhancer in B cells inhibitor, alpha Mus musculus 222-234 16880762-9 2006 Pretreatment with TFDG markedly inhibited TNBS-induced increases in nuclear localization of NF-kappaB, cytosolic IKK activity and preserved IkappaBalpha in colon tissue. Trinitrobenzenesulfonic Acid 42-46 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 92-101 16880762-9 2006 Pretreatment with TFDG markedly inhibited TNBS-induced increases in nuclear localization of NF-kappaB, cytosolic IKK activity and preserved IkappaBalpha in colon tissue. Trinitrobenzenesulfonic Acid 42-46 nuclear factor of kappa light polypeptide gene enhancer in B cells inhibitor, alpha Mus musculus 140-152 16782535-14 2006 In summary, curcumin showed therapeutic effects on TNBS-induced colitis and the mechanisms by which curcumin exerts its effects may involve activation of PPARgamma and its ligands. Trinitrobenzenesulfonic Acid 51-55 peroxisome proliferator-activated receptor gamma Rattus norvegicus 154-163 16838116-2 2006 We sought to evaluate the expression and activity of p38 and JNK MAPK in IBD and 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis; and the effects of a p38 inhibitor, SB203580, in TNBS colitis. Trinitrobenzenesulfonic Acid 81-116 mitogen-activated protein kinase 14 Homo sapiens 53-56 16838116-2 2006 We sought to evaluate the expression and activity of p38 and JNK MAPK in IBD and 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis; and the effects of a p38 inhibitor, SB203580, in TNBS colitis. Trinitrobenzenesulfonic Acid 118-122 mitogen-activated protein kinase 14 Homo sapiens 53-56 16838116-2 2006 We sought to evaluate the expression and activity of p38 and JNK MAPK in IBD and 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis; and the effects of a p38 inhibitor, SB203580, in TNBS colitis. Trinitrobenzenesulfonic Acid 118-122 mitogen-activated protein kinase 8 Homo sapiens 61-64 16890604-5 2006 METHODS: Phex gene expression was evaluated in calvaria of 6-7-week-old mice administered with trinitrobenzene sulfonic acid (TNBS) with or without neutralizing anti-TNF-alpha antibody, dietary curcumin, or systemically with recombinant TNF-alpha. Trinitrobenzenesulfonic Acid 95-124 phosphate regulating endopeptidase homolog, X-linked Mus musculus 9-13 16927145-5 2006 In all TNBS-treated rats, colonic MPO activity and MDA levels were found to be increased significantly compared to those in the sham group. Trinitrobenzenesulfonic Acid 7-11 myeloperoxidase Rattus norvegicus 34-37 16917232-0 2006 Antisense therapy of MAdCAM-1 for trinitrobenzenesulfonic acid-induced murine colitis. Trinitrobenzenesulfonic Acid 34-62 mucosal vascular addressin cell adhesion molecule 1 Mus musculus 21-29 16891783-3 2006 In this study, we examined the kinetics of Card15/Nod2 expression in intestinal tissue during inflammation in the 2, 4, 6-trinitrobenzenesulfonic acid (TNBS)-treated rat experimental colitis model. Trinitrobenzenesulfonic Acid 114-150 nucleotide-binding oligomerization domain containing 2 Rattus norvegicus 43-49 16917232-6 2006 RESULTS: MAdCAM-1 antisense oligonucleotides significantly suppressed the development of trinitrobenzene sulfonate colitis clinically and histopathologically compared with controls. Trinitrobenzenesulfonic Acid 89-114 mucosal vascular addressin cell adhesion molecule 1 Mus musculus 9-17 16888154-5 2006 Trinitrobenzene sulfonic acid (TNBS)-induced colitis is a murine model of human CD and vasoactive intestinal polypeptide (VIP) exerts a beneficial effect, by decreasing both inflammatory and autoimmune components of the disease. Trinitrobenzenesulfonic Acid 0-29 vasoactive intestinal peptide Homo sapiens 87-120 16888154-5 2006 Trinitrobenzene sulfonic acid (TNBS)-induced colitis is a murine model of human CD and vasoactive intestinal polypeptide (VIP) exerts a beneficial effect, by decreasing both inflammatory and autoimmune components of the disease. Trinitrobenzenesulfonic Acid 0-29 vasoactive intestinal peptide Homo sapiens 122-125 16401692-2 2006 The action of nerve growth factor (NGF) on sensory neurones contributes to the development of referred colonic hypersensitivity induced by trinitrobenzene sulfonic acid (TNBS). Trinitrobenzenesulfonic Acid 139-168 nerve growth factor Rattus norvegicus 14-33 16401692-2 2006 The action of nerve growth factor (NGF) on sensory neurones contributes to the development of referred colonic hypersensitivity induced by trinitrobenzene sulfonic acid (TNBS). Trinitrobenzenesulfonic Acid 139-168 nerve growth factor Rattus norvegicus 35-38 16401692-2 2006 The action of nerve growth factor (NGF) on sensory neurones contributes to the development of referred colonic hypersensitivity induced by trinitrobenzene sulfonic acid (TNBS). Trinitrobenzenesulfonic Acid 170-174 nerve growth factor Rattus norvegicus 14-33 16401692-2 2006 The action of nerve growth factor (NGF) on sensory neurones contributes to the development of referred colonic hypersensitivity induced by trinitrobenzene sulfonic acid (TNBS). Trinitrobenzenesulfonic Acid 170-174 nerve growth factor Rattus norvegicus 35-38 16891783-3 2006 In this study, we examined the kinetics of Card15/Nod2 expression in intestinal tissue during inflammation in the 2, 4, 6-trinitrobenzenesulfonic acid (TNBS)-treated rat experimental colitis model. Trinitrobenzenesulfonic Acid 114-150 nucleotide-binding oligomerization domain containing 2 Rattus norvegicus 50-54 16891783-3 2006 In this study, we examined the kinetics of Card15/Nod2 expression in intestinal tissue during inflammation in the 2, 4, 6-trinitrobenzenesulfonic acid (TNBS)-treated rat experimental colitis model. Trinitrobenzenesulfonic Acid 152-156 nucleotide-binding oligomerization domain containing 2 Rattus norvegicus 43-49 16891783-3 2006 In this study, we examined the kinetics of Card15/Nod2 expression in intestinal tissue during inflammation in the 2, 4, 6-trinitrobenzenesulfonic acid (TNBS)-treated rat experimental colitis model. Trinitrobenzenesulfonic Acid 152-156 nucleotide-binding oligomerization domain containing 2 Rattus norvegicus 50-54 16891783-5 2006 Card15/Nod2 mRNA expression increased and peaked at 4 days after the TNBS administration, followed by a gradual decrease in accordance with the amelioration of the inflammatory response. Trinitrobenzenesulfonic Acid 69-73 nucleotide-binding oligomerization domain containing 2 Rattus norvegicus 0-6 16891783-5 2006 Card15/Nod2 mRNA expression increased and peaked at 4 days after the TNBS administration, followed by a gradual decrease in accordance with the amelioration of the inflammatory response. Trinitrobenzenesulfonic Acid 69-73 nucleotide-binding oligomerization domain containing 2 Rattus norvegicus 7-11 16331625-7 2006 When IFN-gamma(-/-) mice were treated with AOM and TNBS, significantly higher number of tumors were seen (8.4 +/- 1.7) than in WT (3.3 +/- 2.9) or IL-4(-/-) (3.1 +/- 3.4) mice, which received identical treatments. Trinitrobenzenesulfonic Acid 51-55 interferon gamma Mus musculus 5-14 16771773-1 2006 Macroscopic and histological analysis revealed that the colonic inflammation induced by 2,4,6-trinitrobenzenesulphonic acid (TNBS) was of lower grade in tumour necrosis factor-alpha (TNF-alpha)(-/-) mice than in wild-type mice. Trinitrobenzenesulfonic Acid 88-123 tumor necrosis factor Mus musculus 183-192 16771773-1 2006 Macroscopic and histological analysis revealed that the colonic inflammation induced by 2,4,6-trinitrobenzenesulphonic acid (TNBS) was of lower grade in tumour necrosis factor-alpha (TNF-alpha)(-/-) mice than in wild-type mice. Trinitrobenzenesulfonic Acid 125-129 tumor necrosis factor Mus musculus 183-192 16771773-3 2006 After the induction of inflammation with TNBS, the levels of proinflammatory cytokines, such as TNF-alpha, interleukin-1beta and interleukin-6, were elevated both in the inflamed mucosa and muscle layers in the wild-type mice; however, the productions of these cytokines were greatly reduced in the TNF-alpha(-/-) mouse colon. Trinitrobenzenesulfonic Acid 41-45 tumor necrosis factor Mus musculus 96-105 16771773-3 2006 After the induction of inflammation with TNBS, the levels of proinflammatory cytokines, such as TNF-alpha, interleukin-1beta and interleukin-6, were elevated both in the inflamed mucosa and muscle layers in the wild-type mice; however, the productions of these cytokines were greatly reduced in the TNF-alpha(-/-) mouse colon. Trinitrobenzenesulfonic Acid 41-45 interleukin 1 beta Mus musculus 107-124 16771773-3 2006 After the induction of inflammation with TNBS, the levels of proinflammatory cytokines, such as TNF-alpha, interleukin-1beta and interleukin-6, were elevated both in the inflamed mucosa and muscle layers in the wild-type mice; however, the productions of these cytokines were greatly reduced in the TNF-alpha(-/-) mouse colon. Trinitrobenzenesulfonic Acid 41-45 interleukin 6 Mus musculus 129-142 16771773-3 2006 After the induction of inflammation with TNBS, the levels of proinflammatory cytokines, such as TNF-alpha, interleukin-1beta and interleukin-6, were elevated both in the inflamed mucosa and muscle layers in the wild-type mice; however, the productions of these cytokines were greatly reduced in the TNF-alpha(-/-) mouse colon. Trinitrobenzenesulfonic Acid 41-45 tumor necrosis factor Mus musculus 299-308 16697735-4 2006 METHODS: We examined the anti-inflammatory action of ghrelin in the colitis induced by intracolonic administration of trinitrobenzene sulfonic acid. Trinitrobenzenesulfonic Acid 118-147 ghrelin Mus musculus 53-60 16697735-7 2006 RESULTS: Ghrelin ameliorated significantly the clinical and histopathologic severity of the trinitrobenzene sulfonic acid-induced colitis; abrogating body weight loss, diarrhea, and inflammation; and increasing survival. Trinitrobenzenesulfonic Acid 92-121 ghrelin Mus musculus 9-16 16630028-2 2006 Recently it has been demonstrated that p38MAPK (mitogen-activated protein kinase) inhibition using SB203580 is effective in reducing disease in both dextran sulphate sodium (DSS)-induced and 2,4,6-trinitrobenzenesulphonic acid (TNBS)-induced murine colitides, underscoring the importance of this pathway in gastrointestinal inflammation. Trinitrobenzenesulfonic Acid 191-226 mitogen-activated protein kinase 14 Mus musculus 39-46 16630028-2 2006 Recently it has been demonstrated that p38MAPK (mitogen-activated protein kinase) inhibition using SB203580 is effective in reducing disease in both dextran sulphate sodium (DSS)-induced and 2,4,6-trinitrobenzenesulphonic acid (TNBS)-induced murine colitides, underscoring the importance of this pathway in gastrointestinal inflammation. Trinitrobenzenesulfonic Acid 228-232 mitogen-activated protein kinase 14 Mus musculus 39-46 16331625-7 2006 When IFN-gamma(-/-) mice were treated with AOM and TNBS, significantly higher number of tumors were seen (8.4 +/- 1.7) than in WT (3.3 +/- 2.9) or IL-4(-/-) (3.1 +/- 3.4) mice, which received identical treatments. Trinitrobenzenesulfonic Acid 51-55 interleukin 4 Mus musculus 147-151 16331625-8 2006 A separate set of experiment, using less doses of AOM and TNBS also showed the higher frequency of tumor formation in IFN-gamma(-/-) mice than in IL-4(-/-) mice. Trinitrobenzenesulfonic Acid 58-62 interferon gamma Mus musculus 118-127 16331625-8 2006 A separate set of experiment, using less doses of AOM and TNBS also showed the higher frequency of tumor formation in IFN-gamma(-/-) mice than in IL-4(-/-) mice. Trinitrobenzenesulfonic Acid 58-62 interleukin 4 Mus musculus 146-150 16689657-4 2006 On day 7 after anal instillation of TNBS, SD and DA rats demonstrated massive lymphocyte infiltration with an interferon-gamma (IFN-gamma) mRNA upregulation, whereas Lewis, F344, and BN rats showed an intense submucosal neutrophil accumulation with high tumor necrosis factor-alpha (TNF-alpha) mRNA levels. Trinitrobenzenesulfonic Acid 36-40 interferon gamma Rattus norvegicus 110-126 16689657-4 2006 On day 7 after anal instillation of TNBS, SD and DA rats demonstrated massive lymphocyte infiltration with an interferon-gamma (IFN-gamma) mRNA upregulation, whereas Lewis, F344, and BN rats showed an intense submucosal neutrophil accumulation with high tumor necrosis factor-alpha (TNF-alpha) mRNA levels. Trinitrobenzenesulfonic Acid 36-40 interferon gamma Rattus norvegicus 128-137 16689657-4 2006 On day 7 after anal instillation of TNBS, SD and DA rats demonstrated massive lymphocyte infiltration with an interferon-gamma (IFN-gamma) mRNA upregulation, whereas Lewis, F344, and BN rats showed an intense submucosal neutrophil accumulation with high tumor necrosis factor-alpha (TNF-alpha) mRNA levels. Trinitrobenzenesulfonic Acid 36-40 tumor necrosis factor Rattus norvegicus 254-281 16689657-4 2006 On day 7 after anal instillation of TNBS, SD and DA rats demonstrated massive lymphocyte infiltration with an interferon-gamma (IFN-gamma) mRNA upregulation, whereas Lewis, F344, and BN rats showed an intense submucosal neutrophil accumulation with high tumor necrosis factor-alpha (TNF-alpha) mRNA levels. Trinitrobenzenesulfonic Acid 36-40 tumor necrosis factor Rattus norvegicus 283-292 16552751-3 2006 Here, we show that expression of ghrelin and its receptor mRNA is significantly increased during acute experimental colitis in mice injected intracolonically with trinitrobenzene sulfate (TNBS). Trinitrobenzenesulfonic Acid 188-192 ghrelin Mus musculus 33-40 16670527-6 2006 RESULTS: Using a model of acute trinitrobenzenesulfonic acid (TNBS)-induced colitis, we found that IL-17 was produced in colon tissue at 24 and 48 hours and that IL-17R knockout mice were significantly protected against TNBS-induced weight loss, IL-6 production, colonic inflammation, and local macrophage inflammatory protein-2 induction. Trinitrobenzenesulfonic Acid 62-66 interleukin 17A Mus musculus 99-104 16670527-6 2006 RESULTS: Using a model of acute trinitrobenzenesulfonic acid (TNBS)-induced colitis, we found that IL-17 was produced in colon tissue at 24 and 48 hours and that IL-17R knockout mice were significantly protected against TNBS-induced weight loss, IL-6 production, colonic inflammation, and local macrophage inflammatory protein-2 induction. Trinitrobenzenesulfonic Acid 62-66 interleukin 17 receptor A Mus musculus 162-168 16670527-6 2006 RESULTS: Using a model of acute trinitrobenzenesulfonic acid (TNBS)-induced colitis, we found that IL-17 was produced in colon tissue at 24 and 48 hours and that IL-17R knockout mice were significantly protected against TNBS-induced weight loss, IL-6 production, colonic inflammation, and local macrophage inflammatory protein-2 induction. Trinitrobenzenesulfonic Acid 220-224 interleukin 17A Mus musculus 99-104 16670527-6 2006 RESULTS: Using a model of acute trinitrobenzenesulfonic acid (TNBS)-induced colitis, we found that IL-17 was produced in colon tissue at 24 and 48 hours and that IL-17R knockout mice were significantly protected against TNBS-induced weight loss, IL-6 production, colonic inflammation, and local macrophage inflammatory protein-2 induction. Trinitrobenzenesulfonic Acid 220-224 interleukin 17 receptor A Mus musculus 162-168 16670527-9 2006 Furthermore, overexpression of an IL-17R IgG1 fusion protein significantly attenuated colonic inflammation after acute TNBS. Trinitrobenzenesulfonic Acid 119-123 interleukin 17 receptor A Mus musculus 34-40 16670527-6 2006 RESULTS: Using a model of acute trinitrobenzenesulfonic acid (TNBS)-induced colitis, we found that IL-17 was produced in colon tissue at 24 and 48 hours and that IL-17R knockout mice were significantly protected against TNBS-induced weight loss, IL-6 production, colonic inflammation, and local macrophage inflammatory protein-2 induction. Trinitrobenzenesulfonic Acid 32-60 interleukin 17A Mus musculus 99-104 16670527-6 2006 RESULTS: Using a model of acute trinitrobenzenesulfonic acid (TNBS)-induced colitis, we found that IL-17 was produced in colon tissue at 24 and 48 hours and that IL-17R knockout mice were significantly protected against TNBS-induced weight loss, IL-6 production, colonic inflammation, and local macrophage inflammatory protein-2 induction. Trinitrobenzenesulfonic Acid 32-60 interleukin 17 receptor A Mus musculus 162-168