PMID-sentid Pub_year Sent_text compound_name comp_offset prot_official_name organism prot_offset 22297444-3 2011 We previously demonstrated that mucosal Hsp60 decreases in UC patients treated with conventional therapies (mesalazine, probiotics), suggesting that this chaperonin could be a reliable biomarker useful for monitoring response to treatment, and that it might play a role in pathogenesis. Mesalamine 108-118 heat shock protein family D (Hsp60) member 1 Homo sapiens 40-45 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. Mesalamine 66-87 myeloperoxidase Homo sapiens 151-166 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. Mesalamine 66-87 myeloperoxidase Homo sapiens 168-171 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. Mesalamine 66-87 nuclear factor kappa B subunit 1 Homo sapiens 174-195 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. Mesalamine 66-87 nuclear factor kappa B subunit 1 Homo sapiens 197-206 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. Mesalamine 89-94 myeloperoxidase Homo sapiens 151-166 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. Mesalamine 89-94 myeloperoxidase Homo sapiens 168-171 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. Mesalamine 89-94 nuclear factor kappa B subunit 1 Homo sapiens 174-195 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. Mesalamine 89-94 nuclear factor kappa B subunit 1 Homo sapiens 197-206 21153768-6 2011 The results showed that manifestation, colonic damage score and MPO activities of the rats treated with 5-ASA or/and rhITFs were improved, serum EGF production was augmented and expression of tissue NF-kappaB was down-regulated. Mesalamine 104-109 myeloperoxidase Rattus norvegicus 64-67 21153768-6 2011 The results showed that manifestation, colonic damage score and MPO activities of the rats treated with 5-ASA or/and rhITFs were improved, serum EGF production was augmented and expression of tissue NF-kappaB was down-regulated. Mesalamine 104-109 nuclear factor kappa B subunit 1 Homo sapiens 199-208 21315419-1 2011 We have previously reported that treatment of colorectal cancer cells with mesalazine results in the up-regulated expression of a novel member of the cadherin protein superfamily, named mu-protocadherin, which is able to sequester beta-catenin on plasmatic membrane of treated cells inhibiting its proliferation signalling pathway. Mesalamine 75-85 cadherin 1 Homo sapiens 150-158 21315419-1 2011 We have previously reported that treatment of colorectal cancer cells with mesalazine results in the up-regulated expression of a novel member of the cadherin protein superfamily, named mu-protocadherin, which is able to sequester beta-catenin on plasmatic membrane of treated cells inhibiting its proliferation signalling pathway. Mesalamine 75-85 cadherin related family member 5 Homo sapiens 186-202 21315419-1 2011 We have previously reported that treatment of colorectal cancer cells with mesalazine results in the up-regulated expression of a novel member of the cadherin protein superfamily, named mu-protocadherin, which is able to sequester beta-catenin on plasmatic membrane of treated cells inhibiting its proliferation signalling pathway. Mesalamine 75-85 catenin beta 1 Homo sapiens 231-243 21354904-7 2011 Huangqin and mesalazine significantly lessened inflammatory cell infiltration and decreased the mast cell number and serum IL-6 level after a one-week treatment. Mesalamine 13-23 interleukin 6 Rattus norvegicus 123-127 21430235-3 2011 Using human embryonic kidney cells stably expressing uptake transporters of the organic anion-transporting polypeptide (OATP) family, which are expressed in human intestine and/or liver, we found that mesalazine uptake is mediated by OATP1B1, OATP1B3, and OATP2B1 but not by OATP1A2 and OATP4A1. Mesalamine 201-211 solute carrier organic anion transporter family member 1A2 Homo sapiens 80-118 21430235-3 2011 Using human embryonic kidney cells stably expressing uptake transporters of the organic anion-transporting polypeptide (OATP) family, which are expressed in human intestine and/or liver, we found that mesalazine uptake is mediated by OATP1B1, OATP1B3, and OATP2B1 but not by OATP1A2 and OATP4A1. Mesalamine 201-211 solute carrier organic anion transporter family member 1A2 Homo sapiens 120-124 21430235-3 2011 Using human embryonic kidney cells stably expressing uptake transporters of the organic anion-transporting polypeptide (OATP) family, which are expressed in human intestine and/or liver, we found that mesalazine uptake is mediated by OATP1B1, OATP1B3, and OATP2B1 but not by OATP1A2 and OATP4A1. Mesalamine 201-211 solute carrier organic anion transporter family member 1B1 Homo sapiens 234-241 21430235-3 2011 Using human embryonic kidney cells stably expressing uptake transporters of the organic anion-transporting polypeptide (OATP) family, which are expressed in human intestine and/or liver, we found that mesalazine uptake is mediated by OATP1B1, OATP1B3, and OATP2B1 but not by OATP1A2 and OATP4A1. Mesalamine 201-211 solute carrier organic anion transporter family member 1B3 Homo sapiens 243-250 21430235-3 2011 Using human embryonic kidney cells stably expressing uptake transporters of the organic anion-transporting polypeptide (OATP) family, which are expressed in human intestine and/or liver, we found that mesalazine uptake is mediated by OATP1B1, OATP1B3, and OATP2B1 but not by OATP1A2 and OATP4A1. Mesalamine 201-211 solute carrier organic anion transporter family member 2B1 Homo sapiens 256-263 21430235-3 2011 Using human embryonic kidney cells stably expressing uptake transporters of the organic anion-transporting polypeptide (OATP) family, which are expressed in human intestine and/or liver, we found that mesalazine uptake is mediated by OATP1B1, OATP1B3, and OATP2B1 but not by OATP1A2 and OATP4A1. Mesalamine 201-211 solute carrier organic anion transporter family member 1A2 Homo sapiens 275-282 21430235-3 2011 Using human embryonic kidney cells stably expressing uptake transporters of the organic anion-transporting polypeptide (OATP) family, which are expressed in human intestine and/or liver, we found that mesalazine uptake is mediated by OATP1B1, OATP1B3, and OATP2B1 but not by OATP1A2 and OATP4A1. Mesalamine 201-211 solute carrier organic anion transporter family member 4A1 Homo sapiens 287-294 21430235-4 2011 Moreover, genetic variations (*1b, *5, *15) in the SLCO1B1 gene encoding OATP1B1 reduced the K(m) value for mesalazine uptake from 55.1 to 16.3, 24.3, and 32.4 muM, respectively, and the respective V(max) values. Mesalamine 108-118 solute carrier organic anion transporter family member 1B1 Homo sapiens 51-58 21430235-4 2011 Moreover, genetic variations (*1b, *5, *15) in the SLCO1B1 gene encoding OATP1B1 reduced the K(m) value for mesalazine uptake from 55.1 to 16.3, 24.3, and 32.4 muM, respectively, and the respective V(max) values. Mesalamine 108-118 solute carrier organic anion transporter family member 1B1 Homo sapiens 73-80 21430235-4 2011 Moreover, genetic variations (*1b, *5, *15) in the SLCO1B1 gene encoding OATP1B1 reduced the K(m) value for mesalazine uptake from 55.1 to 16.3, 24.3, and 32.4 muM, respectively, and the respective V(max) values. Mesalamine 108-118 latexin Homo sapiens 160-163 21430235-5 2011 Finally, budesonide, cyclosporine, and rifampin were identified as inhibitors of OATP1B1-, OATP1B3-, and OATP2B1-meditated mesalazine uptake. Mesalamine 123-133 solute carrier organic anion transporter family member 1B1 Homo sapiens 81-88 21430235-5 2011 Finally, budesonide, cyclosporine, and rifampin were identified as inhibitors of OATP1B1-, OATP1B3-, and OATP2B1-meditated mesalazine uptake. Mesalamine 123-133 solute carrier organic anion transporter family member 1B3 Homo sapiens 91-98 21430235-5 2011 Finally, budesonide, cyclosporine, and rifampin were identified as inhibitors of OATP1B1-, OATP1B3-, and OATP2B1-meditated mesalazine uptake. Mesalamine 123-133 solute carrier organic anion transporter family member 2B1 Homo sapiens 105-112 21430235-6 2011 These in vitro data indicate that OATP-mediated uptake and its modification by genetic factors and comedications may play a role for mesalazine effects. Mesalamine 133-143 solute carrier organic anion transporter family member 1A2 Homo sapiens 34-38 20629092-8 2011 Angiogenin levels were lower in UC patients receiving 5-aminosalicylate (5-ASA) alone, compared to those receiving combined therapy (P = 0.0478). Mesalamine 54-71 angiogenin Homo sapiens 0-10 20629092-8 2011 Angiogenin levels were lower in UC patients receiving 5-aminosalicylate (5-ASA) alone, compared to those receiving combined therapy (P = 0.0478). Mesalamine 73-78 angiogenin Homo sapiens 0-10 21222616-4 2011 Here we demonstrate that 5-ASA alters beta-catenin immunocomplex formation by changing complex binding of seven proteins including translation initiation factors eIF4b. Mesalamine 25-30 LOC100125986 Oryctolagus cuniculus 38-50 21222616-4 2011 Here we demonstrate that 5-ASA alters beta-catenin immunocomplex formation by changing complex binding of seven proteins including translation initiation factors eIF4b. Mesalamine 25-30 eukaryotic translation initiation factor 4B Oryctolagus cuniculus 162-167 21222616-5 2011 OMICs-based cross-testing by reverse in-gel chemogenomics (utilizing 5-ASA"s fluorescent properties), in-silico docking and surface plasmon resonance experiments identified binding of 5-ASA to eIF4e"s cap-binding pocket, a key regulatory site for protein synthesis. Mesalamine 184-189 eukaryotic translation initiation factor 4E Oryctolagus cuniculus 193-198 21222616-7 2011 By using two unbiased and independent OMICs-based experimental approaches two members of the cellular translation machinery, eIF4b and IF4e, were identified as targets of 5-ASA. Mesalamine 171-176 eukaryotic translation initiation factor 4B Oryctolagus cuniculus 125-130 21345224-8 2011 Interestingly, highly expressing foci were consistently observed at the edges of ulcers where flattened, motile epithelial cells are actively involved in restitution, and also in areas of mucosal regeneration.5-aminosalicylate reduced fascin expression in colorectal epithelial cells and inhibited their motility. Mesalamine 209-226 fascin actin-bundling protein 1 Homo sapiens 235-241 19932165-7 2010 5-Aminosalicylic acid, an anti-inflammatory drug routinely used in the management of inflammatory bowel disease, also increased PPARgamma expression but to a lesser extent. Mesalamine 0-21 peroxisome proliferator activated receptor gamma Mus musculus 128-137 20973884-0 2011 Mesalamine-induced B7-H1 expression on hepatic stellate cells attenuates autoimmune liver injury. Mesalamine 0-10 CD274 antigen Mus musculus 19-24 20973884-6 2011 B7-H1 expression on LX-2 cells following mesalamine treatment was examined by using flow cytometry. Mesalamine 41-51 CD274 antigen Mus musculus 0-5 20973884-9 2011 RESULTS: Flow cytometry showed that mesalamine treatment increased the B7-H1-expressing LX-2 cell fraction from 45.4% to 88.2%, of which increment is equivalent to that of positive control (29.9%, interferon gamma-treated cells). Mesalamine 38-48 CD274 molecule Homo sapiens 73-78 20973884-13 2011 CONCLUSION: These results demonstrate that mesalamine enhances B7-H1 expression on HSCs, and thus, induces T-cell apoptosis and attenuates autoimmune liver injury. Mesalamine 45-55 CD274 molecule Homo sapiens 65-70 20061197-9 2010 An association with 5-aminosalicylate therapy (R(2)=0.4) was only detected with RAP1 mRNA expression. Mesalamine 20-37 TERF2 interacting protein Homo sapiens 80-84 20304104-2 2010 It has been reported that 5-aminosalicylate (5-ASA) has an affinity for PPARgamma, but the effects of 5-ASA on the nasal symptoms of allergic rhinitis are unclear. Mesalamine 26-43 peroxisome proliferator activated receptor gamma Mus musculus 72-81 20304104-2 2010 It has been reported that 5-aminosalicylate (5-ASA) has an affinity for PPARgamma, but the effects of 5-ASA on the nasal symptoms of allergic rhinitis are unclear. Mesalamine 45-50 peroxisome proliferator activated receptor gamma Mus musculus 72-81 19760781-0 2010 Effect of EP4 agonist (ONO-4819CD) for patients with mild to moderate ulcerative colitis refractory to 5-aminosalicylates: a randomized phase II, placebo-controlled trial. Mesalamine 103-121 prostaglandin E receptor 4 Homo sapiens 10-13 20631420-2 2010 Recent in vivo and in vitro studies have demonstrated that 5-aminosalicylic acid (5-ASA), regarded as the active moiety in aminosalicylate preparations such as sulfasalazine, can induce the heat shock protein, heme oxygenase-1 (HO-1) and up-regulate HO enzyme activity in the colon. Mesalamine 59-80 heme oxygenase 1 Homo sapiens 210-226 20631420-2 2010 Recent in vivo and in vitro studies have demonstrated that 5-aminosalicylic acid (5-ASA), regarded as the active moiety in aminosalicylate preparations such as sulfasalazine, can induce the heat shock protein, heme oxygenase-1 (HO-1) and up-regulate HO enzyme activity in the colon. Mesalamine 59-80 heme oxygenase 1 Homo sapiens 228-232 20631420-2 2010 Recent in vivo and in vitro studies have demonstrated that 5-aminosalicylic acid (5-ASA), regarded as the active moiety in aminosalicylate preparations such as sulfasalazine, can induce the heat shock protein, heme oxygenase-1 (HO-1) and up-regulate HO enzyme activity in the colon. Mesalamine 82-87 heme oxygenase 1 Homo sapiens 210-226 20631420-2 2010 Recent in vivo and in vitro studies have demonstrated that 5-aminosalicylic acid (5-ASA), regarded as the active moiety in aminosalicylate preparations such as sulfasalazine, can induce the heat shock protein, heme oxygenase-1 (HO-1) and up-regulate HO enzyme activity in the colon. Mesalamine 82-87 heme oxygenase 1 Homo sapiens 228-232 19901345-7 2010 Be-stimulated CBD BAL cell IFN-gamma and TNF-alpha cytokine production was decreased by treatment with sulfasalazine or mesalamine. Mesalamine 120-130 interferon gamma Homo sapiens 27-36 19901345-7 2010 Be-stimulated CBD BAL cell IFN-gamma and TNF-alpha cytokine production was decreased by treatment with sulfasalazine or mesalamine. Mesalamine 120-130 tumor necrosis factor Homo sapiens 41-50 20304104-11 2010 Finally, 5-ASA inhibited both OVA-specific IgE antibody and IL-4 production; however, it had no effect on IL-10 levels. Mesalamine 9-14 interleukin 4 Mus musculus 60-64 23251733-5 2010 The possible synergism between the two drugs, because of the inhibition of thiopurine methyltransferase (TPMT) enzyme activity by 5-ASA, has been postulated as another justification for dual prescription. Mesalamine 130-135 thiopurine S-methyltransferase Homo sapiens 75-103 23251733-5 2010 The possible synergism between the two drugs, because of the inhibition of thiopurine methyltransferase (TPMT) enzyme activity by 5-ASA, has been postulated as another justification for dual prescription. Mesalamine 130-135 thiopurine S-methyltransferase Homo sapiens 105-109 20197483-0 2010 Mesalazine reduces mutations in transforming growth factor beta receptor II and activin type II receptor by improvement of replication fidelity in mononucleotide repeats. Mesalamine 0-10 transforming growth factor beta receptor 2 Homo sapiens 32-75 20197483-9 2010 RESULTS: In HCT116, 5-ASA reduced the mutant fraction at (CA)13 by 48.3%, at A10 by 35.6-43.6%, at G10 by 74.9-83.6%, and at (AAAG)17 by 37.6-44.4%. Mesalamine 20-25 immunoglobulin kappa variable 6D-21 (non-functional) Homo sapiens 77-80 20197483-11 2010 Moreover, the presence of 5-ASA significantly reduced mutations in TGFBR2 (A10) and ACVR2 (A8) by 39.9% and 46.2%, respectively. Mesalamine 26-31 transforming growth factor beta receptor 2 Homo sapiens 67-73 20197483-11 2010 Moreover, the presence of 5-ASA significantly reduced mutations in TGFBR2 (A10) and ACVR2 (A8) by 39.9% and 46.2%, respectively. Mesalamine 26-31 immunoglobulin kappa variable 6D-21 (non-functional) Homo sapiens 75-78 20197483-11 2010 Moreover, the presence of 5-ASA significantly reduced mutations in TGFBR2 (A10) and ACVR2 (A8) by 39.9% and 46.2%, respectively. Mesalamine 26-31 activin A receptor type 2A Homo sapiens 84-89 20197483-12 2010 CONCLUSIONS: 5-ASA increases replication fidelity in mononucleotide, dinucleotide, and tetranucleotide repeats and reduces mutations in tumor suppressor genes TGFBR2 and ACVR2, a finding that may provoke in vivo studies for the prevention of colorectal cancer in hereditary nonpolyposis colorectal cancer. Mesalamine 13-18 transforming growth factor beta receptor 2 Homo sapiens 159-165 20197483-12 2010 CONCLUSIONS: 5-ASA increases replication fidelity in mononucleotide, dinucleotide, and tetranucleotide repeats and reduces mutations in tumor suppressor genes TGFBR2 and ACVR2, a finding that may provoke in vivo studies for the prevention of colorectal cancer in hereditary nonpolyposis colorectal cancer. Mesalamine 13-18 activin A receptor type 2A Homo sapiens 170-175 20151072-6 2010 A mechanism of action for such chemoprevention has been provided by the agonism of the peroxisome proliferator-activated receptor-gamma by 5-ASA, which unifies its efficacy as an anti-inflammatory and chemopreventive agent. Mesalamine 139-144 peroxisome proliferator activated receptor gamma Homo sapiens 87-135 20091560-16 2010 Rectal 5-ASA was superior to rectal corticosteroids for inducing symptomatic improvement and remission with POR 1.56 (6 trials, 95% CI 1.15 to 2.11; P = 0.004) and 1.65 (6 trials, 95% CI 1.11 to 2.45; P = 0.01), respectively. Mesalamine 7-12 ADP ribosylation factor interacting protein 2 Homo sapiens 108-113 19879273-0 2010 Mesalamine inhibits epithelial beta-catenin activation in chronic ulcerative colitis. Mesalamine 0-10 catenin beta 1 Homo sapiens 31-43 19879273-2 2010 The present study addressed the possibility that mesalamine reduces beta-catenin-associated progenitor cell activation, Akt-phosphorylated beta-catenin(Ser552) (P-beta-catenin), and colitis-induced dysplasia (CID). Mesalamine 49-59 catenin beta 1 Homo sapiens 68-80 19879273-2 2010 The present study addressed the possibility that mesalamine reduces beta-catenin-associated progenitor cell activation, Akt-phosphorylated beta-catenin(Ser552) (P-beta-catenin), and colitis-induced dysplasia (CID). Mesalamine 49-59 AKT serine/threonine kinase 1 Homo sapiens 120-123 19879273-2 2010 The present study addressed the possibility that mesalamine reduces beta-catenin-associated progenitor cell activation, Akt-phosphorylated beta-catenin(Ser552) (P-beta-catenin), and colitis-induced dysplasia (CID). Mesalamine 49-59 catenin beta 1 Homo sapiens 139-151 19879273-2 2010 The present study addressed the possibility that mesalamine reduces beta-catenin-associated progenitor cell activation, Akt-phosphorylated beta-catenin(Ser552) (P-beta-catenin), and colitis-induced dysplasia (CID). Mesalamine 49-59 catenin beta 1 Homo sapiens 139-151 19879273-3 2010 METHODS: Effects of mesalamine on P-beta-catenin staining and function were assessed by immunohistochemistry and quantitative reverse-transcription polymerase chain reaction (qRT-PCR) in biopsy specimens of CUC in mild or "refractory" severe mucosal inflammation. Mesalamine 20-30 catenin beta 1 Homo sapiens 36-48 19879273-6 2010 RESULTS: Data from IL-10(-/-) and human colitis samples show that mesalamine reduced Akt activation and P-beta-catenin levels in the middle and upper crypt. Mesalamine 66-76 interleukin 10 Homo sapiens 19-24 19879273-6 2010 RESULTS: Data from IL-10(-/-) and human colitis samples show that mesalamine reduced Akt activation and P-beta-catenin levels in the middle and upper crypt. Mesalamine 66-76 thymoma viral proto-oncogene 1 Mus musculus 85-88 19879273-6 2010 RESULTS: Data from IL-10(-/-) and human colitis samples show that mesalamine reduced Akt activation and P-beta-catenin levels in the middle and upper crypt. Mesalamine 66-76 catenin beta 1 Homo sapiens 106-118 19879273-7 2010 Reductions in P-beta-catenin in CUC biopsy specimens with severe inflammation suggested that mesalamine reduced P-beta-catenin levels in tissue refractory to mesalamine"s anti-inflammatory effects. Mesalamine 93-103 catenin beta 1 Homo sapiens 16-28 19879273-7 2010 Reductions in P-beta-catenin in CUC biopsy specimens with severe inflammation suggested that mesalamine reduced P-beta-catenin levels in tissue refractory to mesalamine"s anti-inflammatory effects. Mesalamine 93-103 catenin beta 1 Homo sapiens 114-126 19879273-8 2010 In IL-10(-/-) mice, mesalamine reduced CID concordant with inhibition of crypt Akt and beta-catenin signaling. Mesalamine 20-30 interleukin 10 Mus musculus 3-8 19879273-9 2010 CONCLUSIONS: The results are consistent with the model that mesalamine contributes to chemoprevention in CAC by reducing beta-catenin signaling within intestinal progenitors. Mesalamine 60-70 catenin beta 1 Homo sapiens 121-133 21208525-8 2010 Sulfasalazine was also able to scavenge these RNS, although with a much lower potency than 5-ASA. Mesalamine 91-96 FAM20C golgi associated secretory pathway kinase Homo sapiens 46-49 19817724-2 2010 AIM: To test the hypothesis that sulfasalazine (SASP) might have a synergistic beneficial effect in acute pouchitis, by combining the anti-inflammatory activity of 5-aminosalicylic Acid and the bacteriostatic effect of sulphapyridine. Mesalamine 164-185 aspartic peptidase retroviral like 1 Homo sapiens 48-52 19541409-0 2010 5-Aminosalicylic acid inhibits TGF-beta1 signalling in colorectal cancer cells. Mesalamine 0-21 transforming growth factor beta 1 Homo sapiens 31-40 19541409-2 2010 We aimed to determine the effects of 5-aminosalicylic acid (5-ASA) on TGF-beta signalling in colorectal cancer cells in vitro. Mesalamine 37-58 transforming growth factor beta 1 Homo sapiens 70-78 19541409-2 2010 We aimed to determine the effects of 5-aminosalicylic acid (5-ASA) on TGF-beta signalling in colorectal cancer cells in vitro. Mesalamine 60-65 transforming growth factor beta 1 Homo sapiens 70-78 19541409-3 2010 5-ASA inhibited TGF-beta1 signalling in HCT116 cells and colonic fibroblasts, as judged by a TGF-beta-specific reporter gene assay, plasminogen activator inhibitor-1 mRNA and protein levels, fibroblast trans-differentiation, Smad3 phosphorylation and nuclear translocation. Mesalamine 0-5 transforming growth factor beta 1 Homo sapiens 16-25 19541409-3 2010 5-ASA inhibited TGF-beta1 signalling in HCT116 cells and colonic fibroblasts, as judged by a TGF-beta-specific reporter gene assay, plasminogen activator inhibitor-1 mRNA and protein levels, fibroblast trans-differentiation, Smad3 phosphorylation and nuclear translocation. Mesalamine 0-5 serpin family E member 1 Homo sapiens 132-165 19541409-3 2010 5-ASA inhibited TGF-beta1 signalling in HCT116 cells and colonic fibroblasts, as judged by a TGF-beta-specific reporter gene assay, plasminogen activator inhibitor-1 mRNA and protein levels, fibroblast trans-differentiation, Smad3 phosphorylation and nuclear translocation. Mesalamine 0-5 SMAD family member 3 Homo sapiens 225-230 19541409-4 2010 We conclude that 5-ASA inhibits TGF-beta1 signalling in colorectal cancer cells, and might be a potent adjuvant therapeutic drug, interfering with aberrant TGF-beta signalling in colorectal cancer. Mesalamine 17-22 transforming growth factor beta 1 Homo sapiens 32-41 19541409-4 2010 We conclude that 5-ASA inhibits TGF-beta1 signalling in colorectal cancer cells, and might be a potent adjuvant therapeutic drug, interfering with aberrant TGF-beta signalling in colorectal cancer. Mesalamine 17-22 transforming growth factor beta 1 Homo sapiens 32-40 20926883-15 2010 Clinical practice should change such that combination therapy with an anti-TNF agent and azathioprine replace azathioprine in patients failing first line therapy with mesalamine and/or steroids. Mesalamine 167-177 tumor necrosis factor Homo sapiens 75-78 18976971-4 2009 The expression of NF-kappaB and metalloproteinases was examined in either HT-29 cells treated with IL-1beta and/or 5-aminosalicylic acid. Mesalamine 115-136 nuclear factor kappa B subunit 1 Homo sapiens 18-27 19616541-0 2009 An anti-inflammatory mechanism of taurine conjugated 5-aminosalicylic acid against experimental colitis: taurine chloramine potentiates inhibitory effect of 5-aminosalicylic acid on IL-1beta-mediated NFkappaB activation. Mesalamine 53-74 interleukin 1 beta Homo sapiens 182-190 19616541-0 2009 An anti-inflammatory mechanism of taurine conjugated 5-aminosalicylic acid against experimental colitis: taurine chloramine potentiates inhibitory effect of 5-aminosalicylic acid on IL-1beta-mediated NFkappaB activation. Mesalamine 53-74 nuclear factor kappa B subunit 1 Homo sapiens 200-208 19369484-10 2009 We conclude that mesalamine, sulfasalazine, and rosiglitazone significantly reduced the cellular expression of TC22, implicating PPARgamma in this modulation. Mesalamine 17-27 peroxisome proliferator activated receptor gamma Homo sapiens 129-138 19222409-5 2009 METHODS: Using published data, we created a computer model with STELLA software to simulate amounts of colonic 5-ASA in the total colon, right, transverse, descending and sigmoid/rectum after daily and three time/day Asacol. Mesalamine 111-116 developmental pluripotency associated 3 Homo sapiens 64-70 19762547-9 2009 Furthermore, 5-ASA treatment significantly diminished increased activity of TNF-alpha and MMP9 in UC. Mesalamine 13-18 tumor necrosis factor Rattus norvegicus 76-85 19762547-9 2009 Furthermore, 5-ASA treatment significantly diminished increased activity of TNF-alpha and MMP9 in UC. Mesalamine 13-18 matrix metallopeptidase 9 Rattus norvegicus 90-94 19762547-10 2009 This is the first demonstration that 5-ASA treatment reverses an imbalance between the angiogenic factor VEGF and antiangiogenic factors endostatin and angiostatin in experimental UC. Mesalamine 37-42 vascular endothelial growth factor A Rattus norvegicus 105-109 19762547-11 2009 The effect of 5-ASA in UC may be caused by the down-regulation of expression of endostatin and angiostatin by modulation of MMP2 and MMP9 via inhibition of TNFalpha. Mesalamine 14-19 matrix metallopeptidase 2 Rattus norvegicus 124-128 19762547-11 2009 The effect of 5-ASA in UC may be caused by the down-regulation of expression of endostatin and angiostatin by modulation of MMP2 and MMP9 via inhibition of TNFalpha. Mesalamine 14-19 matrix metallopeptidase 9 Rattus norvegicus 133-137 19762547-11 2009 The effect of 5-ASA in UC may be caused by the down-regulation of expression of endostatin and angiostatin by modulation of MMP2 and MMP9 via inhibition of TNFalpha. Mesalamine 14-19 tumor necrosis factor Rattus norvegicus 156-164 19616541-0 2009 An anti-inflammatory mechanism of taurine conjugated 5-aminosalicylic acid against experimental colitis: taurine chloramine potentiates inhibitory effect of 5-aminosalicylic acid on IL-1beta-mediated NFkappaB activation. Mesalamine 157-178 interleukin 1 beta Homo sapiens 182-190 19616541-0 2009 An anti-inflammatory mechanism of taurine conjugated 5-aminosalicylic acid against experimental colitis: taurine chloramine potentiates inhibitory effect of 5-aminosalicylic acid on IL-1beta-mediated NFkappaB activation. Mesalamine 157-178 nuclear factor kappa B subunit 1 Homo sapiens 200-208 19616541-6 2009 Treatment with either 5-ASA or taurine chloramine (TauCl) inhibited IL-1beta-mediated NFkappaB dependent luciferase expression and IL-6 secretion. Mesalamine 22-27 interleukin 1 beta Homo sapiens 68-76 19616541-6 2009 Treatment with either 5-ASA or taurine chloramine (TauCl) inhibited IL-1beta-mediated NFkappaB dependent luciferase expression and IL-6 secretion. Mesalamine 22-27 nuclear factor kappa B subunit 1 Homo sapiens 86-94 19616541-6 2009 Treatment with either 5-ASA or taurine chloramine (TauCl) inhibited IL-1beta-mediated NFkappaB dependent luciferase expression and IL-6 secretion. Mesalamine 22-27 interleukin 6 Homo sapiens 131-135 19616541-7 2009 In HCT116 cells, the inhibitory effect by TauCl or 5-ASA was through preventing IL-1beta-induced IkappaB kinase activation and subsequently interfering with IkappaBalpha degradation and p65 nuclear accumulation. Mesalamine 51-56 interleukin 1 beta Homo sapiens 80-88 19616541-7 2009 In HCT116 cells, the inhibitory effect by TauCl or 5-ASA was through preventing IL-1beta-induced IkappaB kinase activation and subsequently interfering with IkappaBalpha degradation and p65 nuclear accumulation. Mesalamine 51-56 NFKB inhibitor alpha Homo sapiens 157-169 19616541-7 2009 In HCT116 cells, the inhibitory effect by TauCl or 5-ASA was through preventing IL-1beta-induced IkappaB kinase activation and subsequently interfering with IkappaBalpha degradation and p65 nuclear accumulation. Mesalamine 51-56 RELA proto-oncogene, NF-kB subunit Homo sapiens 186-189 19616541-8 2009 Furthermore, combined TauCl/5-ASA treatment interfered additively with the activation process, leading to additive inhibitory effect on IL-1beta-mediated NFkappaB activation. Mesalamine 28-33 interleukin 1 beta Homo sapiens 136-144 19616541-8 2009 Furthermore, combined TauCl/5-ASA treatment interfered additively with the activation process, leading to additive inhibitory effect on IL-1beta-mediated NFkappaB activation. Mesalamine 28-33 nuclear factor kappa B subunit 1 Homo sapiens 154-162 18976971-8 2009 The activity of NF-kappaB was also decreased by combined-treatment with IL-1beta and 5-aminosalicylic acid. Mesalamine 85-106 nuclear factor kappa B subunit 1 Homo sapiens 16-25 18976971-9 2009 The use of an ELISA and zymography demonstrated that MMP-2 and MMP-9 enzyme activity were decreased in HT-29 cells by treatment with various concentration of 5-aminosalicylic acid. Mesalamine 158-179 matrix metallopeptidase 2 Homo sapiens 53-58 18976971-9 2009 The use of an ELISA and zymography demonstrated that MMP-2 and MMP-9 enzyme activity were decreased in HT-29 cells by treatment with various concentration of 5-aminosalicylic acid. Mesalamine 158-179 matrix metallopeptidase 9 Homo sapiens 63-68 18976971-12 2009 CONCLUSIONS: This study indicated that 5-aminosalicylic acid suppresses the growth of human colon cancer cells and is able to inhibit MMPs expression via NF-kappaB mediated cell signals and invasiveness. Mesalamine 39-60 matrix metallopeptidase 2 Homo sapiens 134-138 18976971-12 2009 CONCLUSIONS: This study indicated that 5-aminosalicylic acid suppresses the growth of human colon cancer cells and is able to inhibit MMPs expression via NF-kappaB mediated cell signals and invasiveness. Mesalamine 39-60 nuclear factor kappa B subunit 1 Homo sapiens 154-163 19220658-8 2009 Trinitrobenzene sulfonic acid-induced expression of TNF-alpha and IL-1beta was reduced by muscovite and 5-ASA treatment. Mesalamine 104-109 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. Mesalamine 104-109 interleukin 1 beta Rattus norvegicus 66-74 19220658-9 2009 Reduction of MUC2 expression in colitis rats was reversed by muscovite and 5-ASA treatment. Mesalamine 75-80 mucin 2, oligomeric mucus/gel-forming Rattus norvegicus 13-17 19891583-9 2009 Mesalazine significantly improved changes in the length of the colon, tissue MPO activity, WBC, and the histological inflammation score as compared with DSS-induced colitis. Mesalamine 0-10 myeloperoxidase Rattus norvegicus 77-80 18716872-3 2009 NAC alone and in combination with 5-ASA suppressed COX2 gene expression and prostaglandin E(2) (PGE(2)) levels to control values. Mesalamine 34-39 cytochrome c oxidase II, mitochondrial Rattus norvegicus 51-55 18716872-4 2009 Furthermore, NAC plus 5-ASA reduced nitrate generation, an expression of inducible nitric oxide synthase (iNOS) activity, to basal levels and these results were significantly lower than those observed with either NAC or 5-ASA alone. Mesalamine 22-27 nitric oxide synthase 2 Rattus norvegicus 73-104 18716872-4 2009 Furthermore, NAC plus 5-ASA reduced nitrate generation, an expression of inducible nitric oxide synthase (iNOS) activity, to basal levels and these results were significantly lower than those observed with either NAC or 5-ASA alone. Mesalamine 22-27 nitric oxide synthase 2 Rattus norvegicus 106-110 18785066-3 2009 The aim of this study was to investigate the underlying mechanism of NHE-3 isoform expression and its modulation by 5"-aminosalicylate in human CD and UC. Mesalamine 116-134 solute carrier family 9 member A3 Homo sapiens 69-74 19155731-8 2009 Medications associated with PPD are reviewed and the patient"s use of mesalamine and balsalazide for ulcerative colitis are deemed potential triggers, given their relative similarity to aspirin, a known trigger of PPD. Mesalamine 70-80 cellular communication network factor 6 Homo sapiens 214-217 18774638-7 2009 The growth-inhibitory action of mesalazine and butyrate was accompanied by a significant increase in caspase-3 activity, cleavage of PARP and caspase-8, while decreasing the expression of Xiap and Survivin simultaneously. Mesalamine 32-42 caspase 3 Homo sapiens 101-110 18774638-7 2009 The growth-inhibitory action of mesalazine and butyrate was accompanied by a significant increase in caspase-3 activity, cleavage of PARP and caspase-8, while decreasing the expression of Xiap and Survivin simultaneously. Mesalamine 32-42 poly(ADP-ribose) polymerase 1 Homo sapiens 133-137 18774638-7 2009 The growth-inhibitory action of mesalazine and butyrate was accompanied by a significant increase in caspase-3 activity, cleavage of PARP and caspase-8, while decreasing the expression of Xiap and Survivin simultaneously. Mesalamine 32-42 caspase 8 Homo sapiens 142-151 18774638-7 2009 The growth-inhibitory action of mesalazine and butyrate was accompanied by a significant increase in caspase-3 activity, cleavage of PARP and caspase-8, while decreasing the expression of Xiap and Survivin simultaneously. Mesalamine 32-42 X-linked inhibitor of apoptosis Homo sapiens 188-192 19891583-14 2009 These findings suggest that the recovery of mucosal impairment due to treatment with mesalazine may be associated with the protection of the tight junction protein occludin in DSS-induced colitis. Mesalamine 85-95 occludin Rattus norvegicus 164-172 18852012-17 2008 Studies on the eukaryotic enzymes by NMR and crystallography have facilitated understanding substrate specificities of human NAT1 (5-aminosalicylate and p-aminobenzoic acid) and human NAT2 (sulphamethazine). Mesalamine 131-148 N-acetyltransferase 1 Homo sapiens 125-129 18855437-5 2008 In addition, the resultant SPI hydrogel matrix was investigated for the controlled release of 5-aminosalicylic acid as the model drug. Mesalamine 94-115 chromogranin A Homo sapiens 27-30 18557988-9 2008 Concurrent 5-aminosalicylic acid therapy increased 6TU excretion significantly (median 32.9%), consistent with inhibiting TPMT. Mesalamine 11-32 thiopurine S-methyltransferase Homo sapiens 122-126 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. Mesalamine 73-78 myeloperoxidase Rattus norvegicus 0-3 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. Mesalamine 113-118 myeloperoxidase Rattus norvegicus 0-3 18703751-10 2008 alpha-Tocopherol plus 5-ASA, however, was the only treatment strategy that reduced significantly MPO activity below that recorded for 5-ASA alone. Mesalamine 22-27 myeloperoxidase Rattus norvegicus 97-100 18703751-10 2008 alpha-Tocopherol plus 5-ASA, however, was the only treatment strategy that reduced significantly MPO activity below that recorded for 5-ASA alone. Mesalamine 134-139 myeloperoxidase Rattus norvegicus 97-100 18627362-8 2008 5-ASA is now recognized as a ligand for peroxisome proliferator activated receptor-gamma (PPAR-gamma) and it has a role as a chemo-preventive agent in long-standing UC. Mesalamine 0-5 peroxisome proliferator activated receptor gamma Homo sapiens 40-88 18627362-8 2008 5-ASA is now recognized as a ligand for peroxisome proliferator activated receptor-gamma (PPAR-gamma) and it has a role as a chemo-preventive agent in long-standing UC. Mesalamine 0-5 peroxisome proliferator activated receptor gamma Homo sapiens 90-100 18758150-0 2008 Changes of the peptide YY levels in the intestinal tissue of rats with experimental colitis following oral administration of mesalazine and prednisolone. Mesalamine 125-135 peptide YY Rattus norvegicus 15-25 18758150-1 2008 Few studies have reported the changes in the peptide YY (PYY) levels in the intestinal tissue of rats with ulcerative colitis (UC) following oral administration of mesalazine and prednisolone. Mesalamine 164-174 peptide YY Rattus norvegicus 45-55 18758150-1 2008 Few studies have reported the changes in the peptide YY (PYY) levels in the intestinal tissue of rats with ulcerative colitis (UC) following oral administration of mesalazine and prednisolone. Mesalamine 164-174 peptide YY Rattus norvegicus 57-60 18758150-5 2008 The PYY levels in the caecum and colon decreased significantly after administering DSS but increased when mesalazine was administered in a tissue-specific manner. Mesalamine 106-116 peptide YY Rattus norvegicus 4-7 18495657-8 2008 Analysis of upstream kinases that negatively control CDC25A expression showed that mesalazine enhanced the activation of CHK1 and CHK2. Mesalamine 83-93 checkpoint kinase 1 Homo sapiens 121-125 18544567-0 2008 PPARgamma is involved in mesalazine-mediated induction of apoptosis and inhibition of cell growth in colon cancer cells. Mesalamine 25-35 peroxisome proliferator activated receptor gamma Homo sapiens 0-9 18544567-3 2008 The aim of our study was to investigate the involvement of peroxisome proliferator-activated receptor gamma (PPARgamma) in mesalazine"s anticarcinogenic actions in colorectal cancer cells. Mesalamine 123-133 peroxisome proliferator activated receptor gamma Homo sapiens 59-107 18544567-3 2008 The aim of our study was to investigate the involvement of peroxisome proliferator-activated receptor gamma (PPARgamma) in mesalazine"s anticarcinogenic actions in colorectal cancer cells. Mesalamine 123-133 peroxisome proliferator activated receptor gamma Homo sapiens 109-118 18544567-11 2008 The growth-inhibitory effect of mesalazine was partially reduced in dominant-negative PPARgamma mutant cells, whereas the expression of c-Myc was not affected. Mesalamine 32-42 peroxisome proliferator activated receptor gamma Homo sapiens 86-95 18544567-12 2008 Mesalazine-mediated increased caspase-3 activity, the expression of PTEN, cleavage of PARP and caspase-8 as well as reduced levels of survivin and Xiap were completely abolished in the PPARgamma mutant cell lines. Mesalamine 0-10 caspase 3 Homo sapiens 30-39 18544567-12 2008 Mesalazine-mediated increased caspase-3 activity, the expression of PTEN, cleavage of PARP and caspase-8 as well as reduced levels of survivin and Xiap were completely abolished in the PPARgamma mutant cell lines. Mesalamine 0-10 phosphatase and tensin homolog Homo sapiens 68-72 18544567-12 2008 Mesalazine-mediated increased caspase-3 activity, the expression of PTEN, cleavage of PARP and caspase-8 as well as reduced levels of survivin and Xiap were completely abolished in the PPARgamma mutant cell lines. Mesalamine 0-10 poly(ADP-ribose) polymerase 1 Homo sapiens 86-90 18544567-12 2008 Mesalazine-mediated increased caspase-3 activity, the expression of PTEN, cleavage of PARP and caspase-8 as well as reduced levels of survivin and Xiap were completely abolished in the PPARgamma mutant cell lines. Mesalamine 0-10 caspase 8 Homo sapiens 95-104 18544567-12 2008 Mesalazine-mediated increased caspase-3 activity, the expression of PTEN, cleavage of PARP and caspase-8 as well as reduced levels of survivin and Xiap were completely abolished in the PPARgamma mutant cell lines. Mesalamine 0-10 X-linked inhibitor of apoptosis Homo sapiens 147-151 18544567-12 2008 Mesalazine-mediated increased caspase-3 activity, the expression of PTEN, cleavage of PARP and caspase-8 as well as reduced levels of survivin and Xiap were completely abolished in the PPARgamma mutant cell lines. Mesalamine 0-10 peroxisome proliferator activated receptor gamma Homo sapiens 185-194 18544567-13 2008 CONCLUSION: This study clearly demonstrates that mesalazine-mediated pro-apoptotic and anti-proliferative actions are regulated via PPARgamma-dependent and -independent pathways in colonocytes. Mesalamine 49-59 peroxisome proliferator activated receptor gamma Homo sapiens 132-141 18495657-11 2008 Notably, mesalazine also inhibited CDC25A in human CRC explants. Mesalamine 9-19 cell division cycle 25A Homo sapiens 35-41 18495657-12 2008 Finally, we showed that mesalazine downregulated CDC25A in CT26, a murine CRC cell line, and prevented the formation of CT26-derived tumors in mice. Mesalamine 24-34 cell division cycle 25A Mus musculus 49-55 18495657-13 2008 Data show that mesalazine negatively regulates CDC25A protein expression, thus delaying CRC cell progression. Mesalamine 15-25 cell division cycle 25A Homo sapiens 47-53 18215658-0 2008 The involvement of heme oxygenase-1 activity in the therapeutic actions of 5-aminosalicylic acid in rat colitis. Mesalamine 75-96 heme oxygenase 1 Rattus norvegicus 19-35 18495657-0 2008 Mesalazine negatively regulates CDC25A protein expression and promotes accumulation of colon cancer cells in S phase. Mesalamine 0-10 cell division cycle 25A Homo sapiens 32-38 18495657-4 2008 Mesalazine inhibited the growth of HCT-116 and HT-29 cells, two CRC cell lines that express either a wild-type or mutated p53. Mesalamine 0-10 tumor protein p53 Homo sapiens 122-125 18495657-7 2008 Consistently, mesalazine reduced the protein content of CDC25A, a phosphatase that regulates CDK2 phosphorylation status. Mesalamine 14-24 cell division cycle 25A Homo sapiens 56-62 18495657-7 2008 Consistently, mesalazine reduced the protein content of CDC25A, a phosphatase that regulates CDK2 phosphorylation status. Mesalamine 14-24 cyclin dependent kinase 2 Homo sapiens 93-97 18495657-8 2008 Analysis of upstream kinases that negatively control CDC25A expression showed that mesalazine enhanced the activation of CHK1 and CHK2. Mesalamine 83-93 cell division cycle 25A Homo sapiens 53-59 18495657-8 2008 Analysis of upstream kinases that negatively control CDC25A expression showed that mesalazine enhanced the activation of CHK1 and CHK2. Mesalamine 83-93 checkpoint kinase 2 Homo sapiens 130-134 18495657-10 2008 In contrast, CDC25A protein ubiquitination and degradation and accumulation of cells in S phase following mesalazine exposure were reverted by proteasome inhibitors. Mesalamine 106-116 cell division cycle 25A Homo sapiens 13-19 18473409-12 2008 CONCLUSION: In group A (oral NAC combined with mesalamine) contrarily to group B (mesalamine alone), the clinical improvement correlates with a decrease of chemokines such as MCP-1 and IL-8. Mesalamine 47-57 C-C motif chemokine ligand 2 Homo sapiens 175-180 18473409-12 2008 CONCLUSION: In group A (oral NAC combined with mesalamine) contrarily to group B (mesalamine alone), the clinical improvement correlates with a decrease of chemokines such as MCP-1 and IL-8. Mesalamine 47-57 C-X-C motif chemokine ligand 8 Homo sapiens 185-189 18215658-3 2008 The effects of 5-ASA on the colonic expression and activity of HO-1 along with its effect on the inflammatory damage have been evaluated in the colitis provoked by instillation of trinitrobenzene sulphonic acid (TNBS) over 48 h in the rat. Mesalamine 15-20 heme oxygenase 1 Rattus norvegicus 63-67 18215658-4 2008 Intracolonic administration of 5-ASA (8, 25 and 75 mg/kg/day) dose-dependently reduced the TNBS-provoked macroscopic colonic inflammatory injury, myeloperoxidase (MPO) activity and TNF-alpha levels, while also dose-dependently increasing colonic heme oxygenase enzyme activity. Mesalamine 31-36 myeloperoxidase Rattus norvegicus 146-161 18215658-4 2008 Intracolonic administration of 5-ASA (8, 25 and 75 mg/kg/day) dose-dependently reduced the TNBS-provoked macroscopic colonic inflammatory injury, myeloperoxidase (MPO) activity and TNF-alpha levels, while also dose-dependently increasing colonic heme oxygenase enzyme activity. Mesalamine 31-36 myeloperoxidase Rattus norvegicus 163-166 18215658-4 2008 Intracolonic administration of 5-ASA (8, 25 and 75 mg/kg/day) dose-dependently reduced the TNBS-provoked macroscopic colonic inflammatory injury, myeloperoxidase (MPO) activity and TNF-alpha levels, while also dose-dependently increasing colonic heme oxygenase enzyme activity. Mesalamine 31-36 tumor necrosis factor Rattus norvegicus 181-190 18215658-5 2008 Colonic HO-1 protein expression, determined by Western blot analysis in this colitis model, was likewise further induced by 5-ASA. Mesalamine 124-129 heme oxygenase 1 Rattus norvegicus 8-12 18215658-8 2008 These results suggest that 5-ASA may exert its colonic anti-oxidant and anti-inflammatory effects in vivo in part through the up-regulation of HO-1 enzyme expression and activity. Mesalamine 27-32 heme oxygenase 1 Rattus norvegicus 143-147 18077625-0 2008 Reduction of peroxisome proliferation-activated receptor gamma expression by gamma-irradiation as a mechanism contributing to inflammatory response in rat colon: modulation by the 5-aminosalicylic acid agonist. Mesalamine 180-201 peroxisome proliferator activated receptor alpha Rattus norvegicus 13-56 18077625-4 2008 We tested whether irradiation-induced acute inflammatory response could be modulated pharmacologically with the antiinflammatory properties of 5-aminosalicylic acid (5-ASA) (250 mg/kg/day), which is a PPAR activator. Mesalamine 143-164 peroxisome proliferator activated receptor alpha Rattus norvegicus 201-205 18322880-1 2008 BACKGROUND: 5- Aminosalicylic acid (5-ASA) is metabolised in colonic mucosa by N-acetyltransferase 1 (NAT1). Mesalamine 12-34 N-acetyltransferase 1 Homo sapiens 79-100 18322880-1 2008 BACKGROUND: 5- Aminosalicylic acid (5-ASA) is metabolised in colonic mucosa by N-acetyltransferase 1 (NAT1). Mesalamine 12-34 N-acetyltransferase 1 Homo sapiens 102-106 18322880-1 2008 BACKGROUND: 5- Aminosalicylic acid (5-ASA) is metabolised in colonic mucosa by N-acetyltransferase 1 (NAT1). Mesalamine 36-41 N-acetyltransferase 1 Homo sapiens 79-100 18322880-1 2008 BACKGROUND: 5- Aminosalicylic acid (5-ASA) is metabolised in colonic mucosa by N-acetyltransferase 1 (NAT1). Mesalamine 36-41 N-acetyltransferase 1 Homo sapiens 102-106 18322880-8 2008 Clinical response to 5-ASA was determined by medical record review and associated with NAT1 genotypes. Mesalamine 21-26 N-acetyltransferase 1 Homo sapiens 87-91 18077625-4 2008 We tested whether irradiation-induced acute inflammatory response could be modulated pharmacologically with the antiinflammatory properties of 5-aminosalicylic acid (5-ASA) (250 mg/kg/day), which is a PPAR activator. Mesalamine 166-171 peroxisome proliferator activated receptor alpha Rattus norvegicus 201-205 18077625-6 2008 5-ASA treatment normalized both PPARgamma and RXRalpha expression at 3 days postirradiation and PPARalpha at 7 days. Mesalamine 0-5 peroxisome proliferator-activated receptor gamma Rattus norvegicus 32-41 18077625-6 2008 5-ASA treatment normalized both PPARgamma and RXRalpha expression at 3 days postirradiation and PPARalpha at 7 days. Mesalamine 0-5 retinoid X receptor alpha Rattus norvegicus 46-54 18077625-6 2008 5-ASA treatment normalized both PPARgamma and RXRalpha expression at 3 days postirradiation and PPARalpha at 7 days. Mesalamine 0-5 peroxisome proliferator activated receptor alpha Rattus norvegicus 96-105 18077625-7 2008 By promoting PPAR expression and its nuclear translocation, 5-ASA interfered with the nuclear factor (NF)-kappaB pathway, both by reducing irradiation-induced NF-kappaB p65 translocation/activation and increasing the expression of nuclear factor-kappaB inhibitor (IkappaB) mRNA and protein. Mesalamine 60-65 peroxisome proliferator activated receptor alpha Rattus norvegicus 13-17 18077625-7 2008 By promoting PPAR expression and its nuclear translocation, 5-ASA interfered with the nuclear factor (NF)-kappaB pathway, both by reducing irradiation-induced NF-kappaB p65 translocation/activation and increasing the expression of nuclear factor-kappaB inhibitor (IkappaB) mRNA and protein. Mesalamine 60-65 synaptotagmin 1 Rattus norvegicus 169-172 18077625-8 2008 Therefore, 5-ASA prevents irradiation-induced inflammatory processes as well as expression of tumor necrosis factor alpha, monocyte chemotactic protein-1, inducible nitric-oxide synthase, and macrophage infiltration. Mesalamine 11-16 tumor necrosis factor Rattus norvegicus 94-121 18077625-8 2008 Therefore, 5-ASA prevents irradiation-induced inflammatory processes as well as expression of tumor necrosis factor alpha, monocyte chemotactic protein-1, inducible nitric-oxide synthase, and macrophage infiltration. Mesalamine 11-16 C-C motif chemokine ligand 2 Rattus norvegicus 123-186 18077625-9 2008 In addition, 5-ASA restores the interferon gamma/signal transducer and activator of transcription (STAT)-1 and STAT-3 concentrations that were impaired at 3 and 7 days postirradiation and are correlated with suppressor of cytokine signaling-3 repression. Mesalamine 13-18 signal transducer and activator of transcription 3 Rattus norvegicus 111-117 18077625-9 2008 In addition, 5-ASA restores the interferon gamma/signal transducer and activator of transcription (STAT)-1 and STAT-3 concentrations that were impaired at 3 and 7 days postirradiation and are correlated with suppressor of cytokine signaling-3 repression. Mesalamine 13-18 suppressor of cytokine signaling 3 Rattus norvegicus 208-242 17981262-4 2008 We show that 5-ASA down-regulates both constitutive and TNF-alpha or IL-1beta-induced COX-2 in HT-115 and HT-29 cells. Mesalamine 13-18 prostaglandin-endoperoxide synthase 2 Homo sapiens 86-91 17981262-5 2008 Inhibition of COX-2 by 5-ASA occurs at the RNA and protein level, and is associated with a significant decrease in PGE2 synthesis, arrest of growth and enhanced death of CRC cells. Mesalamine 23-28 prostaglandin-endoperoxide synthase 2 Homo sapiens 14-19 17981262-8 2008 Taken together our data indicate that 5-ASA causes both a COX-2-dependent and -independent inhibition of CRC cell growth. Mesalamine 38-43 prostaglandin-endoperoxide synthase 2 Homo sapiens 58-63 17941093-0 2008 Characterization of epithelial IL-8 response to inflammatory bowel disease mucosal E. coli and its inhibition by mesalamine. Mesalamine 113-123 C-X-C motif chemokine ligand 8 Homo sapiens 31-35 17941093-9 2008 IL-8 release was mediated by extracellular-regulated kinase (ERK) and p38 mitogen-activated protein kinase (MAPK) and inhibited by mesalamine, but not hydrocortisone, at therapeutic concentrations. Mesalamine 131-141 C-X-C motif chemokine ligand 8 Homo sapiens 0-4 17941093-12 2008 The IL-8 release is MAPK-dependent and inhibited by mesalamine. Mesalamine 52-62 C-X-C motif chemokine ligand 8 Homo sapiens 4-8 17308963-0 2007 Thrombin generation in mesalazine refractory ulcerative colitis and the influence of low molecular weight heparin. Mesalamine 23-33 coagulation factor II, thrombin Homo sapiens 0-8 17981262-0 2008 Cyclooxygenase-2-dependent and -independent inhibition of proliferation of colon cancer cells by 5-aminosalicylic acid. Mesalamine 97-118 prostaglandin-endoperoxide synthase 2 Homo sapiens 0-16 17981262-4 2008 We show that 5-ASA down-regulates both constitutive and TNF-alpha or IL-1beta-induced COX-2 in HT-115 and HT-29 cells. Mesalamine 13-18 tumor necrosis factor Homo sapiens 56-65 17981262-4 2008 We show that 5-ASA down-regulates both constitutive and TNF-alpha or IL-1beta-induced COX-2 in HT-115 and HT-29 cells. Mesalamine 13-18 interleukin 1 beta Homo sapiens 69-77 17503181-0 2008 5-aminosalicylic acid improves indomethacin-induced enteropathy by inhibiting iNOS transcription in rats. Mesalamine 0-21 nitric oxide synthase 2 Rattus norvegicus 78-82 19052456-7 2008 RESULTS: Compared with unaffected mucosa, BCRP expression was significantly reduced in inflamed mucosa of newly diagnosed drug-naive patients with UC (expression reduced to 30%) as well as in patients not responding to treatment (reduced to 25%) with either 5-aminosalicylates (n = 7) or prednisone (n = 4). Mesalamine 258-276 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 42-46 17308963-13 2007 CONCLUSION: The LMWH reviparine reduces thrombin generation in patients with mild-to-moderately active, mesalazine refractory UC, but is not associated with a reduction in disease activity. Mesalamine 104-114 coagulation factor II, thrombin Homo sapiens 40-48 17334911-8 2007 In the multivariate analysis, gender, hematocrit, and treatment with 5-aminosalicylates/steroids/azathioprine/6-MP statistically influenced TPMT activity, although, probably, in a clinically irrelevant manner. Mesalamine 69-87 thiopurine S-methyltransferase Homo sapiens 140-144 17539984-0 2007 Mesalazine downregulates c-Myc in human colon cancer cells. Mesalamine 0-10 MYC proto-oncogene, bHLH transcription factor Homo sapiens 25-30 17539984-4 2007 AIMS: To examine whether mesalazine affects the expression of c-Myc in human colon cancer cell lines. Mesalamine 25-35 MYC proto-oncogene, bHLH transcription factor Homo sapiens 62-67 17539984-7 2007 RESULTS: Mesalazine significantly reduced expression of c-Myc mRNA and protein. Mesalamine 9-19 MYC proto-oncogene, bHLH transcription factor Homo sapiens 56-61 17539984-8 2007 CONCLUSIONS: Mesalazine downregulates gene and protein expression of c-Myc. Mesalamine 13-23 MYC proto-oncogene, bHLH transcription factor Homo sapiens 69-74 17539984-10 2007 Expression of c-Myc is significantly reduced by mesalazine 40 mm. Mesalamine 48-58 MYC proto-oncogene, bHLH transcription factor Homo sapiens 14-19 17460546-9 2007 Rhesus NAT2 provided relatively high acetylation activity with p-anisidine, lower activity with procainamide, sulphamethazine or 5-aminosalicylate and poor activity with p-aminobenzoic acid. Mesalamine 129-146 N-acetyltransferase 2 Macaca mulatta 7-11 17304143-0 2007 Monitoring of thiopurine methyltransferase activity in postsurgical patients with Crohn"s disease during 1 year of treatment with azathioprine or mesalazine. Mesalamine 146-156 thiopurine S-methyltransferase Homo sapiens 14-42 17304143-2 2007 Evaluation of a possible long-term effect of mesalazine or azathioprine on TPMT activity is of particular clinical importance because both drugs can to be given for several years in inflammatory bowel disease. Mesalamine 45-55 thiopurine S-methyltransferase Homo sapiens 75-79 16944117-3 2006 METHODS: We tested the hypothesis that 5-ASA represents a substrate of P-glycoprotein (P-gp) and/or multidrug resistance-associated protein 2 (MRP2), thereby possibly contributing to variable therapeutic effects. Mesalamine 39-44 ATP binding cassette subfamily B member 1 Homo sapiens 71-85 16728434-0 2006 Protein phosphatase 2A is required for mesalazine-dependent inhibition of Wnt/beta-catenin pathway activity. Mesalamine 39-49 catenin beta 1 Homo sapiens 78-90 16728434-3 2006 The effect of mesalazine on the Wnt/beta-catenin pathway was studied in colorectal cancer cell lines to find a molecular basis underlying its chemopreventive features. Mesalamine 14-24 catenin beta 1 Homo sapiens 36-48 16728434-4 2006 Mesalazine affects the Wnt/beta-catenin pathway in adenomatous polyposis coli mutated cells with intact beta-catenin, judged by luciferase reporter assays. Mesalamine 0-10 catenin beta 1 Homo sapiens 27-39 16728434-4 2006 Mesalazine affects the Wnt/beta-catenin pathway in adenomatous polyposis coli mutated cells with intact beta-catenin, judged by luciferase reporter assays. Mesalamine 0-10 catenin beta 1 Homo sapiens 104-116 16728434-5 2006 Furthermore, mesalazine treatment reduced expression of nuclear beta-catenin and Wnt/beta-catenin target genes, and increased beta-catenin phosphorylation. Mesalamine 13-23 catenin beta 1 Homo sapiens 64-76 16728434-5 2006 Furthermore, mesalazine treatment reduced expression of nuclear beta-catenin and Wnt/beta-catenin target genes, and increased beta-catenin phosphorylation. Mesalamine 13-23 catenin beta 1 Homo sapiens 85-97 16728434-5 2006 Furthermore, mesalazine treatment reduced expression of nuclear beta-catenin and Wnt/beta-catenin target genes, and increased beta-catenin phosphorylation. Mesalamine 13-23 catenin beta 1 Homo sapiens 85-97 16728434-6 2006 This effect on the Wnt/beta-catenin pathway is mediated via protein phosphatase 2A (PP2A): increased phosphorylation of PP2A after mesalazine treatment is observed, which coincides with decreased PP2A enzymatic activity. Mesalamine 131-141 catenin beta 1 Homo sapiens 23-35 16728434-6 2006 This effect on the Wnt/beta-catenin pathway is mediated via protein phosphatase 2A (PP2A): increased phosphorylation of PP2A after mesalazine treatment is observed, which coincides with decreased PP2A enzymatic activity. Mesalamine 131-141 protein phosphatase 2 phosphatase activator Homo sapiens 84-88 16728434-6 2006 This effect on the Wnt/beta-catenin pathway is mediated via protein phosphatase 2A (PP2A): increased phosphorylation of PP2A after mesalazine treatment is observed, which coincides with decreased PP2A enzymatic activity. Mesalamine 131-141 protein phosphatase 2 phosphatase activator Homo sapiens 120-124 16728434-6 2006 This effect on the Wnt/beta-catenin pathway is mediated via protein phosphatase 2A (PP2A): increased phosphorylation of PP2A after mesalazine treatment is observed, which coincides with decreased PP2A enzymatic activity. Mesalamine 131-141 protein phosphatase 2 phosphatase activator Homo sapiens 120-124 16728434-7 2006 The inhibition of PP2A enzymatic activity by mesalazine is essential for its effect on the Wnt/beta-catenin pathway, as shown by transient transfection with siPP2A and mutant PP2A. Mesalamine 45-55 protein phosphatase 2 phosphatase activator Homo sapiens 18-22 16728434-7 2006 The inhibition of PP2A enzymatic activity by mesalazine is essential for its effect on the Wnt/beta-catenin pathway, as shown by transient transfection with siPP2A and mutant PP2A. Mesalamine 45-55 catenin beta 1 Homo sapiens 95-107 16728434-7 2006 The inhibition of PP2A enzymatic activity by mesalazine is essential for its effect on the Wnt/beta-catenin pathway, as shown by transient transfection with siPP2A and mutant PP2A. Mesalamine 45-55 protein phosphatase 2 phosphatase activator Homo sapiens 159-163 16728434-8 2006 This study shows, using concentrations of mesalazine identical to concentrations seen in patients with inflammatory bowel disease, that mesalazine inhibits the Wnt/beta-catenin pathway via inhibition of PP2A. Mesalamine 136-146 catenin beta 1 Homo sapiens 164-176 16728434-8 2006 This study shows, using concentrations of mesalazine identical to concentrations seen in patients with inflammatory bowel disease, that mesalazine inhibits the Wnt/beta-catenin pathway via inhibition of PP2A. Mesalamine 136-146 protein phosphatase 2 phosphatase activator Homo sapiens 203-207 16961744-5 2006 A 1 g Pentasa-suppository once daily induces a quicker clinical and endoscopic remission and was better tolerated than a 500-mg suppository twice daily. Mesalamine 6-13 BCL2 related protein A1 Homo sapiens 0-3 16829624-9 2006 Recombinant rat Nat3 was functional and catalyzed the N-acetylation of several arylamine substrates, including 3-ethylaniline, 3,5-dimethylaniline, 5-aminosalicylic acid, 4-aminobiphenyl, 4,4"-methylenedianiline, 4,4"-methylenebis(2-chloroaniline), and 2-aminofluorene, and the O-acetylation of N-hydroxy-4-aminobiphenyl. Mesalamine 148-169 N-acetyltransferase 3 Rattus norvegicus 16-20 17241873-12 2007 CONCLUSIONS: Our data demonstrate that 5-ASA causes cells to reversibly accumulate in S phase and activate an ATR-dependent checkpoint. Mesalamine 39-44 ATR serine/threonine kinase Homo sapiens 110-113 16914308-8 2006 In contrast, the 5-ASA-mediated Colo205 cell death is preventable by Bcl-2 over-expression. Mesalamine 17-22 BCL2 apoptosis regulator Homo sapiens 69-74 16939425-6 2006 The recent discovery that 5-aminosalicylic acids may act in ulcerative colitis by activating peroxisome proliferator-activated receptor-gamma, a nuclear receptor that plays a role in the control of cell proliferation and apoptosis, has given new impetus to the idea that long-term therapy with 5-aminosalicylic acid may reduce the risk of colorectal cancer. Mesalamine 26-48 peroxisome proliferator activated receptor gamma Homo sapiens 93-141 16939425-6 2006 The recent discovery that 5-aminosalicylic acids may act in ulcerative colitis by activating peroxisome proliferator-activated receptor-gamma, a nuclear receptor that plays a role in the control of cell proliferation and apoptosis, has given new impetus to the idea that long-term therapy with 5-aminosalicylic acid may reduce the risk of colorectal cancer. Mesalamine 26-47 peroxisome proliferator activated receptor gamma Homo sapiens 93-141 16944117-3 2006 METHODS: We tested the hypothesis that 5-ASA represents a substrate of P-glycoprotein (P-gp) and/or multidrug resistance-associated protein 2 (MRP2), thereby possibly contributing to variable therapeutic effects. Mesalamine 39-44 ATP binding cassette subfamily B member 1 Homo sapiens 87-91 16944117-3 2006 METHODS: We tested the hypothesis that 5-ASA represents a substrate of P-glycoprotein (P-gp) and/or multidrug resistance-associated protein 2 (MRP2), thereby possibly contributing to variable therapeutic effects. Mesalamine 39-44 ATP binding cassette subfamily C member 2 Homo sapiens 100-141 16944117-3 2006 METHODS: We tested the hypothesis that 5-ASA represents a substrate of P-glycoprotein (P-gp) and/or multidrug resistance-associated protein 2 (MRP2), thereby possibly contributing to variable therapeutic effects. Mesalamine 39-44 ATP binding cassette subfamily C member 2 Homo sapiens 143-147 16944117-6 2006 RESULTS: In Caco-2 cells a P-gp-mediated efflux of 5-ASA (5-500 muM) could be excluded. Mesalamine 51-56 ATP binding cassette subfamily B member 1 Homo sapiens 27-31 16944117-6 2006 RESULTS: In Caco-2 cells a P-gp-mediated efflux of 5-ASA (5-500 muM) could be excluded. Mesalamine 51-56 latexin Homo sapiens 64-67 16892148-9 2006 Thirty cases were administrated with Sulfasalazine/Mesalazine (SASP/5-ASA) or corticosteroids/immuno-suppressor in which 27 got clinically improved. Mesalamine 51-61 aspartic peptidase retroviral like 1 Homo sapiens 63-67 16165710-0 2005 Mesalamine promotes intestinal epithelial wound healing in vitro through a TGF-beta-independent mechanism. Mesalamine 0-10 transforming growth factor, beta 1 Rattus norvegicus 75-83 16625537-12 2006 These values were also calculated for the trials in which SASP and 5-ASA were compared, revealing an odds ratio of 1.29 (95% CI, 1.05 to 1.57), with a negative NNT value (-19), suggesting a higher degree of therapeutic effectiveness for SASP.SASP and 5-ASA had similar adverse event profiles, with odds ratios of 1.16(0.62 to 2.16), and 1.31(0.86 to 1.99), respectively. Mesalamine 251-256 aspartic peptidase retroviral like 1 Homo sapiens 58-62 16633046-1 2006 BACKGROUND: Small uncontrolled trials have suggested that 5-aminosalicylate (5-ASA) medications increase 6-thioguanine nucleotide (6-TGn) levels in adults with Crohn"s disease (CD) on azathioprine (AZA) or 6-mercaptopurine (6-MP), presumably through the inhibition of thiopurine methyltransferase (TPMT). Mesalamine 58-75 thiopurine S-methyltransferase Homo sapiens 268-296 16633046-1 2006 BACKGROUND: Small uncontrolled trials have suggested that 5-aminosalicylate (5-ASA) medications increase 6-thioguanine nucleotide (6-TGn) levels in adults with Crohn"s disease (CD) on azathioprine (AZA) or 6-mercaptopurine (6-MP), presumably through the inhibition of thiopurine methyltransferase (TPMT). Mesalamine 58-75 thiopurine S-methyltransferase Homo sapiens 298-302 16633046-1 2006 BACKGROUND: Small uncontrolled trials have suggested that 5-aminosalicylate (5-ASA) medications increase 6-thioguanine nucleotide (6-TGn) levels in adults with Crohn"s disease (CD) on azathioprine (AZA) or 6-mercaptopurine (6-MP), presumably through the inhibition of thiopurine methyltransferase (TPMT). Mesalamine 77-82 thiopurine S-methyltransferase Homo sapiens 268-296 16633046-1 2006 BACKGROUND: Small uncontrolled trials have suggested that 5-aminosalicylate (5-ASA) medications increase 6-thioguanine nucleotide (6-TGn) levels in adults with Crohn"s disease (CD) on azathioprine (AZA) or 6-mercaptopurine (6-MP), presumably through the inhibition of thiopurine methyltransferase (TPMT). Mesalamine 77-82 thiopurine S-methyltransferase Homo sapiens 298-302 16407467-10 2006 In addition, 5-ASA inhibited phosphorylation of p65 at serine 536, which is critical for transcriptional activity of NF-kappaB. Mesalamine 13-18 RELA proto-oncogene, NF-kB subunit Homo sapiens 48-51 16407467-11 2006 Furthermore, combined TauCl/5-ASA treatment additively inhibited TNF-dependent NF-kappaB activation. Mesalamine 28-33 tumor necrosis factor Homo sapiens 65-68 16407467-12 2006 Together, our data suggest that the colon-specific carrier taurine contributes to the clinical effect of the prodrug by potentiating the inhibitory effect of the active ingredient 5-ASA on a major proinflammatory signal, TNF-dependent NF-kappaB activation in the inflamed large intestine. Mesalamine 180-185 tumor necrosis factor Homo sapiens 221-224 16614956-10 2006 Myeloperoxidase activity was also reduced significantly by 5-aminosalicylic acid (P < 0.05) but not by hyperbaric oxygen. Mesalamine 59-80 myeloperoxidase Rattus norvegicus 0-15 16159550-10 2005 In the multivariate study, the variables associated with TPMT activity were: sex, treatment with 5-aminosalicylates, steroids and azathioprine/6-mercaptopurine. Mesalamine 97-115 thiopurine S-methyltransferase Homo sapiens 57-61 16939423-5 2006 Other drugs known to act via peroxisome proliferator-activated receptor-gamma, such as rosiglitazone and the selective peroxisome proliferator-activated receptor-gamma ligand GW1929, can be displaced from their binding sites on the peroxisome proliferator-activated receptor-gamma molecule by 5-aminosalicylic acid at concentrations of 5-aminosalicylic acid that correspond with the concentrations found in the lumen of ulcerative colitis patients taking oral mesalazine. Mesalamine 293-314 peroxisome proliferator activated receptor gamma Homo sapiens 29-77 16939423-5 2006 Other drugs known to act via peroxisome proliferator-activated receptor-gamma, such as rosiglitazone and the selective peroxisome proliferator-activated receptor-gamma ligand GW1929, can be displaced from their binding sites on the peroxisome proliferator-activated receptor-gamma molecule by 5-aminosalicylic acid at concentrations of 5-aminosalicylic acid that correspond with the concentrations found in the lumen of ulcerative colitis patients taking oral mesalazine. Mesalamine 293-314 peroxisome proliferator activated receptor gamma Homo sapiens 119-167 16939423-5 2006 Other drugs known to act via peroxisome proliferator-activated receptor-gamma, such as rosiglitazone and the selective peroxisome proliferator-activated receptor-gamma ligand GW1929, can be displaced from their binding sites on the peroxisome proliferator-activated receptor-gamma molecule by 5-aminosalicylic acid at concentrations of 5-aminosalicylic acid that correspond with the concentrations found in the lumen of ulcerative colitis patients taking oral mesalazine. Mesalamine 293-314 peroxisome proliferator activated receptor gamma Homo sapiens 119-167 16939423-5 2006 Other drugs known to act via peroxisome proliferator-activated receptor-gamma, such as rosiglitazone and the selective peroxisome proliferator-activated receptor-gamma ligand GW1929, can be displaced from their binding sites on the peroxisome proliferator-activated receptor-gamma molecule by 5-aminosalicylic acid at concentrations of 5-aminosalicylic acid that correspond with the concentrations found in the lumen of ulcerative colitis patients taking oral mesalazine. Mesalamine 336-357 peroxisome proliferator activated receptor gamma Homo sapiens 29-77 16939423-5 2006 Other drugs known to act via peroxisome proliferator-activated receptor-gamma, such as rosiglitazone and the selective peroxisome proliferator-activated receptor-gamma ligand GW1929, can be displaced from their binding sites on the peroxisome proliferator-activated receptor-gamma molecule by 5-aminosalicylic acid at concentrations of 5-aminosalicylic acid that correspond with the concentrations found in the lumen of ulcerative colitis patients taking oral mesalazine. Mesalamine 336-357 peroxisome proliferator activated receptor gamma Homo sapiens 119-167 16939423-5 2006 Other drugs known to act via peroxisome proliferator-activated receptor-gamma, such as rosiglitazone and the selective peroxisome proliferator-activated receptor-gamma ligand GW1929, can be displaced from their binding sites on the peroxisome proliferator-activated receptor-gamma molecule by 5-aminosalicylic acid at concentrations of 5-aminosalicylic acid that correspond with the concentrations found in the lumen of ulcerative colitis patients taking oral mesalazine. Mesalamine 336-357 peroxisome proliferator activated receptor gamma Homo sapiens 119-167 16939423-5 2006 Other drugs known to act via peroxisome proliferator-activated receptor-gamma, such as rosiglitazone and the selective peroxisome proliferator-activated receptor-gamma ligand GW1929, can be displaced from their binding sites on the peroxisome proliferator-activated receptor-gamma molecule by 5-aminosalicylic acid at concentrations of 5-aminosalicylic acid that correspond with the concentrations found in the lumen of ulcerative colitis patients taking oral mesalazine. Mesalamine 460-470 peroxisome proliferator activated receptor gamma Homo sapiens 29-77 16939423-5 2006 Other drugs known to act via peroxisome proliferator-activated receptor-gamma, such as rosiglitazone and the selective peroxisome proliferator-activated receptor-gamma ligand GW1929, can be displaced from their binding sites on the peroxisome proliferator-activated receptor-gamma molecule by 5-aminosalicylic acid at concentrations of 5-aminosalicylic acid that correspond with the concentrations found in the lumen of ulcerative colitis patients taking oral mesalazine. Mesalamine 460-470 peroxisome proliferator activated receptor gamma Homo sapiens 119-167 16939423-5 2006 Other drugs known to act via peroxisome proliferator-activated receptor-gamma, such as rosiglitazone and the selective peroxisome proliferator-activated receptor-gamma ligand GW1929, can be displaced from their binding sites on the peroxisome proliferator-activated receptor-gamma molecule by 5-aminosalicylic acid at concentrations of 5-aminosalicylic acid that correspond with the concentrations found in the lumen of ulcerative colitis patients taking oral mesalazine. Mesalamine 460-470 peroxisome proliferator activated receptor gamma Homo sapiens 119-167 16625536-1 2006 BACKGROUND: The newer 5-ASA preparations were intended to avoid the adverse effects of SASP while maintaining its therapeutic benefits. Mesalamine 22-27 aspartic peptidase retroviral like 1 Homo sapiens 87-91 16625536-14 2006 AUTHORS" CONCLUSIONS: The newer 5-ASA preparations were superior to placebo and tended towards therapeutic benefit over SASP. Mesalamine 32-37 aspartic peptidase retroviral like 1 Homo sapiens 120-124 16625537-1 2006 BACKGROUND: The newer 5-ASA preparations were intended to avoid the adverse effects of SASP while maintaining its therapeutic benefits. Mesalamine 22-27 aspartic peptidase retroviral like 1 Homo sapiens 87-91 16534883-1 2006 AIM: To observe if the total amount of platelet P-selectin (tP-selectin) in patients with inflammatory bowel disease (IBD) was related to disease entity or activity, 5-aminosalicylic acid (5-ASA) medication or gender. Mesalamine 166-187 selectin P Homo sapiens 48-58 16534883-1 2006 AIM: To observe if the total amount of platelet P-selectin (tP-selectin) in patients with inflammatory bowel disease (IBD) was related to disease entity or activity, 5-aminosalicylic acid (5-ASA) medication or gender. Mesalamine 189-194 selectin P Homo sapiens 48-58 16082388-0 2006 Silencing of SH-PTP2 defines a crucial role in the inactivation of epidermal growth factor receptor by 5-aminosalicylic acid in colon cancer cells. Mesalamine 103-124 protein tyrosine phosphatase non-receptor type 11 Homo sapiens 13-20 16082388-0 2006 Silencing of SH-PTP2 defines a crucial role in the inactivation of epidermal growth factor receptor by 5-aminosalicylic acid in colon cancer cells. Mesalamine 103-124 epidermal growth factor receptor Homo sapiens 67-99 16082388-3 2006 We here examined the effect of 5-ASA on epidermal growth factor receptor (EGFR) activation, a pathway that triggers mitogenic signals in CRC cells. Mesalamine 31-36 epidermal growth factor receptor Homo sapiens 40-72 16082388-3 2006 We here examined the effect of 5-ASA on epidermal growth factor receptor (EGFR) activation, a pathway that triggers mitogenic signals in CRC cells. Mesalamine 31-36 epidermal growth factor receptor Homo sapiens 74-78 16082388-4 2006 We show that 5-ASA inhibits EGFR activation, through a mechanism that does not rely on CRC cell death induction. Mesalamine 13-18 epidermal growth factor receptor Homo sapiens 28-32 16082388-5 2006 5-ASA enhances the activity, but not expression, of phosphorylated (p)-EGFR-targeting phosphatases (PTPs), and treatment of cells with PTP inhibitors abrogates the 5-ASA-mediated EGFR dephosphorylation. Mesalamine 0-5 epidermal growth factor receptor Homo sapiens 71-75 16082388-5 2006 5-ASA enhances the activity, but not expression, of phosphorylated (p)-EGFR-targeting phosphatases (PTPs), and treatment of cells with PTP inhibitors abrogates the 5-ASA-mediated EGFR dephosphorylation. Mesalamine 0-5 protein tyrosine phosphatase receptor type U Homo sapiens 100-103 16082388-5 2006 5-ASA enhances the activity, but not expression, of phosphorylated (p)-EGFR-targeting phosphatases (PTPs), and treatment of cells with PTP inhibitors abrogates the 5-ASA-mediated EGFR dephosphorylation. Mesalamine 0-5 epidermal growth factor receptor Homo sapiens 179-183 16082388-5 2006 5-ASA enhances the activity, but not expression, of phosphorylated (p)-EGFR-targeting phosphatases (PTPs), and treatment of cells with PTP inhibitors abrogates the 5-ASA-mediated EGFR dephosphorylation. Mesalamine 164-169 epidermal growth factor receptor Homo sapiens 71-75 16082388-5 2006 5-ASA enhances the activity, but not expression, of phosphorylated (p)-EGFR-targeting phosphatases (PTPs), and treatment of cells with PTP inhibitors abrogates the 5-ASA-mediated EGFR dephosphorylation. Mesalamine 164-169 protein tyrosine phosphatase receptor type U Homo sapiens 100-103 16082388-5 2006 5-ASA enhances the activity, but not expression, of phosphorylated (p)-EGFR-targeting phosphatases (PTPs), and treatment of cells with PTP inhibitors abrogates the 5-ASA-mediated EGFR dephosphorylation. Mesalamine 164-169 epidermal growth factor receptor Homo sapiens 179-183 16082388-6 2006 Both SH-PTP1 and SH-PTP2 interact with EGFR upon 5-ASA treatment. Mesalamine 49-54 protein tyrosine phosphatase non-receptor type 6 Homo sapiens 5-12 16082388-6 2006 Both SH-PTP1 and SH-PTP2 interact with EGFR upon 5-ASA treatment. Mesalamine 49-54 protein tyrosine phosphatase non-receptor type 11 Homo sapiens 17-24 16082388-6 2006 Both SH-PTP1 and SH-PTP2 interact with EGFR upon 5-ASA treatment. Mesalamine 49-54 epidermal growth factor receptor Homo sapiens 39-43 16082388-7 2006 However, knockdown of SH-PTP2 but not SH-PTP1 by small interference RNAs prevents the 5-ASA-induced EGFR dephosphorylation. Mesalamine 86-91 protein tyrosine phosphatase non-receptor type 11 Homo sapiens 22-29 16082388-7 2006 However, knockdown of SH-PTP2 but not SH-PTP1 by small interference RNAs prevents the 5-ASA-induced EGFR dephosphorylation. Mesalamine 86-91 epidermal growth factor receptor Homo sapiens 100-104 16082388-8 2006 Finally, we show that 5-ASA attenuates p-EGFR in ex vivo organ cultures of CRC explants. Mesalamine 22-27 epidermal growth factor receptor Homo sapiens 41-45 16082388-9 2006 Data indicate that 5-ASA disrupts EGFR signalling by enhancing SH-PTP2 activity, and suggest a mechanism by which 5-ASA interferes with CRC growth. Mesalamine 19-24 epidermal growth factor receptor Homo sapiens 34-38 16082388-9 2006 Data indicate that 5-ASA disrupts EGFR signalling by enhancing SH-PTP2 activity, and suggest a mechanism by which 5-ASA interferes with CRC growth. Mesalamine 19-24 protein tyrosine phosphatase non-receptor type 11 Homo sapiens 63-70 16461476-0 2006 Effects of topical treatment of sodium butyrate and 5-aminosalicylic acid on expression of trefoil factor 3, interleukin 1beta, and nuclear factor kappaB in trinitrobenzene sulphonic acid induced colitis in rats. Mesalamine 52-73 trefoil factor 3 Rattus norvegicus 91-107 16461476-0 2006 Effects of topical treatment of sodium butyrate and 5-aminosalicylic acid on expression of trefoil factor 3, interleukin 1beta, and nuclear factor kappaB in trinitrobenzene sulphonic acid induced colitis in rats. Mesalamine 52-73 interleukin 1 beta Rattus norvegicus 109-126 16461476-2 2006 This study evaluates effects of topical treatment of sodium butyrate (NaB) and 5-aminosalicylic acid (5-ASA) on the expression of trefoil factor 3 (TFF3), interleukin 1beta (IL1beta), and nuclear factor kappaB (NFkappaB) in trinitrobenzene sulphonic acid (TNBS) induced colitis in rats. Mesalamine 79-100 trefoil factor 3 Rattus norvegicus 130-146 16461476-2 2006 This study evaluates effects of topical treatment of sodium butyrate (NaB) and 5-aminosalicylic acid (5-ASA) on the expression of trefoil factor 3 (TFF3), interleukin 1beta (IL1beta), and nuclear factor kappaB (NFkappaB) in trinitrobenzene sulphonic acid (TNBS) induced colitis in rats. Mesalamine 79-100 trefoil factor 3 Rattus norvegicus 148-152 16461476-2 2006 This study evaluates effects of topical treatment of sodium butyrate (NaB) and 5-aminosalicylic acid (5-ASA) on the expression of trefoil factor 3 (TFF3), interleukin 1beta (IL1beta), and nuclear factor kappaB (NFkappaB) in trinitrobenzene sulphonic acid (TNBS) induced colitis in rats. Mesalamine 79-100 interleukin 1 beta Rattus norvegicus 155-172 16461476-2 2006 This study evaluates effects of topical treatment of sodium butyrate (NaB) and 5-aminosalicylic acid (5-ASA) on the expression of trefoil factor 3 (TFF3), interleukin 1beta (IL1beta), and nuclear factor kappaB (NFkappaB) in trinitrobenzene sulphonic acid (TNBS) induced colitis in rats. Mesalamine 102-107 trefoil factor 3 Rattus norvegicus 130-146 16461476-2 2006 This study evaluates effects of topical treatment of sodium butyrate (NaB) and 5-aminosalicylic acid (5-ASA) on the expression of trefoil factor 3 (TFF3), interleukin 1beta (IL1beta), and nuclear factor kappaB (NFkappaB) in trinitrobenzene sulphonic acid (TNBS) induced colitis in rats. Mesalamine 102-107 trefoil factor 3 Rattus norvegicus 148-152 16461476-2 2006 This study evaluates effects of topical treatment of sodium butyrate (NaB) and 5-aminosalicylic acid (5-ASA) on the expression of trefoil factor 3 (TFF3), interleukin 1beta (IL1beta), and nuclear factor kappaB (NFkappaB) in trinitrobenzene sulphonic acid (TNBS) induced colitis in rats. Mesalamine 102-107 interleukin 1 beta Rattus norvegicus 155-172 16461476-5 2006 RESULTS: Treatment of NaB, 5-ASA, and the combination improved diarrhoea, colonic damage score, and MPO activities, increased TFF3 mRNA expression, and decreased serum IL1beta production and tissue NFkappaB expression. Mesalamine 27-32 myeloperoxidase Rattus norvegicus 100-103 16461476-5 2006 RESULTS: Treatment of NaB, 5-ASA, and the combination improved diarrhoea, colonic damage score, and MPO activities, increased TFF3 mRNA expression, and decreased serum IL1beta production and tissue NFkappaB expression. Mesalamine 27-32 trefoil factor 3 Rattus norvegicus 126-130 16461476-5 2006 RESULTS: Treatment of NaB, 5-ASA, and the combination improved diarrhoea, colonic damage score, and MPO activities, increased TFF3 mRNA expression, and decreased serum IL1beta production and tissue NFkappaB expression. Mesalamine 27-32 interleukin 1 beta Rattus norvegicus 168-175 16461476-7 2006 CONCLUSIONS: The combination of topical treatment of NaB and 5-ASA was effective for relieving and repairing colonic inflammation and the effects were related to stimulation of TFF3 mRNA expression and down-regulation of IL1beta production and NFkappaB expression. Mesalamine 61-66 trefoil factor 3 Rattus norvegicus 177-181 16461476-7 2006 CONCLUSIONS: The combination of topical treatment of NaB and 5-ASA was effective for relieving and repairing colonic inflammation and the effects were related to stimulation of TFF3 mRNA expression and down-regulation of IL1beta production and NFkappaB expression. Mesalamine 61-66 interleukin 1 beta Rattus norvegicus 221-228 16306769-7 2005 Supporting these findings, results from a 3-month follow-up study revealed that the UC groups treated with 5-aminosalicylic acid and glucocorticoid exhibited dramatic decreases of CCL20 mRNA in PBMCs, accompanied by ameliorated disease states. Mesalamine 107-128 C-C motif chemokine ligand 20 Homo sapiens 180-185 16306769-8 2005 Moreover, tumor necrosis factor-alpha- or interleukin-1beta-induced CCL20 secretion was greatly diminished by 5-aminosalicylic acid and/or glucocorticoid treatment of human intestinal epithelial HT-29 cells. Mesalamine 110-131 tumor necrosis factor Homo sapiens 10-37 16306769-8 2005 Moreover, tumor necrosis factor-alpha- or interleukin-1beta-induced CCL20 secretion was greatly diminished by 5-aminosalicylic acid and/or glucocorticoid treatment of human intestinal epithelial HT-29 cells. Mesalamine 110-131 interleukin 1 beta Homo sapiens 42-59 16306769-8 2005 Moreover, tumor necrosis factor-alpha- or interleukin-1beta-induced CCL20 secretion was greatly diminished by 5-aminosalicylic acid and/or glucocorticoid treatment of human intestinal epithelial HT-29 cells. Mesalamine 110-131 C-C motif chemokine ligand 20 Homo sapiens 68-73 16181300-1 2005 BACKGROUND: In vitro studies suggest interactions between mesalazine (mesalamine) and thiopurines by thiopurine S-methyltransferase (TPMT) inhibition, influencing the balance of hepatotoxic 6-methylmercaptopurine ribonucleotide and immunosuppressive tioguanine (thioguanine) metabolites. Mesalamine 58-68 thiopurine S-methyltransferase Homo sapiens 101-131 16181300-1 2005 BACKGROUND: In vitro studies suggest interactions between mesalazine (mesalamine) and thiopurines by thiopurine S-methyltransferase (TPMT) inhibition, influencing the balance of hepatotoxic 6-methylmercaptopurine ribonucleotide and immunosuppressive tioguanine (thioguanine) metabolites. Mesalamine 58-68 thiopurine S-methyltransferase Homo sapiens 133-137 16181300-1 2005 BACKGROUND: In vitro studies suggest interactions between mesalazine (mesalamine) and thiopurines by thiopurine S-methyltransferase (TPMT) inhibition, influencing the balance of hepatotoxic 6-methylmercaptopurine ribonucleotide and immunosuppressive tioguanine (thioguanine) metabolites. Mesalamine 70-80 thiopurine S-methyltransferase Homo sapiens 101-131 16181300-1 2005 BACKGROUND: In vitro studies suggest interactions between mesalazine (mesalamine) and thiopurines by thiopurine S-methyltransferase (TPMT) inhibition, influencing the balance of hepatotoxic 6-methylmercaptopurine ribonucleotide and immunosuppressive tioguanine (thioguanine) metabolites. Mesalamine 70-80 thiopurine S-methyltransferase Homo sapiens 133-137 16181300-13 2005 Theoretically, mesalazine inhibits thiopurine S-methyltransferase activity. Mesalamine 15-25 thiopurine S-methyltransferase Homo sapiens 35-65 24764591-3 2004 METHODS: THREE GROUPS OF FEMALE SPRAGUE DAWLEY RATS WERE ASSIGNED TO RECEIVE TREATMENT AS FOLLOWS: mesalamine enema (60 mg/mL) BID + irradiation (IR) was given to the mesalamine + IR group, and isotonic saline enema BID + irradiation to the control group. Mesalamine 99-109 BH3 interacting domain death agonist Rattus norvegicus 127-130 15909923-3 2004 There are some suggestions in the literature that the intestinal bacterial azo-reductases are involved in biotransformation of SAS into 5-aminosalicylic acid (5-ASA) and sulphapyridine (SP). Mesalamine 136-157 tetraspanin 31 Homo sapiens 127-130 15909923-3 2004 There are some suggestions in the literature that the intestinal bacterial azo-reductases are involved in biotransformation of SAS into 5-aminosalicylic acid (5-ASA) and sulphapyridine (SP). Mesalamine 159-164 tetraspanin 31 Homo sapiens 127-130 15909923-5 2004 No enzymatic systems presumably exist in Caco-2, which could be responsible for SAS metabolism, because after 72 h-incubation of cell cultures with 1 mM SAS, its metabolites i.e., 5-ASA and SP were not detected in cells, neither in culture media. Mesalamine 180-185 tetraspanin 31 Homo sapiens 153-156 15854172-1 2005 BACKGROUND: Based on in vitro experiments using recombinant human thiopurine S-methyltransferase this enzyme is inhibited by sulfasalazine (sulphasalazine) and 5-aminosalicylate. Mesalamine 160-177 thiopurine S-methyltransferase Homo sapiens 66-96 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. Mesalamine 113-123 T cell leukemia, homeobox 2 Mus musculus 125-128 15824083-0 2005 Intestinal antiinflammatory effect of 5-aminosalicylic acid is dependent on peroxisome proliferator-activated receptor-gamma. Mesalamine 38-59 peroxisome proliferator activated receptor gamma Mus musculus 76-124 15824083-1 2005 5-aminosalicylic acid (5-ASA) is an antiinflammatory drug widely used in the treatment of inflammatory bowel diseases. Mesalamine 0-21 anti-sarcolemmal autoantibodies Mus musculus 25-28 24764591-12 2004 With the topical application of mesalamine, the GSH and MDA levels and MPO activities were similar to those of the sham group. Mesalamine 32-42 myeloperoxidase Rattus norvegicus 71-74 12878742-0 2003 Epidermal growth factor enemas with oral mesalamine for mild-to-moderate left-sided ulcerative colitis or proctitis. Mesalamine 41-51 epidermal growth factor Homo sapiens 0-23 15094390-2 2004 Here, we report a dual-function anti-oxidant conjugate comprising an anti-inflammatory agent (5-aminosalicylic acid) and a chelator with potential as a superoxide dismutase mimic. Mesalamine 94-115 superoxide dismutase 1 Homo sapiens 152-172 15094390-5 2004 In inflamed tissues, peptidase mediated release of active 5-ASA would also release the EDTA chelator which has significant SOD mimic activity when complexed to Cu(II) ions. Mesalamine 58-63 superoxide dismutase 1 Homo sapiens 123-126 14742690-3 2004 This induction was especially pronounced when cells were treated with interleukin-1alpha (IL-1) plus aspirin for 24 h. Sodium salicylate, a poor COX inhibitor, likewise enhanced IL-1-mediated COX-2 gene expression whereas 5-aminosalicylic acid (5-ASA) or indomethacin had no effect. Mesalamine 222-243 interleukin 1 alpha Homo sapiens 70-88 14742690-3 2004 This induction was especially pronounced when cells were treated with interleukin-1alpha (IL-1) plus aspirin for 24 h. Sodium salicylate, a poor COX inhibitor, likewise enhanced IL-1-mediated COX-2 gene expression whereas 5-aminosalicylic acid (5-ASA) or indomethacin had no effect. Mesalamine 222-243 interleukin 1 beta Homo sapiens 90-94 14742690-3 2004 This induction was especially pronounced when cells were treated with interleukin-1alpha (IL-1) plus aspirin for 24 h. Sodium salicylate, a poor COX inhibitor, likewise enhanced IL-1-mediated COX-2 gene expression whereas 5-aminosalicylic acid (5-ASA) or indomethacin had no effect. Mesalamine 245-250 interleukin 1 alpha Homo sapiens 70-88 14742690-3 2004 This induction was especially pronounced when cells were treated with interleukin-1alpha (IL-1) plus aspirin for 24 h. Sodium salicylate, a poor COX inhibitor, likewise enhanced IL-1-mediated COX-2 gene expression whereas 5-aminosalicylic acid (5-ASA) or indomethacin had no effect. Mesalamine 245-250 interleukin 1 beta Homo sapiens 90-94 14742690-3 2004 This induction was especially pronounced when cells were treated with interleukin-1alpha (IL-1) plus aspirin for 24 h. Sodium salicylate, a poor COX inhibitor, likewise enhanced IL-1-mediated COX-2 gene expression whereas 5-aminosalicylic acid (5-ASA) or indomethacin had no effect. Mesalamine 245-250 interleukin 1 beta Homo sapiens 178-182 12950415-6 2003 It is hypothesized that 5-ASAs may prevent the enhancing effect of prostaglandins on PPARdelta binding to DNA by its COX inhibitory properties, decreasing proliferation of colorectal mucosal cells in non-inflammatory bowel disease patients with sporadic polyps of the large bowel. Mesalamine 24-30 peroxisome proliferator activated receptor delta Homo sapiens 85-94 12663503-11 2003 In addition, mesalazine induced apoptosis in colon cancer cells possibly through activation of caspase-3 whereas the levels of bcl-2 family proteins were not altered. Mesalamine 13-23 caspase 3 Homo sapiens 95-104 12858458-3 2003 METHODS: In an open study, mesalazine (3-4 g/day) was prescribed for 24 weeks to 20 patients (aged 18-70 yrs) with active AS, defined as the presence of at least one clinical criterion (morning stiffness > 30 min, peripheral synovitis, enthesopathy, or pain score > 2 on a visual analog scale of 10 cm) and one laboratory criterion [erythrocyte sedimentation rate (ESR) > 20 mm/h or C-reactive protein (CRP) > 20 mg/l]. Mesalamine 27-37 C-reactive protein Homo sapiens 392-410 12858458-3 2003 METHODS: In an open study, mesalazine (3-4 g/day) was prescribed for 24 weeks to 20 patients (aged 18-70 yrs) with active AS, defined as the presence of at least one clinical criterion (morning stiffness > 30 min, peripheral synovitis, enthesopathy, or pain score > 2 on a visual analog scale of 10 cm) and one laboratory criterion [erythrocyte sedimentation rate (ESR) > 20 mm/h or C-reactive protein (CRP) > 20 mg/l]. Mesalamine 27-37 C-reactive protein Homo sapiens 412-415 12106976-10 2002 When 5-ASA was orally administered using chitosan capsules in TNBS-induced colitis rats, we found better therapeutic effects with 5-ASA than with a 5-ASA CMC suspension, as evaluated by the MPO activities, C/B ratio and the damage score. Mesalamine 5-10 myeloperoxidase Rattus norvegicus 190-193 12519386-9 2003 Pharmacological inhibition of protein tyrosine phosphatases or treatment with mesalamine or sulphasalazine diminished IL-1 beta-stimulated IL-8 secretion by butyrate-exposed HT-29 cells substantially. Mesalamine 78-88 interleukin 1 beta Homo sapiens 118-127 12519386-9 2003 Pharmacological inhibition of protein tyrosine phosphatases or treatment with mesalamine or sulphasalazine diminished IL-1 beta-stimulated IL-8 secretion by butyrate-exposed HT-29 cells substantially. Mesalamine 78-88 C-X-C motif chemokine ligand 8 Homo sapiens 139-143 12917894-1 2003 BACKGROUND: The newer 5-ASA preparations were intended to avoid the adverse effects of SASP while maintaining its therapeutic benefits. Mesalamine 22-27 aspartic peptidase retroviral like 1 Homo sapiens 87-91 12917894-14 2003 REVIEWER"S CONCLUSIONS: The newer 5-ASA preparations were superior to placebo and tended towards therapeutic benefit over SASP. Mesalamine 34-39 aspartic peptidase retroviral like 1 Homo sapiens 122-126 12231210-5 2002 5ASA had no effect on RA synovial tissue explant production of IL-8 and MCP-1, while increasing GROalpha production. Mesalamine 0-4 C-X-C motif chemokine ligand 1 Homo sapiens 96-104 12135032-1 2002 OBJECTIVES: 5-Aminosalicylate is metabolized in colonic mucosa by N-acetyltransferase 1 (NAT1), and sulfapyridine is metabolized in the liver by N-acetyltransferase 2 (NAT2). Mesalamine 12-29 N-acetyltransferase 1 Homo sapiens 66-87 12135032-1 2002 OBJECTIVES: 5-Aminosalicylate is metabolized in colonic mucosa by N-acetyltransferase 1 (NAT1), and sulfapyridine is metabolized in the liver by N-acetyltransferase 2 (NAT2). Mesalamine 12-29 N-acetyltransferase 1 Homo sapiens 89-93 12135032-1 2002 OBJECTIVES: 5-Aminosalicylate is metabolized in colonic mucosa by N-acetyltransferase 1 (NAT1), and sulfapyridine is metabolized in the liver by N-acetyltransferase 2 (NAT2). Mesalamine 12-29 N-acetyltransferase 2 Homo sapiens 168-172 11604271-1 2001 We found that N-acetylation polymorphism can be evaluated from the disposition kinetics of sulfapyridine (SP) and 5-aminosalicylic acid (5-ASA) and their acetylated metabolites generated by N-acetyltransferase (NAT2) after oral administration of salicylazosulfapyridine (SASP). Mesalamine 137-142 N-acetyltransferase 2 Homo sapiens 211-215 12519547-1 2002 BACKGROUND: The newer 5-ASA preparations were intended to avoid the adverse effects of SASP while maintaining its therapeutic benefits. Mesalamine 22-27 aspartic peptidase retroviral like 1 Homo sapiens 87-91 11557525-0 2001 Mesalamine induces manganese superoxide dismutase in rat intestinal epithelial cell lines and in vivo. Mesalamine 0-10 superoxide dismutase 2 Rattus norvegicus 19-49 11557525-3 2001 IEC-6 and IRD-98, nontransformed rat small intestinal epithelial cell lines, were used to examine the effect of 5-ASA on the expression of manganese superoxide dismutase (MnSOD). Mesalamine 112-117 superoxide dismutase 2 Rattus norvegicus 139-169 11557525-3 2001 IEC-6 and IRD-98, nontransformed rat small intestinal epithelial cell lines, were used to examine the effect of 5-ASA on the expression of manganese superoxide dismutase (MnSOD). Mesalamine 112-117 superoxide dismutase 2 Rattus norvegicus 171-176 11557525-5 2001 Treatment with 5-ASA at 0.02 or 2 mg/ml induced MnSOD mRNA levels 2.67-fold or 5.66-fold, respectively. Mesalamine 15-20 superoxide dismutase 2 Rattus norvegicus 48-53 11557525-8 2001 MnSOD protein levels were induced 2-fold at 24 h and 4.23-fold at 48 h following treatment with 1 mg/ml 5-ASA. Mesalamine 104-109 superoxide dismutase 2 Rattus norvegicus 0-5 11557525-9 2001 5-ASA increased MnSOD 1.7-fold in vivo. Mesalamine 0-5 superoxide dismutase 2 Rattus norvegicus 16-21 11557525-10 2001 Pretreatment with 5-ASA significantly protected IRD-98 cells from tumor necrosis factor-alpha cytotoxicity. Mesalamine 18-23 tumor necrosis factor Rattus norvegicus 66-93 11557525-12 2001 The induction of MnSOD by 5-ASA may contribute to the therapeutic mechanism of 5-ASA. Mesalamine 26-31 superoxide dismutase 2 Rattus norvegicus 17-22 11557525-12 2001 The induction of MnSOD by 5-ASA may contribute to the therapeutic mechanism of 5-ASA. Mesalamine 79-84 superoxide dismutase 2 Rattus norvegicus 17-22 11515847-7 2001 However, 5-aminosalicylic acid (5-ASA) use was significantly correlated with reduced IL-12 p40 levels in the patients with CD, but not in UC cases. Mesalamine 9-30 interleukin 9 Homo sapiens 91-94 11520209-0 2001 Novel azo derivatives as prodrugs of 5-aminosalicylic acid and amino derivatives with potent platelet activating factor antagonist activity. Mesalamine 37-58 PCNA clamp associated factor Rattus norvegicus 93-119 11515847-7 2001 However, 5-aminosalicylic acid (5-ASA) use was significantly correlated with reduced IL-12 p40 levels in the patients with CD, but not in UC cases. Mesalamine 32-37 interleukin 9 Homo sapiens 91-94 11430933-5 2001 Sulfasalazine and 5-aminosalicylic acid, therapeutic drugs for inflammatory bowel disease, inhibited 5-lipoxygenase activity with an IC(50) of 293 and 970 microM, respectively. Mesalamine 18-39 arachidonate 5-lipoxygenase Homo sapiens 101-115 11358278-5 2001 5-Aminosalicylic acid also was evaluated by means of FRAP (the ferric reducing ability of plasma) test as a potential antioxidant. Mesalamine 0-21 mechanistic target of rapamycin kinase Homo sapiens 53-57 18968310-4 2001 The efficacy of employing sonolinear sweep voltammetry to the determination of this compound within a compositionally complex tissue culture medium has been assessed with the recovery of 5 muM 5-ASA found to be 102% (RSD=5%, N=3). Mesalamine 193-198 latexin Homo sapiens 189-192 11529938-4 2001 In the present study, we investigated the effect of sulphasalazine and two related compounds - sulphapyridine and 5-aminosalicylic acid - on M phi activation induced by bacterial lipopolysaccharide (LPS) and interferon-gamma (IFN-gamma). Mesalamine 114-135 interferon regulatory factor 6 Homo sapiens 199-202 11529938-4 2001 In the present study, we investigated the effect of sulphasalazine and two related compounds - sulphapyridine and 5-aminosalicylic acid - on M phi activation induced by bacterial lipopolysaccharide (LPS) and interferon-gamma (IFN-gamma). Mesalamine 114-135 interferon gamma Homo sapiens 208-224 11707060-8 2001 Rapid acetylation in the intestinal wall and liver (t1/2beta 0.5 to 2 hours) and transport probably by P-glycoprotein affect mucosal concentrations of mesalazine, which apparently determine clinical response. Mesalamine 151-161 CD5 molecule Homo sapiens 52-60 11358278-5 2001 5-Aminosalicylic acid also was evaluated by means of FRAP (the ferric reducing ability of plasma) test as a potential antioxidant. Mesalamine 0-21 mechanistic target of rapamycin kinase Homo sapiens 63-96 11151876-0 2000 Mesalazine inhibits activation of transcription factor NF-kappaB in inflamed mucosa of patients with ulcerative colitis. Mesalamine 0-10 nuclear factor kappa B subunit 1 Homo sapiens 55-64 11215357-12 2001 This can be interpreted as evidence for the efficacy of H15 according to the state of art in the treatment of active Crohn"s disease with Boswellia serrata extract, since the efficacy of mesalazine for this indication has been approved by the health authorities. Mesalamine 187-197 H1.5 linker histone, cluster member Homo sapiens 56-59 11151876-2 2000 Because transcription factor NF-kappaB plays an important role in inflammatory bowel diseases, we investigated the effects of mesalazine therapy on NF-kappaB activation in patients with ulcerative colitis. Mesalamine 126-136 nuclear factor kappa B subunit 1 Homo sapiens 29-38 11151876-2 2000 Because transcription factor NF-kappaB plays an important role in inflammatory bowel diseases, we investigated the effects of mesalazine therapy on NF-kappaB activation in patients with ulcerative colitis. Mesalamine 126-136 nuclear factor kappa B subunit 1 Homo sapiens 148-157 11151876-6 2000 Mesalazine therapy resulted, in a strong abrogation of NF-kappaB activation in situ. Mesalamine 0-10 nuclear factor kappa B subunit 1 Homo sapiens 55-64 11151876-7 2000 CONCLUSIONS: Our results suggest that the therapeutic properties of mesalazine rely at least in part on the inhibition of NF-kappaB activation, resulting in the suppression of proinflammatory gene expression in the inflamed mucosa. Mesalamine 68-78 nuclear factor kappa B subunit 1 Homo sapiens 122-131 11095375-0 2000 Correction of mesalazine-induced neutropenia with high-dose G-CSF. Mesalamine 14-24 colony stimulating factor 3 Homo sapiens 60-65 11054378-2 2000 Various drugs used in the treatment of IBD, such as glucocorticoids, 5-aminosalicylic acid, and sulfasalazine, interfere with NF-kappaB/Rel signaling. Mesalamine 69-90 nuclear factor kappa B subunit 1 Homo sapiens 126-135 10940280-13 2000 CONCLUSIONS: In patients with UC, in the same area of the intestinal tract, we found that the higher the 5-ASA mucosal concentrations, the lower the IL-2R levels and endoscopic and histological scores. Mesalamine 105-110 interleukin 2 receptor subunit alpha Homo sapiens 149-154 10796555-10 2000 REVIEWER"S CONCLUSIONS: The newer 5-ASA preparations were superior to placebo and tended towards therapeutic benefit over SASP. Mesalamine 34-39 aspartic peptidase retroviral like 1 Homo sapiens 122-126 10593965-3 1999 We recently reported that 5-aminosalicylic acid (5-ASA) inhibits TNFalpha-regulated IkappaB degradation and NFkappaB activation. Mesalamine 26-47 tumor necrosis factor Mus musculus 65-73 10593965-3 1999 We recently reported that 5-aminosalicylic acid (5-ASA) inhibits TNFalpha-regulated IkappaB degradation and NFkappaB activation. Mesalamine 26-47 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 108-116 10593965-3 1999 We recently reported that 5-aminosalicylic acid (5-ASA) inhibits TNFalpha-regulated IkappaB degradation and NFkappaB activation. Mesalamine 49-54 tumor necrosis factor Mus musculus 65-73 10593965-3 1999 We recently reported that 5-aminosalicylic acid (5-ASA) inhibits TNFalpha-regulated IkappaB degradation and NFkappaB activation. Mesalamine 49-54 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 108-116 10593965-5 1999 We show 5-ASA inhibits TNFalpha-stimulated phosphorylation of IkappaBalpha in intact YAMC cells. Mesalamine 8-13 tumor necrosis factor Mus musculus 23-31 10593965-5 1999 We show 5-ASA inhibits TNFalpha-stimulated phosphorylation of IkappaBalpha in intact YAMC cells. Mesalamine 8-13 nuclear factor of kappa light polypeptide gene enhancer in B cells inhibitor, alpha Mus musculus 62-74 10593965-6 1999 Phosphorylation of a glutathione S-transferase-IkappaBalpha fusion protein by cellular extracts or immunoprecipitated IKKalpha isolated from cells treated with TNFalpha is inhibited by 5-ASA. Mesalamine 185-190 nuclear factor of kappa light polypeptide gene enhancer in B cells inhibitor, alpha Mus musculus 47-59 10593965-6 1999 Phosphorylation of a glutathione S-transferase-IkappaBalpha fusion protein by cellular extracts or immunoprecipitated IKKalpha isolated from cells treated with TNFalpha is inhibited by 5-ASA. Mesalamine 185-190 conserved helix-loop-helix ubiquitous kinase Mus musculus 118-126 10593965-6 1999 Phosphorylation of a glutathione S-transferase-IkappaBalpha fusion protein by cellular extracts or immunoprecipitated IKKalpha isolated from cells treated with TNFalpha is inhibited by 5-ASA. Mesalamine 185-190 tumor necrosis factor Mus musculus 160-168 10593965-7 1999 Recombinant IKKalpha and IKKbeta autophosphorylation and their phosphorylation of glutathione S-transferase-IkappaBalpha are inhibited by 5-ASA. Mesalamine 138-143 conserved helix-loop-helix ubiquitous kinase Mus musculus 12-20 10593965-7 1999 Recombinant IKKalpha and IKKbeta autophosphorylation and their phosphorylation of glutathione S-transferase-IkappaBalpha are inhibited by 5-ASA. Mesalamine 138-143 inhibitor of kappaB kinase beta Mus musculus 25-32 10593965-7 1999 Recombinant IKKalpha and IKKbeta autophosphorylation and their phosphorylation of glutathione S-transferase-IkappaBalpha are inhibited by 5-ASA. Mesalamine 138-143 nuclear factor of kappa light polypeptide gene enhancer in B cells inhibitor, alpha Mus musculus 108-120 10593965-10 1999 In summary, 5-ASA inhibits TNFalpha-stimulated IKKalpha kinase activity toward IkappaBalpha in intestinal epithelial cells. Mesalamine 12-17 tumor necrosis factor Mus musculus 27-35 10593965-10 1999 In summary, 5-ASA inhibits TNFalpha-stimulated IKKalpha kinase activity toward IkappaBalpha in intestinal epithelial cells. Mesalamine 12-17 conserved helix-loop-helix ubiquitous kinase Mus musculus 47-55 10593965-10 1999 In summary, 5-ASA inhibits TNFalpha-stimulated IKKalpha kinase activity toward IkappaBalpha in intestinal epithelial cells. Mesalamine 12-17 nuclear factor of kappa light polypeptide gene enhancer in B cells inhibitor, alpha Mus musculus 79-91 10593965-11 1999 These findings suggest a novel role for 5-ASA in the management of IBD by disrupting TNFalpha activation of NFkappaB. Mesalamine 40-45 tumor necrosis factor Mus musculus 85-93 10593965-11 1999 These findings suggest a novel role for 5-ASA in the management of IBD by disrupting TNFalpha activation of NFkappaB. Mesalamine 40-45 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 108-116 10422769-9 1999 At this time mesalazine markedly reduced the macroscopic score, myeloperoxidase activity and plasma protein extravasation induced by 7.5% acetic acid. Mesalamine 13-23 myeloperoxidase Homo sapiens 64-79 10493988-0 1999 5-aminosalicylic acid inhibits iNOS transcription in human intestinal epithelial cells. Mesalamine 0-21 nitric oxide synthase 2 Homo sapiens 31-35 10493988-3 1999 Given the lack of conserved regulation of iNOS expression in rodent and human systems, we sought to test the effect of 5-ASA on the expression of human iNOS in cultured enterocytes. Mesalamine 119-124 nitric oxide synthase 2 Homo sapiens 152-156 10493988-7 1999 5-ASA also inhibited the expression of iNOS protein and mRNA and blocked cytokine-induced transcriptional upregulation of the iNOS gene. Mesalamine 0-5 nitric oxide synthase 2 Homo sapiens 39-43 10493988-7 1999 5-ASA also inhibited the expression of iNOS protein and mRNA and blocked cytokine-induced transcriptional upregulation of the iNOS gene. Mesalamine 0-5 nitric oxide synthase 2 Homo sapiens 126-130 10493988-9 1999 We conclude that 5-ASA inhibits iNOS expression and NO production at therapeutically relevant concentrations. Mesalamine 17-22 nitric oxide synthase 2 Homo sapiens 32-36 10473604-0 1999 Inhibition of interleukin-1-stimulated NF-kappaB RelA/p65 phosphorylation by mesalamine is accompanied by decreased transcriptional activity. Mesalamine 77-87 nuclear factor kappa B subunit 1 Homo sapiens 39-48 10473604-0 1999 Inhibition of interleukin-1-stimulated NF-kappaB RelA/p65 phosphorylation by mesalamine is accompanied by decreased transcriptional activity. Mesalamine 77-87 RELA proto-oncogene, NF-kB subunit Homo sapiens 49-53 10473604-0 1999 Inhibition of interleukin-1-stimulated NF-kappaB RelA/p65 phosphorylation by mesalamine is accompanied by decreased transcriptional activity. Mesalamine 77-87 RELA proto-oncogene, NF-kB subunit Homo sapiens 54-57 10473604-6 1999 In this report, we demonstrate that mesalamine, an anti-inflammatory aminosalicylate, dose-dependently inhibits IL-1-stimulated NF-kappaB-dependent transcription without preventing IkappaB degradation or nuclear translocation and DNA binding of the transcriptionally active NF-kappaB proteins, RelA, c-Rel, or RelB. Mesalamine 36-46 nuclear factor kappa B subunit 1 Homo sapiens 128-137 10473604-6 1999 In this report, we demonstrate that mesalamine, an anti-inflammatory aminosalicylate, dose-dependently inhibits IL-1-stimulated NF-kappaB-dependent transcription without preventing IkappaB degradation or nuclear translocation and DNA binding of the transcriptionally active NF-kappaB proteins, RelA, c-Rel, or RelB. Mesalamine 36-46 nuclear factor kappa B subunit 1 Homo sapiens 274-283 10473604-6 1999 In this report, we demonstrate that mesalamine, an anti-inflammatory aminosalicylate, dose-dependently inhibits IL-1-stimulated NF-kappaB-dependent transcription without preventing IkappaB degradation or nuclear translocation and DNA binding of the transcriptionally active NF-kappaB proteins, RelA, c-Rel, or RelB. Mesalamine 36-46 RELA proto-oncogene, NF-kB subunit Homo sapiens 294-298 10473604-6 1999 In this report, we demonstrate that mesalamine, an anti-inflammatory aminosalicylate, dose-dependently inhibits IL-1-stimulated NF-kappaB-dependent transcription without preventing IkappaB degradation or nuclear translocation and DNA binding of the transcriptionally active NF-kappaB proteins, RelA, c-Rel, or RelB. Mesalamine 36-46 REL proto-oncogene, NF-kB subunit Homo sapiens 300-305 10473604-6 1999 In this report, we demonstrate that mesalamine, an anti-inflammatory aminosalicylate, dose-dependently inhibits IL-1-stimulated NF-kappaB-dependent transcription without preventing IkappaB degradation or nuclear translocation and DNA binding of the transcriptionally active NF-kappaB proteins, RelA, c-Rel, or RelB. Mesalamine 36-46 RELB proto-oncogene, NF-kB subunit Homo sapiens 310-314 10473604-7 1999 Mesalamine was found to inhibit IL-1-stimulated RelA phosphorylation. Mesalamine 0-10 RELA proto-oncogene, NF-kB subunit Homo sapiens 48-52 10513809-3 1999 METHODS: SSZ, SP, and 5-ASA were assayed for their effects on basic fibroblast growth factor (bFGF)-induced human dermal microvascular endothelial cell (HMVEC) chemotaxis and proliferation. Mesalamine 22-27 fibroblast growth factor 2 Homo sapiens 62-92 10513809-3 1999 METHODS: SSZ, SP, and 5-ASA were assayed for their effects on basic fibroblast growth factor (bFGF)-induced human dermal microvascular endothelial cell (HMVEC) chemotaxis and proliferation. Mesalamine 22-27 fibroblast growth factor 2 Homo sapiens 94-98 10513809-10 1999 Tumor necrosis factor alpha-stimulated HMVEC shedding of sICAM-1 was reduced by incubation with either SSZ (19%) or 5-ASA (23%) (P<0.05; [n = 6]). Mesalamine 116-121 tumor necrosis factor Homo sapiens 0-27 10602313-3 1999 The aim of the present study was to investigate if sulfasalazine and its colonic metabolites 5-aminosalicylic acid (5ASA) and sulfapyridine affect NF-kappaB/Rel activation and viability of T-lymphocytes. Mesalamine 93-114 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 147-156 10602313-3 1999 The aim of the present study was to investigate if sulfasalazine and its colonic metabolites 5-aminosalicylic acid (5ASA) and sulfapyridine affect NF-kappaB/Rel activation and viability of T-lymphocytes. Mesalamine 116-120 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 147-156 16498335-11 1999 In conclusion, supplementary treatment with mesalazine in patients affected with MDC--at a follow-up limited to 48 months--proved to be well tolerated and effective in reducing the frequency of symptomatic relapses and microhemorrhagic phenomena and in reducing the duration of abdominal pain. Mesalamine 44-54 C-C motif chemokine ligand 22 Homo sapiens 81-84 10572418-2 1999 In addition to it, mechanisms of salicylazosulfapyridine, 5-aminosalicylic acid, and glucocorticoid have been clarified at molecular levels as cell transcription factors of NF-kappa B. Mesalamine 58-79 nuclear factor kappa B subunit 1 Homo sapiens 173-183 10029619-0 1999 Mesalamine blocks tumor necrosis factor growth inhibition and nuclear factor kappaB activation in mouse colonocytes. Mesalamine 0-10 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 77-83 10029619-2 1999 Because tumor necrosis factor (TNF)-alpha is important in the pathogenesis of inflammatory bowel disease, we investigated the effect of mesalamine on TNF-alpha-regulated signal transduction and proliferation in intestinal epithelial cells. Mesalamine 136-146 tumor necrosis factor Mus musculus 150-159 10029619-7 1999 RESULTS: The antiproliferative effects of TNF-alpha were blocked by mesalamine. Mesalamine 68-78 tumor necrosis factor Mus musculus 42-51 10029619-8 1999 TNF-alpha and ceramide activation of MAP kinase were inhibited by mesalamine, whereas epidermal growth factor activation of MAP kinase was unaffected. Mesalamine 66-76 tumor necrosis factor Mus musculus 0-9 10029619-9 1999 TNF-alpha-stimulated NF-kappaB activation and nuclear translocation and the degradation of Ikappa-Balpha were blocked by mesalamine. Mesalamine 121-131 tumor necrosis factor Mus musculus 0-9 10029619-9 1999 TNF-alpha-stimulated NF-kappaB activation and nuclear translocation and the degradation of Ikappa-Balpha were blocked by mesalamine. Mesalamine 121-131 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 21-30 10029619-10 1999 CONCLUSIONS: Mesalamine inhibits TNF-alpha-mediated effects on intestinal epithelial cell proliferation and activation of MAP kinase and NF-kappaB. Mesalamine 13-23 tumor necrosis factor Mus musculus 33-42 10029619-10 1999 CONCLUSIONS: Mesalamine inhibits TNF-alpha-mediated effects on intestinal epithelial cell proliferation and activation of MAP kinase and NF-kappaB. Mesalamine 13-23 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 137-146 9895376-0 1999 5-aminosalicylic acid prevents oxidant mediated damage of glyceraldehyde-3-phosphate dehydrogenase in colon epithelial cells. Mesalamine 0-21 glyceraldehyde-3-phosphate dehydrogenase Homo sapiens 58-98 10194945-1 1999 Sulfasalazine (SASP), since 60 years standard in the treatment of ulcerative colitis, is a double molecule where 5-aminosalicylic acid (5-ASA) and sulfapyridine (SP) are linked together by an azobond. Mesalamine 113-134 aspartic peptidase retroviral like 1 Homo sapiens 15-19 10194945-1 1999 Sulfasalazine (SASP), since 60 years standard in the treatment of ulcerative colitis, is a double molecule where 5-aminosalicylic acid (5-ASA) and sulfapyridine (SP) are linked together by an azobond. Mesalamine 136-141 aspartic peptidase retroviral like 1 Homo sapiens 15-19 10194945-2 1999 Bacterial splitting of SASP within the colon allows delivery of 5-ASA for its topical action (prodrug system). Mesalamine 64-69 aspartic peptidase retroviral like 1 Homo sapiens 23-27 9895376-11 1999 Studies at ratios of HOCl:5-ASA achievable in the mucosa showed direct scavenging to be the mechanism of protection of GAPDH activity. Mesalamine 26-31 glyceraldehyde-3-phosphate dehydrogenase Homo sapiens 119-124 9895376-12 1999 Mixing 5-ASA and HOCl before addition to the cells resulted in significantly greater protection of GAPDH activity than when HOCl was added to cells preincubated with 5-ASA. Mesalamine 7-12 glyceraldehyde-3-phosphate dehydrogenase Homo sapiens 99-104 9895376-14 1999 CONCLUSIONS: Therapies based on 5-ASA may play a direct role in scavenging the potent neutrophil oxidant HOCl, thereby protecting mucosal GAPDH from oxidative inhibition. Mesalamine 32-37 glyceraldehyde-3-phosphate dehydrogenase Homo sapiens 138-143 9895377-6 1999 However, pretreatment with either DEX or 5-ASA significantly attenuated LPS induced increases in expression of P- and E-selectin, and VCAM-1 in the majority of tissues evaluated. Mesalamine 41-46 selectin, platelet Mus musculus 111-128 9895377-6 1999 However, pretreatment with either DEX or 5-ASA significantly attenuated LPS induced increases in expression of P- and E-selectin, and VCAM-1 in the majority of tissues evaluated. Mesalamine 41-46 vascular cell adhesion molecule 1 Mus musculus 134-140 9885444-4 1998 Hematological complications of mesalazine are rare, but if bone marrow suppression is detected, immediate cessation of the drug and intensive immunosuppressive treatment with G-CSF should be considered. Mesalamine 31-41 colony stimulating factor 3 Homo sapiens 175-180 9893931-5 1998 5-ASA and 4-ABA weakly affected the PMN cell chemotaxis induced by zymosan-activated serum (both IC50 values > or = 10 mmol/l) and by FMLP (IC50 > or = 10 and 8.05 mmol/l, respectively). Mesalamine 0-5 formyl peptide receptor 1 Homo sapiens 137-141 9893931-7 1998 BX661A, SASP and SP concentration-dependently inhibited human PMN cell chemotaxis induced by FMLP with IC50 values of 0.68, 0.05 and 2.68 mmol/l, respectively, but both IC50 values of 5-ASA and 4-ABA were > 10 mmol/l. Mesalamine 184-189 aspartic peptidase retroviral like 1 Homo sapiens 8-12 9893931-7 1998 BX661A, SASP and SP concentration-dependently inhibited human PMN cell chemotaxis induced by FMLP with IC50 values of 0.68, 0.05 and 2.68 mmol/l, respectively, but both IC50 values of 5-ASA and 4-ABA were > 10 mmol/l. Mesalamine 184-189 formyl peptide receptor 1 Homo sapiens 93-97 9893931-9 1998 BX661A, SASP, 5-ASA, 4-ABA and SP inhibited ROS production from rat PMN cells stimulated by FMLP in a concentration-dependent manner (IC50 = 58.4, 27.5, 0.61, 1242 and 13.9 mmol/l, respectively). Mesalamine 14-19 formyl peptide receptor 1 Homo sapiens 92-96 9893931-11 1998 BX661A, SASP, 5-ASA, 4-ABA and SP inhibited ROS production from human PMN cells stimulated by FMLP in a concentration-dependent manner (IC50 = 67.4, 46.1, 0.69, 748 and 8.31 mumol/l, respectively). Mesalamine 14-19 formyl peptide receptor 1 Homo sapiens 94-98 9885444-0 1998 Mesalazine-associated severe aplastic anemia successfully treated with antithymocyte globulin, cyclosporine and granulocyte colony-stimulating factor. Mesalamine 0-10 colony stimulating factor 3 Homo sapiens 112-149 9577349-2 1998 Other substrates include the sulphonamide 5-aminosalicylic acid (5-ASA), which is an NAT1 specific substrate; N-acetylation of 5-ASA is a major route of metabolism. Mesalamine 65-70 N-acetyltransferase 1 Homo sapiens 85-89 9780130-9 1998 Sulfasalazine and its metabolite 5-aminosalicylic acid inhibit TPMT, and concurrent furosemide therapy could influence the S-methylation of thiopurines. Mesalamine 33-54 thiopurine S-methyltransferase Homo sapiens 63-67 9571233-6 1998 Under the conditions used, mouse Nat2 had 20-, 2.4-, and 5.4-fold higher catalytic activity for p-aminobenzoic acid, 5-aminosalicylic acid, and 2-aminofluorene, respectively, than Nat1. Mesalamine 117-138 N-acetyltransferase 2 (arylamine N-acetyltransferase) Mus musculus 33-37 9571233-6 1998 Under the conditions used, mouse Nat2 had 20-, 2.4-, and 5.4-fold higher catalytic activity for p-aminobenzoic acid, 5-aminosalicylic acid, and 2-aminofluorene, respectively, than Nat1. Mesalamine 117-138 N-acetyl transferase 1 Mus musculus 180-184 9571233-8 1998 For the substrates tested in this study, mouse Nat3 exhibited activity only toward 5-aminosalicylic acid and only at 1/20 the activity shown by Nat2. Mesalamine 83-104 N-acetyltransferase 3 Mus musculus 47-51 9577349-4 1998 AIMS: To investigate NAT expression in apparently healthy human intestines in order to understand the possible role of NAT in colorectal cancer and in the therapeutic response to 5-ASA. Mesalamine 179-184 bromodomain containing 2 Homo sapiens 21-24 9577349-15 1998 CONCLUSIONS: The interindividual variation in NAT1 and NAT2 in the colon could affect how individuals respond to exposure to specific NAT substrates including carcinogens and 5-ASA. Mesalamine 175-180 N-acetyltransferase 1 Homo sapiens 46-50 9577349-15 1998 CONCLUSIONS: The interindividual variation in NAT1 and NAT2 in the colon could affect how individuals respond to exposure to specific NAT substrates including carcinogens and 5-ASA. Mesalamine 175-180 N-acetyltransferase 2 Homo sapiens 55-59 9577349-15 1998 CONCLUSIONS: The interindividual variation in NAT1 and NAT2 in the colon could affect how individuals respond to exposure to specific NAT substrates including carcinogens and 5-ASA. Mesalamine 175-180 bromodomain containing 2 Homo sapiens 46-49 9391781-12 1997 Looking specifically at two homogeneous subgroups including either naturally/5-aminosalicylic acid (5-ASA) quiescent or corticoid quiescent patients, a very good predictive value for interleukin-6 serum concentration was also found. Mesalamine 77-98 interleukin 6 Homo sapiens 183-196 9352849-0 1997 Effects of mesalamine on the hsp72 stress response in rat IEC-18 intestinal epithelial cells. Mesalamine 11-21 heat shock protein family A (Hsp70) member 1A Rattus norvegicus 29-34 9352849-2 1997 Because sodium salicylate, a related compound, modulates the heat shock protein (hsp72) response in nonepithelial cells, the possibility that mesalamine confers cell protection by increasing intestinal epithelial hsp72 expression was examined. Mesalamine 142-152 heat shock protein family A (Hsp70) member 1A Rattus norvegicus 213-218 9352849-5 1997 RESULTS: Although mesalamine had no effects on the basal hsp72 expression or its thermal activation threshold in IEC-18 cells, it accelerated and augmented thermal induction of hsp72 within the first 2 hours of exposure. Mesalamine 18-28 heat shock protein family A (Hsp70) member 1A Rattus norvegicus 177-182 9352849-8 1997 CONCLUSIONS: Mesalamine augments thermal induction of the intestinal epithelial hsp72 expression in a manner that differs from that in nonintestinal epithelial cells. Mesalamine 13-23 heat shock protein family A (Hsp70) member 1A Rattus norvegicus 80-85 20948062-1 1996 Mesalazine- a 5 lipoxygenase inhibitor was tried in this open trial on 20 psoriatics. Mesalamine 0-10 arachidonate 5-lipoxygenase Homo sapiens 14-28 7496871-8 1995 5-Aminosalicylic acid did not modulate IL-6 synthesis, but significantly reduced IL-1 and enhanced TNF synthesis. Mesalamine 0-21 interleukin 1 beta Homo sapiens 81-85 8862941-0 1996 The effect of 5-aminosalicylate and para-aminosalicylate on the synthesis of prostaglandin E2 and leukotriene B4 in isolated colonic mucosal cells. Mesalamine 14-31 cystatin 12, pseudogene Homo sapiens 91-112 8566837-3 1996 The effect of 5-aminosalicylic acid (5-ASA) on IFN gamma induced changes in transepithelial resistance and permeability was investigated in HT29 clone 19A and Caco 2 monolayers. Mesalamine 14-35 interferon gamma Homo sapiens 47-56 8566837-3 1996 The effect of 5-aminosalicylic acid (5-ASA) on IFN gamma induced changes in transepithelial resistance and permeability was investigated in HT29 clone 19A and Caco 2 monolayers. Mesalamine 37-42 interferon gamma Homo sapiens 47-56 8566837-6 1996 HT29:19A monolayers incubated with both IFN gamma and 5-ASA showed lower HLA-DR expression compared with monolayers incubated with IFN gamma alone. Mesalamine 54-59 interferon gamma Homo sapiens 131-140 8566837-8 1996 Addition of both IFN gamma and 5-ASA to the basolateral surface of the monolayers significantly reduced paracellular permeability compared with addition of IFN gamma alone. Mesalamine 31-36 interferon gamma Homo sapiens 156-165 8566837-9 1996 These data show that IFN gamma is able to induce HLA-DR expression and to impair the barrier function of HT29:19A monolayers, and that 5-ASA reduces IFN gamma induced HLA-DR expression and inhibits the effects of IFN gamma on epithelial barrier function. Mesalamine 135-140 interferon gamma Homo sapiens 149-158 8566837-9 1996 These data show that IFN gamma is able to induce HLA-DR expression and to impair the barrier function of HT29:19A monolayers, and that 5-ASA reduces IFN gamma induced HLA-DR expression and inhibits the effects of IFN gamma on epithelial barrier function. Mesalamine 135-140 interferon gamma Homo sapiens 149-158 7496871-8 1995 5-Aminosalicylic acid did not modulate IL-6 synthesis, but significantly reduced IL-1 and enhanced TNF synthesis. Mesalamine 0-21 tumor necrosis factor Homo sapiens 99-102 7640156-3 1995 The hypothesis was tested that TPMT might be inhibited by sulphasalazine or isomers of ASA. Mesalamine 87-90 thiopurine S-methyltransferase Homo sapiens 31-35 7640156-5 1995 Kinetic studies demonstrated that the inhibition of TPMT by sulphasalazine and ASA isomers was non-competitive with regard to the thiopurine substrate, 6-MP, and was uncompetitive with regard to the methyl donor for the reaction, S-adenosyl-L-methionine. Mesalamine 79-82 thiopurine S-methyltransferase Homo sapiens 52-56 8691064-7 1996 Blood monocytes stimulated by lipopolysaccharide and treated with hydrocortisone, 5-aminosalicylic acid, or cyclosporin A showed reduced MCP-1 expression and production in the presence of these agents. Mesalamine 82-103 chemokine (C-C motif) ligand 2 Mus musculus 137-142 1358240-7 1992 By contrast, 5-aminosalicylic acid induced a threefold increase in the IL-8 release. Mesalamine 13-34 C-X-C motif chemokine ligand 8 Homo sapiens 71-75 7938083-0 1994 5-Aminosalicylic acid inhibits leukotriene B4 omega-hydroxylase activity in human polymorphonuclear leukocytes. Mesalamine 0-21 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 31-63 7938083-2 1994 To investigate the action of 5-aminosalicylic acid (5-ASA) on LTB4 omega-hydroxylase activity, we incubated human polymorphonuclear leukocytes (PMNLs) with 3H-labeled LTB4 after pre-incubation with various concentrations of 5-ASA. Mesalamine 52-57 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 62-84 7938083-4 1994 LTB4 omega-hydroxylase activity was inhibited by 5-ASA in a concentration-dependent fashion. Mesalamine 49-54 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 0-22 8281849-6 1994 At the cellular level, 5-aminosalicylic acid inhibited phorbol myristate acetate (100 ng/ml)-activated superoxide generation to 82.3 +/- 9.3%, the formylmethionyl leucyl peptide (10(-5) M) to 61.0 +/- 6.8%, and the NaF (20 mM)-stimulated production to 32.3 +/- 3.2% (mean +/- SD, P < 0.01). Mesalamine 23-44 C-X-C motif chemokine ligand 8 Homo sapiens 215-218 7815356-0 1995 5-Aminosalicylic acid abrogates T-cell proliferation by blocking interleukin-2 production in peripheral blood mononuclear cells. Mesalamine 0-21 interleukin 2 Homo sapiens 65-78 7815356-3 1995 We tested whether SS or its metabolites 5-aminosalicylic acid (5-ASA) and sulfapyridine (SP) inhibited the T-cell activation products interleukin 2 (IL-2) and interleukin 2 receptor alpha-chain (IL-2R alpha). Mesalamine 40-61 interleukin 2 Homo sapiens 134-147 7815356-3 1995 We tested whether SS or its metabolites 5-aminosalicylic acid (5-ASA) and sulfapyridine (SP) inhibited the T-cell activation products interleukin 2 (IL-2) and interleukin 2 receptor alpha-chain (IL-2R alpha). Mesalamine 40-61 interleukin 2 Homo sapiens 149-153 7815356-3 1995 We tested whether SS or its metabolites 5-aminosalicylic acid (5-ASA) and sulfapyridine (SP) inhibited the T-cell activation products interleukin 2 (IL-2) and interleukin 2 receptor alpha-chain (IL-2R alpha). Mesalamine 40-61 interleukin 2 Homo sapiens 159-172 7815356-3 1995 We tested whether SS or its metabolites 5-aminosalicylic acid (5-ASA) and sulfapyridine (SP) inhibited the T-cell activation products interleukin 2 (IL-2) and interleukin 2 receptor alpha-chain (IL-2R alpha). Mesalamine 63-68 interleukin 2 Homo sapiens 134-147 7815356-3 1995 We tested whether SS or its metabolites 5-aminosalicylic acid (5-ASA) and sulfapyridine (SP) inhibited the T-cell activation products interleukin 2 (IL-2) and interleukin 2 receptor alpha-chain (IL-2R alpha). Mesalamine 63-68 interleukin 2 Homo sapiens 149-153 7815356-3 1995 We tested whether SS or its metabolites 5-aminosalicylic acid (5-ASA) and sulfapyridine (SP) inhibited the T-cell activation products interleukin 2 (IL-2) and interleukin 2 receptor alpha-chain (IL-2R alpha). Mesalamine 63-68 interleukin 2 Homo sapiens 159-172 7815356-9 1995 5-ASA (625 microM) markedly reduced culture supernatant IL-2 protein levels by 92% and steady-state IL-2 messenger RNA levels 4.4-fold at 24 and 18 hr, respectively. Mesalamine 0-5 interleukin 2 Homo sapiens 56-60 7815356-9 1995 5-ASA (625 microM) markedly reduced culture supernatant IL-2 protein levels by 92% and steady-state IL-2 messenger RNA levels 4.4-fold at 24 and 18 hr, respectively. Mesalamine 0-5 interleukin 2 Homo sapiens 100-104 7815356-10 1995 The supplementation of IL-2 restored T-cell proliferation only in 5-ASA-treated cultures. Mesalamine 66-71 interleukin 2 Homo sapiens 23-27 7815356-13 1995 5-ASA inhibits T-cell proliferation in part by blocking IL-2 messenger RNA accumulation and protein production downstream of the rise in cytosolic calcium. Mesalamine 0-5 interleukin 2 Homo sapiens 56-60 7815356-14 1995 Inhibition of IL-2 production is an additional mechanism of action for 5-ASA. Mesalamine 71-76 interleukin 2 Homo sapiens 14-18 1446859-1 1992 5-Aminosalicylic acid (5ASA), 4ASA, their N-acetylated metabolites N-acetyl-5ASA and N-acetyl-4ASA, olsalazine, and colchicine impair interferon-gamma (IFN gamma) induced HLA-DR expression on a colonic cell line, HT-29. Mesalamine 0-21 interferon gamma Homo sapiens 134-150 1446859-1 1992 5-Aminosalicylic acid (5ASA), 4ASA, their N-acetylated metabolites N-acetyl-5ASA and N-acetyl-4ASA, olsalazine, and colchicine impair interferon-gamma (IFN gamma) induced HLA-DR expression on a colonic cell line, HT-29. Mesalamine 0-21 interferon gamma Homo sapiens 152-161 1351726-1 1992 Although it has been proposed that sulphasalazine (SASP) and its metabolite 5-aminosalicylic acid (5-ASA) act therapeutically by inhibiting production of vasoactive and immunoregulatory prostaglandins (PGs), in previous in vitro studies these drugs have both inhibited and promoted PG production. Mesalamine 76-97 aspartic peptidase retroviral like 1 Homo sapiens 51-55 1360533-0 1992 PAF formation by human gastrointestinal mucosa/submucosa in-vitro: release by ricinoleic acid, and inhibition by 5-aminosalicylic acid. Mesalamine 113-134 PCNA clamp associated factor Homo sapiens 0-3 1499439-9 1992 Furthermore, 5-aminosalicylic acid partially protected Cl.16E cells against cellular injury caused by IFN-gamma and TNF-alpha. Mesalamine 13-34 interferon gamma Homo sapiens 102-111 1499439-9 1992 Furthermore, 5-aminosalicylic acid partially protected Cl.16E cells against cellular injury caused by IFN-gamma and TNF-alpha. Mesalamine 13-34 tumor necrosis factor Homo sapiens 116-125 1360533-2 1992 5-Aminosalicylic acid (25-100 micrograms mL-1) inhibited PAF release by ricinoleic acid in a concentration-dependent manner, and 50 micrograms mL-1 reduced the effect of A23187. Mesalamine 0-21 L1 cell adhesion molecule Mus musculus 41-45 1360533-2 1992 5-Aminosalicylic acid (25-100 micrograms mL-1) inhibited PAF release by ricinoleic acid in a concentration-dependent manner, and 50 micrograms mL-1 reduced the effect of A23187. Mesalamine 0-21 PCNA clamp associated factor Homo sapiens 57-60 1351726-1 1992 Although it has been proposed that sulphasalazine (SASP) and its metabolite 5-aminosalicylic acid (5-ASA) act therapeutically by inhibiting production of vasoactive and immunoregulatory prostaglandins (PGs), in previous in vitro studies these drugs have both inhibited and promoted PG production. Mesalamine 99-104 aspartic peptidase retroviral like 1 Homo sapiens 51-55 1359744-5 1992 The enhanced stimulation of PAF induced by A23187 was dose-dependently inhibited by sulphasalazine, 5-aminosalicylic acid and prednisolone, but not by sulfapyridine. Mesalamine 100-121 PCNA clamp associated factor Homo sapiens 28-31 1364279-6 1992 It was found that SASP and its metabolites, such as 5-amino-salicylic acid (5-ASA), and acetyl-5-amino-salicylic acid (AC-5-ASA), but not sulfapyridine (SP) and acetyl-sulfapyridine (Ac-SP) have a direct O2- and .OH scavenging activity in vitro systems. Mesalamine 52-74 aspartic peptidase retroviral like 1 Homo sapiens 18-22 1364279-6 1992 It was found that SASP and its metabolites, such as 5-amino-salicylic acid (5-ASA), and acetyl-5-amino-salicylic acid (AC-5-ASA), but not sulfapyridine (SP) and acetyl-sulfapyridine (Ac-SP) have a direct O2- and .OH scavenging activity in vitro systems. Mesalamine 76-81 aspartic peptidase retroviral like 1 Homo sapiens 18-22 1563100-10 1992 Suppression of mucosal IL-2 production represents an important therapeutic mechanism of drugs used in the management of IBD including HC, 5-ASA and CyA. Mesalamine 138-143 interleukin 2 Homo sapiens 23-27 1630544-2 1992 These drugs are known to ameliorate urinary abnormalities and histological lesions of IgAN associated with ulcerative colitis or Crohn"s disease [5-aminosalicylic acid (5-ASA)] or to prevent, in mice, the induction of IgAN-like disease by oral immunization [disodium cromoglycate (SCG)]. Mesalamine 146-167 IGAN1 Homo sapiens 86-90 1630544-4 1992 The 5-ASA group showed a slight but not significant decrease in s-Cr, 24-hour/proteinuria, IgA circulating immune complexes (IgA-CIC) and IgA rheumatoid factor (IgA-RF); serum beta 2-microglobulin and serum IgA were unchanged; 2 of 9 treated patients showed, after 6 months of therapy, a reduction in proteinuria of more than 50% that lasted for the subsequent 18 months. Mesalamine 4-9 beta-2-microglobulin Homo sapiens 176-196 18475455-1 1992 5-Aminosalicylic Acid (5-ASA) has been used for over 50 years in the treatment of inflammatory bowel disease in the pro-drug form sulphasalazine (SASP). Mesalamine 0-21 aspartic peptidase retroviral like 1 Homo sapiens 146-150 18475455-1 1992 5-Aminosalicylic Acid (5-ASA) has been used for over 50 years in the treatment of inflammatory bowel disease in the pro-drug form sulphasalazine (SASP). Mesalamine 23-28 aspartic peptidase retroviral like 1 Homo sapiens 146-150 1685923-3 1991 Degranulation and release of lysozyme and beta-glucuronidase by activated polymorphonuclear neutrophils was inhibited by sulphasalazine but inhibited by sulphasalazine (IC50: 2 x 10(-4) M) and to a lesser extent by 5-ASA (IC50: 10(-3) M). Mesalamine 215-220 glucuronidase beta Homo sapiens 42-60 1794301-0 1991 Release of platelet-activating factor (PAF) from human colon mucosa and its inhibition by 5-aminosalicylic acid. Mesalamine 90-111 PCNA clamp associated factor Homo sapiens 11-37 1885075-1 1991 5-Aminosalicylic acid (5-ASA), the active moiety of sulphasalazine (SASP), was given as a rectal enema to patients with mild to moderate distal ulcerative colitis to determine the minimum effective dosage. Mesalamine 0-21 aspartic peptidase retroviral like 1 Homo sapiens 68-72 1885075-1 1991 5-Aminosalicylic acid (5-ASA), the active moiety of sulphasalazine (SASP), was given as a rectal enema to patients with mild to moderate distal ulcerative colitis to determine the minimum effective dosage. Mesalamine 23-28 aspartic peptidase retroviral like 1 Homo sapiens 68-72 1647912-8 1991 In cell-free systems, sulfasalazine (SAP) and its metabolite, 5-amino-salicylic acid, had a direct SSA within a millimolar range. Mesalamine 62-84 SH2 domain containing 1A Homo sapiens 37-40 1794301-0 1991 Release of platelet-activating factor (PAF) from human colon mucosa and its inhibition by 5-aminosalicylic acid. Mesalamine 90-111 PCNA clamp associated factor Homo sapiens 39-42 1794301-4 1991 5-ASA 25-100 micrograms/ml caused a 5-100% inhibition of the PAF release by 50 micrograms/ml ricinoleic acid. Mesalamine 0-5 PCNA clamp associated factor Homo sapiens 61-64 1794301-5 1991 The authors conclude that PAF can be released by damage to human colonic mucosa/submucosa, and that the inhibition of PAF release in ulcerative colitis may at least partly explain the therapeutic effect of 5-ASA. Mesalamine 206-211 PCNA clamp associated factor Homo sapiens 26-29 1794301-5 1991 The authors conclude that PAF can be released by damage to human colonic mucosa/submucosa, and that the inhibition of PAF release in ulcerative colitis may at least partly explain the therapeutic effect of 5-ASA. Mesalamine 206-211 PCNA clamp associated factor Homo sapiens 118-121 1846838-0 1991 5-Aminosalicylic acid is a potent inhibitor of interleukin 1 beta production in organ culture of colonic biopsy specimens from patients with inflammatory bowel disease. Mesalamine 0-21 interleukin 1 beta Homo sapiens 47-65 2255590-5 1990 The behaviour of Asacol at different pH values corresponds with the expectations: no release at pH 6 and pH 1, fast release at pH 7.5. Mesalamine 17-23 alanine--glyoxylate and serine--pyruvate aminotransferase Homo sapiens 96-109 33588031-20 2021 5-ASA significantly decreased apoptotic cell death (caspase-3 immunoexpression) while Vit. Mesalamine 0-5 caspase 3 Rattus norvegicus 45-61 2155024-10 1990 With 5-aminosalicylic acid present, however, the myeloperoxidase activity remained at a much higher level, namely about 150 s-1 per haem during the time interval from 100 ms to 5 s after mixing. Mesalamine 5-26 myeloperoxidase Homo sapiens 49-64 2155024-13 1990 In the presence of 5-aminosalicylic acid during the time interval in which the myeloperoxidase activity remained constant, a Km for H2O2 at pH 7.2 was determined of about 30 microM at 200 mM chloride. Mesalamine 19-40 myeloperoxidase Homo sapiens 79-94 33588031-0 2021 Vitamin E and 5-amino salicylic acid ameliorates acrylamide-induced peripheral neuropathy by inhibiting caspase-3 and inducible nitric oxide synthase immunoexpression. Mesalamine 14-36 caspase 3 Rattus norvegicus 104-113 33588031-23 2021 E and 5-ASA significantly decreased iNOS immunoexpression in the sciatic nerve, where 5-ASA was superior to Vit. Mesalamine 6-11 nitric oxide synthase 2 Rattus norvegicus 36-40 33588031-0 2021 Vitamin E and 5-amino salicylic acid ameliorates acrylamide-induced peripheral neuropathy by inhibiting caspase-3 and inducible nitric oxide synthase immunoexpression. Mesalamine 14-36 nitric oxide synthase 2 Rattus norvegicus 118-149 33588031-25 2021 E and 5-ASA protect against acrylamide-induced peripheral neuropathy through downregulation of both caspase-3 and iNOS immunoexpression. Mesalamine 6-11 caspase 3 Rattus norvegicus 100-109 33588031-25 2021 E and 5-ASA protect against acrylamide-induced peripheral neuropathy through downregulation of both caspase-3 and iNOS immunoexpression. Mesalamine 6-11 nitric oxide synthase 2 Rattus norvegicus 114-118 34929577-0 2022 Mesalazine initiates an anti-oncogenic beta-catenin / MUCDHL negative feed-back loop in colon cancer cells by cell-specific mechanisms. Mesalamine 0-10 catenin beta 1 Homo sapiens 39-51 33793375-2 2021 As mesalazine (5-ASA) could be involved in ER stress, proinflammatory and ER stress-associated cytokines and markers were measured.Results: Mesalazine (5-ASA) suppressed IL-6 mRNA in healthy donors and in HLA-B27+ and HLA-B27- patients but did not lead to induction and secretion of IL-1beta. Mesalamine 140-150 interleukin 6 Homo sapiens 170-174 33793375-2 2021 As mesalazine (5-ASA) could be involved in ER stress, proinflammatory and ER stress-associated cytokines and markers were measured.Results: Mesalazine (5-ASA) suppressed IL-6 mRNA in healthy donors and in HLA-B27+ and HLA-B27- patients but did not lead to induction and secretion of IL-1beta. Mesalamine 140-150 major histocompatibility complex, class I, B Homo sapiens 205-212 33793375-2 2021 As mesalazine (5-ASA) could be involved in ER stress, proinflammatory and ER stress-associated cytokines and markers were measured.Results: Mesalazine (5-ASA) suppressed IL-6 mRNA in healthy donors and in HLA-B27+ and HLA-B27- patients but did not lead to induction and secretion of IL-1beta. Mesalamine 140-150 major histocompatibility complex, class I, B Homo sapiens 218-225 33793375-2 2021 As mesalazine (5-ASA) could be involved in ER stress, proinflammatory and ER stress-associated cytokines and markers were measured.Results: Mesalazine (5-ASA) suppressed IL-6 mRNA in healthy donors and in HLA-B27+ and HLA-B27- patients but did not lead to induction and secretion of IL-1beta. Mesalamine 140-150 interleukin 1 alpha Homo sapiens 283-291 33793375-2 2021 As mesalazine (5-ASA) could be involved in ER stress, proinflammatory and ER stress-associated cytokines and markers were measured.Results: Mesalazine (5-ASA) suppressed IL-6 mRNA in healthy donors and in HLA-B27+ and HLA-B27- patients but did not lead to induction and secretion of IL-1beta. Mesalamine 152-157 interleukin 6 Homo sapiens 170-174 33793375-2 2021 As mesalazine (5-ASA) could be involved in ER stress, proinflammatory and ER stress-associated cytokines and markers were measured.Results: Mesalazine (5-ASA) suppressed IL-6 mRNA in healthy donors and in HLA-B27+ and HLA-B27- patients but did not lead to induction and secretion of IL-1beta. Mesalamine 152-157 major histocompatibility complex, class I, B Homo sapiens 205-212 33793375-2 2021 As mesalazine (5-ASA) could be involved in ER stress, proinflammatory and ER stress-associated cytokines and markers were measured.Results: Mesalazine (5-ASA) suppressed IL-6 mRNA in healthy donors and in HLA-B27+ and HLA-B27- patients but did not lead to induction and secretion of IL-1beta. Mesalamine 152-157 major histocompatibility complex, class I, B Homo sapiens 218-225 33793375-2 2021 As mesalazine (5-ASA) could be involved in ER stress, proinflammatory and ER stress-associated cytokines and markers were measured.Results: Mesalazine (5-ASA) suppressed IL-6 mRNA in healthy donors and in HLA-B27+ and HLA-B27- patients but did not lead to induction and secretion of IL-1beta. Mesalamine 152-157 interleukin 1 alpha Homo sapiens 283-291 33793375-3 2021 In HLA-B27 + or - patients the ER stress-associated markers CHOP (DDIT3) and ATF6 were suppressed.Conclusions: Here we show that mesalazine (5-ASA) inhibits the transcription of proinflammatory and (ER) stress associated cytokines and markers, independently of the HLA-B27 status. Mesalamine 129-139 major histocompatibility complex, class I, B Homo sapiens 3-10 33793375-3 2021 In HLA-B27 + or - patients the ER stress-associated markers CHOP (DDIT3) and ATF6 were suppressed.Conclusions: Here we show that mesalazine (5-ASA) inhibits the transcription of proinflammatory and (ER) stress associated cytokines and markers, independently of the HLA-B27 status. Mesalamine 129-139 DNA damage inducible transcript 3 Homo sapiens 60-64 33793375-3 2021 In HLA-B27 + or - patients the ER stress-associated markers CHOP (DDIT3) and ATF6 were suppressed.Conclusions: Here we show that mesalazine (5-ASA) inhibits the transcription of proinflammatory and (ER) stress associated cytokines and markers, independently of the HLA-B27 status. Mesalamine 129-139 DNA damage inducible transcript 3 Homo sapiens 66-71 33793375-3 2021 In HLA-B27 + or - patients the ER stress-associated markers CHOP (DDIT3) and ATF6 were suppressed.Conclusions: Here we show that mesalazine (5-ASA) inhibits the transcription of proinflammatory and (ER) stress associated cytokines and markers, independently of the HLA-B27 status. Mesalamine 129-139 activating transcription factor 6 Homo sapiens 77-81 33793375-3 2021 In HLA-B27 + or - patients the ER stress-associated markers CHOP (DDIT3) and ATF6 were suppressed.Conclusions: Here we show that mesalazine (5-ASA) inhibits the transcription of proinflammatory and (ER) stress associated cytokines and markers, independently of the HLA-B27 status. Mesalamine 129-139 major histocompatibility complex, class I, B Homo sapiens 265-272 33793375-3 2021 In HLA-B27 + or - patients the ER stress-associated markers CHOP (DDIT3) and ATF6 were suppressed.Conclusions: Here we show that mesalazine (5-ASA) inhibits the transcription of proinflammatory and (ER) stress associated cytokines and markers, independently of the HLA-B27 status. Mesalamine 141-146 major histocompatibility complex, class I, B Homo sapiens 3-10 33793375-3 2021 In HLA-B27 + or - patients the ER stress-associated markers CHOP (DDIT3) and ATF6 were suppressed.Conclusions: Here we show that mesalazine (5-ASA) inhibits the transcription of proinflammatory and (ER) stress associated cytokines and markers, independently of the HLA-B27 status. Mesalamine 141-146 DNA damage inducible transcript 3 Homo sapiens 60-64 33793375-3 2021 In HLA-B27 + or - patients the ER stress-associated markers CHOP (DDIT3) and ATF6 were suppressed.Conclusions: Here we show that mesalazine (5-ASA) inhibits the transcription of proinflammatory and (ER) stress associated cytokines and markers, independently of the HLA-B27 status. Mesalamine 141-146 DNA damage inducible transcript 3 Homo sapiens 66-71 33793375-3 2021 In HLA-B27 + or - patients the ER stress-associated markers CHOP (DDIT3) and ATF6 were suppressed.Conclusions: Here we show that mesalazine (5-ASA) inhibits the transcription of proinflammatory and (ER) stress associated cytokines and markers, independently of the HLA-B27 status. Mesalamine 141-146 activating transcription factor 6 Homo sapiens 77-81 33793375-3 2021 In HLA-B27 + or - patients the ER stress-associated markers CHOP (DDIT3) and ATF6 were suppressed.Conclusions: Here we show that mesalazine (5-ASA) inhibits the transcription of proinflammatory and (ER) stress associated cytokines and markers, independently of the HLA-B27 status. Mesalamine 141-146 major histocompatibility complex, class I, B Homo sapiens 265-272 33793375-1 2021 Purpose: The aim is to unravel the mechanism of mesalazine (5-ASA) on proinflammatory cytokines in PBMCs of patients with HLA-B27 +and HLA-B27 -acute anterior uveitis (AAU), and whether this may explain the different effects of 5-ASA in both disoders.Methods: PBMCs from 12 HLA-B27+ and 4 HLA-B27- AAU patients were preincubated with 5-ASA and stimulated with LPS. Mesalamine 48-58 major histocompatibility complex, class I, B Homo sapiens 122-129 33793375-1 2021 Purpose: The aim is to unravel the mechanism of mesalazine (5-ASA) on proinflammatory cytokines in PBMCs of patients with HLA-B27 +and HLA-B27 -acute anterior uveitis (AAU), and whether this may explain the different effects of 5-ASA in both disoders.Methods: PBMCs from 12 HLA-B27+ and 4 HLA-B27- AAU patients were preincubated with 5-ASA and stimulated with LPS. Mesalamine 48-58 major histocompatibility complex, class I, B Homo sapiens 135-142 33793375-1 2021 Purpose: The aim is to unravel the mechanism of mesalazine (5-ASA) on proinflammatory cytokines in PBMCs of patients with HLA-B27 +and HLA-B27 -acute anterior uveitis (AAU), and whether this may explain the different effects of 5-ASA in both disoders.Methods: PBMCs from 12 HLA-B27+ and 4 HLA-B27- AAU patients were preincubated with 5-ASA and stimulated with LPS. Mesalamine 48-58 major histocompatibility complex, class I, B Homo sapiens 135-142 33793375-1 2021 Purpose: The aim is to unravel the mechanism of mesalazine (5-ASA) on proinflammatory cytokines in PBMCs of patients with HLA-B27 +and HLA-B27 -acute anterior uveitis (AAU), and whether this may explain the different effects of 5-ASA in both disoders.Methods: PBMCs from 12 HLA-B27+ and 4 HLA-B27- AAU patients were preincubated with 5-ASA and stimulated with LPS. Mesalamine 48-58 major histocompatibility complex, class I, B Homo sapiens 135-142 33793375-1 2021 Purpose: The aim is to unravel the mechanism of mesalazine (5-ASA) on proinflammatory cytokines in PBMCs of patients with HLA-B27 +and HLA-B27 -acute anterior uveitis (AAU), and whether this may explain the different effects of 5-ASA in both disoders.Methods: PBMCs from 12 HLA-B27+ and 4 HLA-B27- AAU patients were preincubated with 5-ASA and stimulated with LPS. Mesalamine 60-65 major histocompatibility complex, class I, B Homo sapiens 122-129 33793375-1 2021 Purpose: The aim is to unravel the mechanism of mesalazine (5-ASA) on proinflammatory cytokines in PBMCs of patients with HLA-B27 +and HLA-B27 -acute anterior uveitis (AAU), and whether this may explain the different effects of 5-ASA in both disoders.Methods: PBMCs from 12 HLA-B27+ and 4 HLA-B27- AAU patients were preincubated with 5-ASA and stimulated with LPS. Mesalamine 60-65 major histocompatibility complex, class I, B Homo sapiens 135-142 33793375-1 2021 Purpose: The aim is to unravel the mechanism of mesalazine (5-ASA) on proinflammatory cytokines in PBMCs of patients with HLA-B27 +and HLA-B27 -acute anterior uveitis (AAU), and whether this may explain the different effects of 5-ASA in both disoders.Methods: PBMCs from 12 HLA-B27+ and 4 HLA-B27- AAU patients were preincubated with 5-ASA and stimulated with LPS. Mesalamine 60-65 major histocompatibility complex, class I, B Homo sapiens 135-142 33793375-1 2021 Purpose: The aim is to unravel the mechanism of mesalazine (5-ASA) on proinflammatory cytokines in PBMCs of patients with HLA-B27 +and HLA-B27 -acute anterior uveitis (AAU), and whether this may explain the different effects of 5-ASA in both disoders.Methods: PBMCs from 12 HLA-B27+ and 4 HLA-B27- AAU patients were preincubated with 5-ASA and stimulated with LPS. Mesalamine 60-65 major histocompatibility complex, class I, B Homo sapiens 135-142 34929577-0 2022 Mesalazine initiates an anti-oncogenic beta-catenin / MUCDHL negative feed-back loop in colon cancer cells by cell-specific mechanisms. Mesalamine 0-10 cadherin related family member 5 Homo sapiens 54-60 34929577-5 2022 Here, we showed that mesalazine increase mRNA levels of MUCDHL and of other genes involved in the intestinal barrier function in most intestinal cell lines. Mesalamine 21-31 cadherin related family member 5 Homo sapiens 56-62 34929577-6 2022 In addition, using gain / loss of function experiments (agonists, plasmid or siRNAs transfections), luciferase reporter genes and chromatin immunoprecipitation, we thoroughly investigated the molecular mechanisms triggered by mesalazine that lead to the up-regulation of MUCDHL expression. Mesalamine 226-236 cadherin related family member 5 Homo sapiens 271-277 34929577-8 2022 However, mesalazine-stimulation of MUCDHL transcription is controlled by cell-specific mechanisms, involving either enhanced activation of CDX2 and PPAR-gamma or repression of the beta-catenin inhibitory effect. Mesalamine 9-19 cadherin related family member 5 Homo sapiens 35-41 34874516-10 2022 Meanwhile, HQD-H and 5-ASA significantly decreased the serum IL-1beta, IL-6 and TNF-alpha levels of mice (P<0.05). Mesalamine 21-26 interleukin 1 alpha Mus musculus 61-69 34929577-8 2022 However, mesalazine-stimulation of MUCDHL transcription is controlled by cell-specific mechanisms, involving either enhanced activation of CDX2 and PPAR-gamma or repression of the beta-catenin inhibitory effect. Mesalamine 9-19 caudal type homeobox 2 Homo sapiens 139-143 34874516-10 2022 Meanwhile, HQD-H and 5-ASA significantly decreased the serum IL-1beta, IL-6 and TNF-alpha levels of mice (P<0.05). Mesalamine 21-26 interleukin 6 Mus musculus 71-75 34874516-10 2022 Meanwhile, HQD-H and 5-ASA significantly decreased the serum IL-1beta, IL-6 and TNF-alpha levels of mice (P<0.05). Mesalamine 21-26 tumor necrosis factor Mus musculus 80-89 34929577-8 2022 However, mesalazine-stimulation of MUCDHL transcription is controlled by cell-specific mechanisms, involving either enhanced activation of CDX2 and PPAR-gamma or repression of the beta-catenin inhibitory effect. Mesalamine 9-19 peroxisome proliferator activated receptor gamma Homo sapiens 148-158 34929577-8 2022 However, mesalazine-stimulation of MUCDHL transcription is controlled by cell-specific mechanisms, involving either enhanced activation of CDX2 and PPAR-gamma or repression of the beta-catenin inhibitory effect. Mesalamine 9-19 catenin beta 1 Homo sapiens 180-192 34913070-11 2022 In addition, the results showed that 5-ASA attenuated the upregulation of transforming growth factor-beta1 and phosphorylated-SMAD3, and the reduction of peroxisome proliferator activated receptor gamma induced by PQ in lung tissue of rats and human lung fibroblast WI-38 VA13 cells. Mesalamine 37-42 transforming growth factor, beta 1 Rattus norvegicus 74-106 34913070-11 2022 In addition, the results showed that 5-ASA attenuated the upregulation of transforming growth factor-beta1 and phosphorylated-SMAD3, and the reduction of peroxisome proliferator activated receptor gamma induced by PQ in lung tissue of rats and human lung fibroblast WI-38 VA13 cells. Mesalamine 37-42 SMAD family member 3 Rattus norvegicus 126-131 34913070-11 2022 In addition, the results showed that 5-ASA attenuated the upregulation of transforming growth factor-beta1 and phosphorylated-SMAD3, and the reduction of peroxisome proliferator activated receptor gamma induced by PQ in lung tissue of rats and human lung fibroblast WI-38 VA13 cells. Mesalamine 37-42 peroxisome proliferator-activated receptor gamma Rattus norvegicus 154-202 34913070-12 2022 In conclusion, the results suggested that 5-ASA had an alleviating effect on PQ-induced pulmonary fibrosis, partly by suppressing the activation of the TGF-beta1 signaling pathway. Mesalamine 42-47 transforming growth factor, beta 1 Rattus norvegicus 152-161 34915497-0 2022 5-Aminosalicylic Acid, A Weak Agonist for Aryl Hydrocarbon Receptor That Induces Splenic Regulatory T Cells. Mesalamine 0-21 aryl-hydrocarbon receptor Mus musculus 42-67 34915497-2 2022 It has been recently reported that 5-ASA induces CD4 + Foxp3 + regulatory T cells (Tregs) in the colon via the aryl hydrocarbon receptor (AhR), a ligand-activated transcription factor that regulates inflammation. Mesalamine 35-40 CD4 antigen Mus musculus 49-52 34915497-2 2022 It has been recently reported that 5-ASA induces CD4 + Foxp3 + regulatory T cells (Tregs) in the colon via the aryl hydrocarbon receptor (AhR), a ligand-activated transcription factor that regulates inflammation. Mesalamine 35-40 forkhead box P3 Mus musculus 55-60 34915497-2 2022 It has been recently reported that 5-ASA induces CD4 + Foxp3 + regulatory T cells (Tregs) in the colon via the aryl hydrocarbon receptor (AhR), a ligand-activated transcription factor that regulates inflammation. Mesalamine 35-40 aryl-hydrocarbon receptor Mus musculus 111-136 34915497-2 2022 It has been recently reported that 5-ASA induces CD4 + Foxp3 + regulatory T cells (Tregs) in the colon via the aryl hydrocarbon receptor (AhR), a ligand-activated transcription factor that regulates inflammation. Mesalamine 35-40 aryl-hydrocarbon receptor Mus musculus 138-141 34915497-3 2022 However, the role of 5-ASA as an AhR agonist that induces Tregs in the spleen remains unknown. Mesalamine 21-26 aryl-hydrocarbon receptor Mus musculus 33-36 34915497-6 2022 RESULTS: The DR-EcoScreen cell-based transactivation assay revealed that 5-ASA acted as a weak AhR agonist at concentrations of >=300 muM (1.31-1.45-fold), and that a typical AhR agonist, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), activated AhR at a concentration of 0.1 nM (22.8-fold). Mesalamine 73-78 aryl-hydrocarbon receptor Mus musculus 95-98 34915497-6 2022 RESULTS: The DR-EcoScreen cell-based transactivation assay revealed that 5-ASA acted as a weak AhR agonist at concentrations of >=300 muM (1.31-1.45-fold), and that a typical AhR agonist, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), activated AhR at a concentration of 0.1 nM (22.8-fold). Mesalamine 73-78 aryl-hydrocarbon receptor Mus musculus 242-245 34915497-7 2022 In addition, the treatment of mouse splenic cells with 300 muM 5-ASA in a primary culture assay significantly induced CD4+CD25 + Foxp3 + Tregs (control vs. 5-ASA: 9.0% vs. 12.65%, p < 0.05), while 0.1 nM TCDD also showed significant induction of Tregs (control vs. TCDD: 9.0% vs. 14.1%, p < 0.05). Mesalamine 63-68 CD4 antigen Mus musculus 118-121 34915497-7 2022 In addition, the treatment of mouse splenic cells with 300 muM 5-ASA in a primary culture assay significantly induced CD4+CD25 + Foxp3 + Tregs (control vs. 5-ASA: 9.0% vs. 12.65%, p < 0.05), while 0.1 nM TCDD also showed significant induction of Tregs (control vs. TCDD: 9.0% vs. 14.1%, p < 0.05). Mesalamine 63-68 interleukin 2 receptor, alpha chain Mus musculus 122-126 34915497-7 2022 In addition, the treatment of mouse splenic cells with 300 muM 5-ASA in a primary culture assay significantly induced CD4+CD25 + Foxp3 + Tregs (control vs. 5-ASA: 9.0% vs. 12.65%, p < 0.05), while 0.1 nM TCDD also showed significant induction of Tregs (control vs. TCDD: 9.0% vs. 14.1%, p < 0.05). Mesalamine 63-68 forkhead box P3 Mus musculus 129-134 34915497-7 2022 In addition, the treatment of mouse splenic cells with 300 muM 5-ASA in a primary culture assay significantly induced CD4+CD25 + Foxp3 + Tregs (control vs. 5-ASA: 9.0% vs. 12.65%, p < 0.05), while 0.1 nM TCDD also showed significant induction of Tregs (control vs. TCDD: 9.0% vs. 14.1%, p < 0.05). Mesalamine 156-161 CD4 antigen Mus musculus 118-121 34915497-7 2022 In addition, the treatment of mouse splenic cells with 300 muM 5-ASA in a primary culture assay significantly induced CD4+CD25 + Foxp3 + Tregs (control vs. 5-ASA: 9.0% vs. 12.65%, p < 0.05), while 0.1 nM TCDD also showed significant induction of Tregs (control vs. TCDD: 9.0% vs. 14.1%, p < 0.05). Mesalamine 156-161 interleukin 2 receptor, alpha chain Mus musculus 122-126 34915497-7 2022 In addition, the treatment of mouse splenic cells with 300 muM 5-ASA in a primary culture assay significantly induced CD4+CD25 + Foxp3 + Tregs (control vs. 5-ASA: 9.0% vs. 12.65%, p < 0.05), while 0.1 nM TCDD also showed significant induction of Tregs (control vs. TCDD: 9.0% vs. 14.1%, p < 0.05). Mesalamine 156-161 forkhead box P3 Mus musculus 129-134 34915497-9 2022 DISCUSSION: These results suggest that 5-ASA is a weak agonist of AhR and thereby induces Tregs in spleen cells. Mesalamine 39-44 aryl-hydrocarbon receptor Mus musculus 66-69 34951226-7 2021 Compared with the model group,mesalazine and JWBTW at each dose obviously increased the body weight, lowered the DAI, injury severity and histopathological scores and serum endotoxin content, down-regulated the protein expression levels of p38 MAPK, MLCK, MLC2 and p-MLC, and up-regulated the ZO-1, occludin and claudin-1, with the most obvious changes noticed in the H-JWBTW group. Mesalamine 30-40 myosin light chain kinase 3 Rattus norvegicus 250-254 34631051-11 2021 Future comparative clinical studies are required to clearly define the subgroups of patients that should be treated preferably with constant or pH-dependent release formulations of mesalazine. Mesalamine 181-191 phenylalanine hydroxylase Homo sapiens 144-146 34410453-0 2021 Systemic mesalazine treatment prevents spontaneous skin fibrosis in PLK2-deficient mice. Mesalamine 9-19 polo like kinase 2 Mus musculus 68-72 34410453-8 2021 In vitro, 72 h of treatment with 10 mmol/L mesalazine induced phenotype conversion in PLK2 KO fibroblasts and attenuated OPN expression by inhibiting ERK1/2. Mesalamine 43-53 polo like kinase 2 Mus musculus 86-90 34410453-8 2021 In vitro, 72 h of treatment with 10 mmol/L mesalazine induced phenotype conversion in PLK2 KO fibroblasts and attenuated OPN expression by inhibiting ERK1/2. Mesalamine 43-53 secreted phosphoprotein 1 Mus musculus 121-124 34410453-8 2021 In vitro, 72 h of treatment with 10 mmol/L mesalazine induced phenotype conversion in PLK2 KO fibroblasts and attenuated OPN expression by inhibiting ERK1/2. Mesalamine 43-53 mitogen-activated protein kinase 3 Mus musculus 150-156 34410453-9 2021 In vivo, dermal myofibroblast differentiation, collagen accumulation, and skin thickening were prevented by mesalazine in PLK2 KO. Mesalamine 108-118 polo like kinase 2 Mus musculus 122-126 34951226-7 2021 Compared with the model group,mesalazine and JWBTW at each dose obviously increased the body weight, lowered the DAI, injury severity and histopathological scores and serum endotoxin content, down-regulated the protein expression levels of p38 MAPK, MLCK, MLC2 and p-MLC, and up-regulated the ZO-1, occludin and claudin-1, with the most obvious changes noticed in the H-JWBTW group. Mesalamine 30-40 myosin light chain 2 Rattus norvegicus 256-260 34951226-7 2021 Compared with the model group,mesalazine and JWBTW at each dose obviously increased the body weight, lowered the DAI, injury severity and histopathological scores and serum endotoxin content, down-regulated the protein expression levels of p38 MAPK, MLCK, MLC2 and p-MLC, and up-regulated the ZO-1, occludin and claudin-1, with the most obvious changes noticed in the H-JWBTW group. Mesalamine 30-40 tight junction protein 1 Rattus norvegicus 293-297 34951226-7 2021 Compared with the model group,mesalazine and JWBTW at each dose obviously increased the body weight, lowered the DAI, injury severity and histopathological scores and serum endotoxin content, down-regulated the protein expression levels of p38 MAPK, MLCK, MLC2 and p-MLC, and up-regulated the ZO-1, occludin and claudin-1, with the most obvious changes noticed in the H-JWBTW group. Mesalamine 30-40 occludin Rattus norvegicus 299-307 34951226-7 2021 Compared with the model group,mesalazine and JWBTW at each dose obviously increased the body weight, lowered the DAI, injury severity and histopathological scores and serum endotoxin content, down-regulated the protein expression levels of p38 MAPK, MLCK, MLC2 and p-MLC, and up-regulated the ZO-1, occludin and claudin-1, with the most obvious changes noticed in the H-JWBTW group. Mesalamine 30-40 claudin 1 Rattus norvegicus 312-321 34059563-4 2021 Intrarectal treatment of moderate and severe colitis with 5-ASA alone or HA alone at a dose of 30 mg/kg led to a significant decrease in clinical activity and histology scores, myeloperoxidase activity (MPO), TNF-alpha, IL-6 and IL-1beta in colitis mice compared to untreated animals. Mesalamine 58-63 myeloperoxidase Mus musculus 177-192 34712949-5 2021 Mesalamine and the HT diminished the length of the lesions formed in the colon, in addition to reducing the levels of myeloperoxidase and interleukin-1beta. Mesalamine 0-10 myeloperoxidase Rattus norvegicus 118-133 34712949-5 2021 Mesalamine and the HT diminished the length of the lesions formed in the colon, in addition to reducing the levels of myeloperoxidase and interleukin-1beta. Mesalamine 0-10 interleukin 1 beta Rattus norvegicus 138-155 34712949-6 2021 Mesalamine was able to significantly reverse the body weight loss, while HT improved the activity of glutathione reductase and catalase. Mesalamine 0-10 glutathione-disulfide reductase Rattus norvegicus 101-122 34712949-6 2021 Mesalamine was able to significantly reverse the body weight loss, while HT improved the activity of glutathione reductase and catalase. Mesalamine 0-10 catalase Rattus norvegicus 127-135 34433292-10 2021 Finally, oral treatment with the clinically-available drug mesalazine, known to inhibit ERK1/2, prevented cardiac OPN overexpression and reversed the pathological PLK2 KO phenotype in PLK2 KO-mice. Mesalamine 59-69 mitogen-activated protein kinase 3 Mus musculus 88-94 34433292-10 2021 Finally, oral treatment with the clinically-available drug mesalazine, known to inhibit ERK1/2, prevented cardiac OPN overexpression and reversed the pathological PLK2 KO phenotype in PLK2 KO-mice. Mesalamine 59-69 secreted phosphoprotein 1 Mus musculus 114-117 34433292-10 2021 Finally, oral treatment with the clinically-available drug mesalazine, known to inhibit ERK1/2, prevented cardiac OPN overexpression and reversed the pathological PLK2 KO phenotype in PLK2 KO-mice. Mesalamine 59-69 polo like kinase 2 Mus musculus 163-167 34433292-10 2021 Finally, oral treatment with the clinically-available drug mesalazine, known to inhibit ERK1/2, prevented cardiac OPN overexpression and reversed the pathological PLK2 KO phenotype in PLK2 KO-mice. Mesalamine 59-69 polo like kinase 2 Mus musculus 184-188 34059563-4 2021 Intrarectal treatment of moderate and severe colitis with 5-ASA alone or HA alone at a dose of 30 mg/kg led to a significant decrease in clinical activity and histology scores, myeloperoxidase activity (MPO), TNF-alpha, IL-6 and IL-1beta in colitis mice compared to untreated animals. Mesalamine 58-63 myeloperoxidase Mus musculus 203-206 34059563-4 2021 Intrarectal treatment of moderate and severe colitis with 5-ASA alone or HA alone at a dose of 30 mg/kg led to a significant decrease in clinical activity and histology scores, myeloperoxidase activity (MPO), TNF-alpha, IL-6 and IL-1beta in colitis mice compared to untreated animals. Mesalamine 58-63 tumor necrosis factor Mus musculus 209-218 34059563-4 2021 Intrarectal treatment of moderate and severe colitis with 5-ASA alone or HA alone at a dose of 30 mg/kg led to a significant decrease in clinical activity and histology scores, myeloperoxidase activity (MPO), TNF-alpha, IL-6 and IL-1beta in colitis mice compared to untreated animals. Mesalamine 58-63 interleukin 6 Mus musculus 220-224 34059563-4 2021 Intrarectal treatment of moderate and severe colitis with 5-ASA alone or HA alone at a dose of 30 mg/kg led to a significant decrease in clinical activity and histology scores, myeloperoxidase activity (MPO), TNF-alpha, IL-6 and IL-1beta in colitis mice compared to untreated animals. Mesalamine 58-63 interleukin 1 alpha Mus musculus 229-237 34059563-5 2021 The combination of HA (30 mg/kg) and 5-ASA in severe colitis led to a significant improvement of colitis compared to 5-ASA alone (MPO, moderate, 5-ASA: 1,776 +- 315, 5-ASA+HA: 1,157 +- 561; severe, 5-ASA: 5,742 +- 611, 5-ASA+HA: 2,953 +- 2,611 U/g tissue). Mesalamine 37-42 myeloperoxidase Mus musculus 130-133 34259316-8 2021 Compared with those in the DSS group, the expressions of IL-1beta, IL-6, IL-17, and TNF-alpha in the DSS+DHA and DSS+5-aminosalicylic acid (5-ASA) groups were decreased, while the expressions of IL-4 and IL-10 were significantly upregulated. Mesalamine 117-138 interleukin 1 alpha Homo sapiens 57-65 34259316-8 2021 Compared with those in the DSS group, the expressions of IL-1beta, IL-6, IL-17, and TNF-alpha in the DSS+DHA and DSS+5-aminosalicylic acid (5-ASA) groups were decreased, while the expressions of IL-4 and IL-10 were significantly upregulated. Mesalamine 117-138 interleukin 6 Homo sapiens 67-71 34259316-8 2021 Compared with those in the DSS group, the expressions of IL-1beta, IL-6, IL-17, and TNF-alpha in the DSS+DHA and DSS+5-aminosalicylic acid (5-ASA) groups were decreased, while the expressions of IL-4 and IL-10 were significantly upregulated. Mesalamine 117-138 interleukin 17A Homo sapiens 73-78 34259316-8 2021 Compared with those in the DSS group, the expressions of IL-1beta, IL-6, IL-17, and TNF-alpha in the DSS+DHA and DSS+5-aminosalicylic acid (5-ASA) groups were decreased, while the expressions of IL-4 and IL-10 were significantly upregulated. Mesalamine 117-138 tumor necrosis factor Homo sapiens 84-93 34259316-8 2021 Compared with those in the DSS group, the expressions of IL-1beta, IL-6, IL-17, and TNF-alpha in the DSS+DHA and DSS+5-aminosalicylic acid (5-ASA) groups were decreased, while the expressions of IL-4 and IL-10 were significantly upregulated. Mesalamine 117-138 interleukin 4 Homo sapiens 195-199 34259316-8 2021 Compared with those in the DSS group, the expressions of IL-1beta, IL-6, IL-17, and TNF-alpha in the DSS+DHA and DSS+5-aminosalicylic acid (5-ASA) groups were decreased, while the expressions of IL-4 and IL-10 were significantly upregulated. Mesalamine 117-138 interleukin 10 Homo sapiens 204-209 35557658-2 2022 The silica-coated MNPs functionalized with the Cu(*II)-mesalamine complex was (Fe3O4@SiO2@NH2-TCT-mesalamine-Cu(II) MNPs) completely characterized by FT-IR, XRD, EDX, FESEM, TEM, VSM, TGA, and BET analyses. Mesalamine 55-65 T-box transcription factor 1 Homo sapiens 184-187 34462641-14 2021 The RIP1, RIP3, Drp1, IL-1beta, IL-18, and caspase-1 mRNA levels in the QYSX, 5-ASA, SX, and QY groups were significantly lower than those in the DSS group (P < 0.05), but there were no differences between the QYSX group and the 5-ASA group. Mesalamine 78-83 receptor (TNFRSF)-interacting serine-threonine kinase 1 Mus musculus 4-8 34462641-14 2021 The RIP1, RIP3, Drp1, IL-1beta, IL-18, and caspase-1 mRNA levels in the QYSX, 5-ASA, SX, and QY groups were significantly lower than those in the DSS group (P < 0.05), but there were no differences between the QYSX group and the 5-ASA group. Mesalamine 78-83 receptor-interacting serine-threonine kinase 3 Mus musculus 10-14 34462641-14 2021 The RIP1, RIP3, Drp1, IL-1beta, IL-18, and caspase-1 mRNA levels in the QYSX, 5-ASA, SX, and QY groups were significantly lower than those in the DSS group (P < 0.05), but there were no differences between the QYSX group and the 5-ASA group. Mesalamine 78-83 dynamin 1-like Mus musculus 16-20 34462641-14 2021 The RIP1, RIP3, Drp1, IL-1beta, IL-18, and caspase-1 mRNA levels in the QYSX, 5-ASA, SX, and QY groups were significantly lower than those in the DSS group (P < 0.05), but there were no differences between the QYSX group and the 5-ASA group. Mesalamine 78-83 interleukin 1 alpha Mus musculus 22-30 34462641-14 2021 The RIP1, RIP3, Drp1, IL-1beta, IL-18, and caspase-1 mRNA levels in the QYSX, 5-ASA, SX, and QY groups were significantly lower than those in the DSS group (P < 0.05), but there were no differences between the QYSX group and the 5-ASA group. Mesalamine 78-83 interleukin 18 Mus musculus 32-37 34462641-16 2021 The levels of Drp1, caspase-1, FIS1, and LC3a/b in the QYSX group and the 5-ASA group were lower than those in the DSS group (P < 0.05). Mesalamine 74-79 dynamin 1-like Mus musculus 14-18 34462641-16 2021 The levels of Drp1, caspase-1, FIS1, and LC3a/b in the QYSX group and the 5-ASA group were lower than those in the DSS group (P < 0.05). Mesalamine 74-79 fission, mitochondrial 1 Mus musculus 31-35 34462641-16 2021 The levels of Drp1, caspase-1, FIS1, and LC3a/b in the QYSX group and the 5-ASA group were lower than those in the DSS group (P < 0.05). Mesalamine 74-79 microtubule-associated protein 1 light chain 3 alpha Mus musculus 41-47 34456974-7 2021 In addition, ingenuity pathway analysis of the gene network further revealed the inhibitory action of mesalazine on C-C motif chemokine ligands (CCL11 and CCL21) and C-X-C motif chemokine ligands (CXCL3 and CXCR2). Mesalamine 102-112 chemokine (C-C motif) ligand 11 Mus musculus 145-150 34456974-7 2021 In addition, ingenuity pathway analysis of the gene network further revealed the inhibitory action of mesalazine on C-C motif chemokine ligands (CCL11 and CCL21) and C-X-C motif chemokine ligands (CXCL3 and CXCR2). Mesalamine 102-112 chemokine (C-X-C motif) ligand 3 Mus musculus 197-202 34456974-7 2021 In addition, ingenuity pathway analysis of the gene network further revealed the inhibitory action of mesalazine on C-C motif chemokine ligands (CCL11 and CCL21) and C-X-C motif chemokine ligands (CXCL3 and CXCR2). Mesalamine 102-112 chemokine (C-X-C motif) receptor 2 Mus musculus 207-212 34456974-8 2021 Taken together, the current transcriptomic findings revealed anti-UC pharmacological targets, including the newly discovered biotargets CCL11, CCL21, CXCL3, and CXCR2, of mesalazine against DSS-induced intestinal inflammation. Mesalamine 171-181 chemokine (C-C motif) ligand 11 Mus musculus 136-141 34456974-8 2021 Taken together, the current transcriptomic findings revealed anti-UC pharmacological targets, including the newly discovered biotargets CCL11, CCL21, CXCL3, and CXCR2, of mesalazine against DSS-induced intestinal inflammation. Mesalamine 171-181 chemokine (C-X-C motif) ligand 3 Mus musculus 150-155 34456974-8 2021 Taken together, the current transcriptomic findings revealed anti-UC pharmacological targets, including the newly discovered biotargets CCL11, CCL21, CXCL3, and CXCR2, of mesalazine against DSS-induced intestinal inflammation. Mesalamine 171-181 chemokine (C-X-C motif) receptor 2 Mus musculus 161-166 34093178-6 2021 Methods: We started our study with protein-metabolite analysis based on peroxisome proliferator-activated receptor gamma (PPARG), the therapeutic target of 5-ASA, to identify more additional potential drug targets. Mesalamine 156-161 peroxisome proliferator activated receptor gamma Homo sapiens 122-127 34093178-9 2021 Results: The combination of 5-ASA and vorinostat (SAHA) showed lower toxicity and mRNA expression of p65 in human colonic epithelial cell lines (Caco-2 and HCT-116), and more efficiently alleviated the symptoms of dextran sulfate sodium (DSS)-induced colitis than treatment with 5-ASA and SAHA alone. Mesalamine 28-33 RELA proto-oncogene, NF-kB subunit Homo sapiens 101-104 34093178-9 2021 Results: The combination of 5-ASA and vorinostat (SAHA) showed lower toxicity and mRNA expression of p65 in human colonic epithelial cell lines (Caco-2 and HCT-116), and more efficiently alleviated the symptoms of dextran sulfate sodium (DSS)-induced colitis than treatment with 5-ASA and SAHA alone. Mesalamine 279-284 RELA proto-oncogene, NF-kB subunit Homo sapiens 101-104 34374246-9 2021 Results: Compared with the model group, in the mesalazine group and the formular group, the clinical symptoms and intestinal mucosal healing of rats were improved significantly, the expression level of NF-kappaB P65 protein in the rectal tissues and the serum contents of ICAM-1 and VCAM-1 were decreased with statistically significant differences (P<0.05). Mesalamine 47-57 intercellular adhesion molecule 1 Rattus norvegicus 272-278 34374246-9 2021 Results: Compared with the model group, in the mesalazine group and the formular group, the clinical symptoms and intestinal mucosal healing of rats were improved significantly, the expression level of NF-kappaB P65 protein in the rectal tissues and the serum contents of ICAM-1 and VCAM-1 were decreased with statistically significant differences (P<0.05). Mesalamine 47-57 vascular cell adhesion molecule 1 Rattus norvegicus 283-289 35584442-0 2022 C-reactive protein levels and prevalence of leukopenia in patients with inflammatory bowel disease treated with azathioprine and/or mesalazine: a real-life study. Mesalamine 132-142 C-reactive protein Homo sapiens 0-18 35584442-1 2022 OBJECTIVE: To examine serum C-reactive protein levels and the prevalence of leukopenia in patients with Crohn"s disease or ulcerative colitis undergoing treatment with azathioprine and/or mesalazine. Mesalamine 188-198 C-reactive protein Homo sapiens 28-46 34373857-0 2021 Mesalamine Reduces Intestinal ACE2 Expression Without Modifying SARS-CoV-2 Infection or Disease Severity in Mice. Mesalamine 0-10 angiotensin converting enzyme 2 Homo sapiens 30-34 34373857-13 2021 Expression of ACE2 was reduced following mesalamine treatment in enteroids, while CTSL expression was increased. Mesalamine 41-51 angiotensin converting enzyme 2 Homo sapiens 14-18 34373857-18 2021 Mesalamine treatment reduced expression of the viral receptor ACE2 while concurrently increasing CTSL expression in human ileum organoids. Mesalamine 0-10 angiotensin converting enzyme 2 Homo sapiens 62-66 34373857-18 2021 Mesalamine treatment reduced expression of the viral receptor ACE2 while concurrently increasing CTSL expression in human ileum organoids. Mesalamine 0-10 cathepsin L Homo sapiens 97-101 34987126-3 2021 Stimulation of human intestinal epithelial cells (Caco-2) with 1000 muM of 5-ASA suppressed the levels of miR-125b, miR-150, miR-155, miR-346 and miR-506, which are known to be involved in the regulation of colitis and/or colorectal cancer in patients with inflammatory bowel disease. Mesalamine 75-80 microRNA 150 Homo sapiens 116-123 34987126-3 2021 Stimulation of human intestinal epithelial cells (Caco-2) with 1000 muM of 5-ASA suppressed the levels of miR-125b, miR-150, miR-155, miR-346 and miR-506, which are known to be involved in the regulation of colitis and/or colorectal cancer in patients with inflammatory bowel disease. Mesalamine 75-80 microRNA 155 Homo sapiens 125-132 34987126-3 2021 Stimulation of human intestinal epithelial cells (Caco-2) with 1000 muM of 5-ASA suppressed the levels of miR-125b, miR-150, miR-155, miR-346 and miR-506, which are known to be involved in the regulation of colitis and/or colorectal cancer in patients with inflammatory bowel disease. Mesalamine 75-80 microRNA 346 Homo sapiens 134-141 34987126-3 2021 Stimulation of human intestinal epithelial cells (Caco-2) with 1000 muM of 5-ASA suppressed the levels of miR-125b, miR-150, miR-155, miR-346 and miR-506, which are known to be involved in the regulation of colitis and/or colorectal cancer in patients with inflammatory bowel disease. Mesalamine 75-80 microRNA 506 Homo sapiens 146-153 34987126-4 2021 The 5-ASA-induced inhibitions of these miRNAs were associated with significant inductions of their target genes such as vitamin D receptor (VDR), suppressor of cytokine signaling (SOCS1), Forkhead box O (FOXO3a) and DNA methyltransferase 1 (DNMT1). Mesalamine 4-9 vitamin D receptor Homo sapiens 120-138 34987126-4 2021 The 5-ASA-induced inhibitions of these miRNAs were associated with significant inductions of their target genes such as vitamin D receptor (VDR), suppressor of cytokine signaling (SOCS1), Forkhead box O (FOXO3a) and DNA methyltransferase 1 (DNMT1). Mesalamine 4-9 vitamin D receptor Homo sapiens 140-143 34987126-4 2021 The 5-ASA-induced inhibitions of these miRNAs were associated with significant inductions of their target genes such as vitamin D receptor (VDR), suppressor of cytokine signaling (SOCS1), Forkhead box O (FOXO3a) and DNA methyltransferase 1 (DNMT1). Mesalamine 4-9 suppressor of cytokine signaling 1 Homo sapiens 180-185 34987126-4 2021 The 5-ASA-induced inhibitions of these miRNAs were associated with significant inductions of their target genes such as vitamin D receptor (VDR), suppressor of cytokine signaling (SOCS1), Forkhead box O (FOXO3a) and DNA methyltransferase 1 (DNMT1). Mesalamine 4-9 forkhead box O3 Homo sapiens 204-210 34987126-4 2021 The 5-ASA-induced inhibitions of these miRNAs were associated with significant inductions of their target genes such as vitamin D receptor (VDR), suppressor of cytokine signaling (SOCS1), Forkhead box O (FOXO3a) and DNA methyltransferase 1 (DNMT1). Mesalamine 4-9 DNA methyltransferase 1 Homo sapiens 216-239 34987126-4 2021 The 5-ASA-induced inhibitions of these miRNAs were associated with significant inductions of their target genes such as vitamin D receptor (VDR), suppressor of cytokine signaling (SOCS1), Forkhead box O (FOXO3a) and DNA methyltransferase 1 (DNMT1). Mesalamine 4-9 DNA methyltransferase 1 Homo sapiens 241-246 34987126-6 2021 Moreover, we showed that 5-ASA has the potential to hinder miR-155 expression induced by the transfection of miR-155 mimic into Caco-2 cells. Mesalamine 25-30 microRNA 155 Homo sapiens 59-66 34987126-6 2021 Moreover, we showed that 5-ASA has the potential to hinder miR-155 expression induced by the transfection of miR-155 mimic into Caco-2 cells. Mesalamine 25-30 microRNA 155 Homo sapiens 109-116 35557658-2 2022 The silica-coated MNPs functionalized with the Cu(*II)-mesalamine complex was (Fe3O4@SiO2@NH2-TCT-mesalamine-Cu(II) MNPs) completely characterized by FT-IR, XRD, EDX, FESEM, TEM, VSM, TGA, and BET analyses. Mesalamine 55-65 delta/notch like EGF repeat containing Homo sapiens 193-196 35557658-2 2022 The silica-coated MNPs functionalized with the Cu(*II)-mesalamine complex was (Fe3O4@SiO2@NH2-TCT-mesalamine-Cu(II) MNPs) completely characterized by FT-IR, XRD, EDX, FESEM, TEM, VSM, TGA, and BET analyses. Mesalamine 98-108 T-box transcription factor 1 Homo sapiens 184-187 35557658-2 2022 The silica-coated MNPs functionalized with the Cu(*II)-mesalamine complex was (Fe3O4@SiO2@NH2-TCT-mesalamine-Cu(II) MNPs) completely characterized by FT-IR, XRD, EDX, FESEM, TEM, VSM, TGA, and BET analyses. Mesalamine 98-108 delta/notch like EGF repeat containing Homo sapiens 193-196 35303008-5 2022 Furthermore, results suggested that the nuclear factor-kappa B (NF-kappaB) pathway may be involved in the promotion of SAA1 expression by flagellin, which was inhibited by treatment with 5-aminosalicylic acid (5-ASA). Mesalamine 187-208 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 40-62 35303008-5 2022 Furthermore, results suggested that the nuclear factor-kappa B (NF-kappaB) pathway may be involved in the promotion of SAA1 expression by flagellin, which was inhibited by treatment with 5-aminosalicylic acid (5-ASA). Mesalamine 187-208 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 64-73 35303008-5 2022 Furthermore, results suggested that the nuclear factor-kappa B (NF-kappaB) pathway may be involved in the promotion of SAA1 expression by flagellin, which was inhibited by treatment with 5-aminosalicylic acid (5-ASA). Mesalamine 187-208 serum amyloid A 1 Mus musculus 119-123 35303008-5 2022 Furthermore, results suggested that the nuclear factor-kappa B (NF-kappaB) pathway may be involved in the promotion of SAA1 expression by flagellin, which was inhibited by treatment with 5-aminosalicylic acid (5-ASA). Mesalamine 210-215 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 40-62 35303008-5 2022 Furthermore, results suggested that the nuclear factor-kappa B (NF-kappaB) pathway may be involved in the promotion of SAA1 expression by flagellin, which was inhibited by treatment with 5-aminosalicylic acid (5-ASA). Mesalamine 210-215 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 64-73 35303008-5 2022 Furthermore, results suggested that the nuclear factor-kappa B (NF-kappaB) pathway may be involved in the promotion of SAA1 expression by flagellin, which was inhibited by treatment with 5-aminosalicylic acid (5-ASA). Mesalamine 210-215 serum amyloid A 1 Mus musculus 119-123 35303008-6 2022 Therefore, the flagellin/NF-kappaB/SAA1 axis may represent one of the mechanisms by which 5-ASA suppresses intestinal inflammation. Mesalamine 90-95 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 25-34 35303008-6 2022 Therefore, the flagellin/NF-kappaB/SAA1 axis may represent one of the mechanisms by which 5-ASA suppresses intestinal inflammation. Mesalamine 90-95 serum amyloid A 1 Mus musculus 35-39 35601773-4 2022 In this study, the effect of mesalazine as a NF-kappaB inhibitor on growth and apoptosis of K562 cells has been investigated. Mesalamine 29-39 nuclear factor kappa B subunit 1 Homo sapiens 45-54 35359771-11 2022 The non-response to the 5-ASA group had significantly higher CAR and CLR levels. Mesalamine 24-29 calcium sensing receptor Homo sapiens 61-64 35359771-12 2022 CAR had a greater predictive accuracy for non-response to 5-ASA than CLR (AUC = 0.781 and 0.759). Mesalamine 58-63 calcium sensing receptor Homo sapiens 0-3 35601773-11 2022 Immuno-cytochemical results showed that mesalazine decreased c-Myc in treated cells. Mesalamine 41-51 MYC proto-oncogene, bHLH transcription factor Homo sapiens 62-67 35601773-12 2022 The RT-PCR results also showed an increase in Bax and a decrease in Bcl-2 expressions in mesalazine-treated cells. Mesalamine 89-99 BCL2 associated X, apoptosis regulator Homo sapiens 46-49 35601773-12 2022 The RT-PCR results also showed an increase in Bax and a decrease in Bcl-2 expressions in mesalazine-treated cells. Mesalamine 89-99 BCL2 apoptosis regulator Homo sapiens 68-73 2890198-1 1987 Fifty patients intolerant of or allergic to sulphasalazine (SASP) or sulphonamides were treated with mesalazine. Mesalamine 101-111 aspartic peptidase retroviral like 1 Homo sapiens 60-64 34849936-0 2022 Mesalamine Reduces Intestinal ACE2 Expression Without Modifying SARS-CoV-2 Infection or Disease Severity in Mice. Mesalamine 0-10 angiotensin converting enzyme 2 Homo sapiens 30-34 2574700-6 1989 Superoxide release from fMLP + CB stimulated neutrophils was also inhibited slightly by 5ASA (50 microM) by 35.6% and by sulphasalazine (50 microM) by 7.9%. Mesalamine 88-92 formyl peptide receptor 1 Homo sapiens 24-28 2574700-7 1989 Similarly, there was little inhibition in the rate of oxygen consumption by fMLP + CB stimulated neutrophils by either 5ASA or sulphasalazine at concentrations which produced near total abolition of luminol dependent chemiluminescence. Mesalamine 119-123 formyl peptide receptor 1 Homo sapiens 76-80 2563347-9 1989 5-Aminosalicylic acid, 4-ASA, and dapsone demonstrated a powerful inhibitory effect on the catalytic activity of myeloperoxidase, whereas all drugs were equally effective in scavenging HOCl. Mesalamine 0-21 myeloperoxidase Rattus norvegicus 113-128 2563347-11 1989 Our results indicate that inhibition of neutrophilic myeloperoxidase may be an important mechanism by which 5-ASA, 4-ASA, and dapsone attenuate FMLP-induced mucosal injury. Mesalamine 108-113 myeloperoxidase Rattus norvegicus 53-68 34433783-5 2022 Our primary outcome was CS-free remission on mesalamine at Week 52. Mesalamine 45-55 citrate synthase Homo sapiens 24-26 2902897-5 1988 Administration of SP plus 5-ASA to parallel cultures that were profoundly suppressed by the molecular equivalent amount of SASP resulted in no suppression. Mesalamine 26-31 aspartic peptidase retroviral like 1 Homo sapiens 123-127 2906888-1 1988 Benzalazine (salicylazobenzoic acid, SAB), a 5-azo derivative of 5-aminosalicylic acid, has been designed as a new therapeutic agent for the treatment of inflammatory bowel disease which might lack the frequent side effects caused by the sulfapyridine moiety of the sulfasalazine molecule (SASP). Mesalamine 65-86 SH3 domain binding protein 5 Homo sapiens 37-40 2890198-3 1987 The patients with allergic reactions, including rash, fever, and systemic manifestations from SASP, were most likely to be intolerant of or allergic to mesalazine (four of seven patients); two of them developed a similar reaction from both SASP and mesalazine. Mesalamine 152-162 aspartic peptidase retroviral like 1 Homo sapiens 94-98 2890198-9 1987 Patients with severe allergic reactions with systemic manifestations from SASP should be treated with caution with 5-aminosalicylic acid preparations. Mesalamine 115-136 aspartic peptidase retroviral like 1 Homo sapiens 74-78 2882965-0 1987 Inhibition of 5-lipoxygenase pathway of arachidonic acid metabolism in human neutrophils by sulfasalazine and 5-aminosalicylic acid. Mesalamine 110-131 arachidonate 5-lipoxygenase Homo sapiens 14-28 2877884-2 1986 The pharmacokinetics of 5-aminosalicylic acid (5-ASA) from sulphasalazine (SASP) and the slow-release 5-ASA preparation Pentasa was investigated in a cross-over study in 9 otherwise healthy patients with an ileo-rectal anastomosis. Mesalamine 24-45 aspartic peptidase retroviral like 1 Homo sapiens 75-79 2883067-3 1987 Sulfasalazine or its therapeutically active metabolite 5-aminosalicylic acid suppressed the loss of deoxyribonucleic acid into the colonic lumen and the subsequent increases in mucosal ornithine decarboxylase activity and tritiated thymidine incorporation into deoxyribonucleic acid induced by sodium deoxycholate. Mesalamine 55-76 ornithine decarboxylase 1 Homo sapiens 185-208 3017804-0 1986 Effects of topical 5-aminosalicylic acid and prednisolone on prostaglandin E2 and leukotriene B4 levels determined by equilibrium in vivo dialysis of rectum in relapsing ulcerative colitis. Mesalamine 19-40 cystatin 12, pseudogene Homo sapiens 75-96 2875632-4 1986 Sulfasalazine (SASP), a drug used in inflammatory bowel diseases, and its active metabolite 5-aminosalicylic acid (5-ASA) were found to inhibit colonic mucosal SP-LT formation, while only 5-ASA inhibited simultaneously synthesis of another arachidonic acid-derived inflammatory mediator, prostaglandin (PG) E2. Mesalamine 92-113 aspartic peptidase retroviral like 1 Homo sapiens 15-19 2875632-4 1986 Sulfasalazine (SASP), a drug used in inflammatory bowel diseases, and its active metabolite 5-aminosalicylic acid (5-ASA) were found to inhibit colonic mucosal SP-LT formation, while only 5-ASA inhibited simultaneously synthesis of another arachidonic acid-derived inflammatory mediator, prostaglandin (PG) E2. Mesalamine 115-120 aspartic peptidase retroviral like 1 Homo sapiens 15-19 2875632-4 1986 Sulfasalazine (SASP), a drug used in inflammatory bowel diseases, and its active metabolite 5-aminosalicylic acid (5-ASA) were found to inhibit colonic mucosal SP-LT formation, while only 5-ASA inhibited simultaneously synthesis of another arachidonic acid-derived inflammatory mediator, prostaglandin (PG) E2. Mesalamine 188-193 aspartic peptidase retroviral like 1 Homo sapiens 15-19 2877884-2 1986 The pharmacokinetics of 5-aminosalicylic acid (5-ASA) from sulphasalazine (SASP) and the slow-release 5-ASA preparation Pentasa was investigated in a cross-over study in 9 otherwise healthy patients with an ileo-rectal anastomosis. Mesalamine 47-52 aspartic peptidase retroviral like 1 Homo sapiens 75-79 2877884-4 1986 The median release of 5-ASA from SASP was 50% and from Pentasa 75%. Mesalamine 22-27 aspartic peptidase retroviral like 1 Homo sapiens 33-37 2877884-8 1986 The present findings also demonstrate that bacterial azo-reduction of SASP in patients with ileorectal anastomosis may be an adequate way to deliver 5-ASA in this type of patient. Mesalamine 149-154 aspartic peptidase retroviral like 1 Homo sapiens 70-74 6428914-2 1984 In an extension of a recent study which showed that therapeutically active compounds, such as sulphasalazine and its colonic metabolite 5-aminosalicylic acid were soybean lipoxygenase inhibitors, it has now been shown that N-acetylaminosalicylic acid, the principal metabolite of 5-aminosalicylic acid, also inhibits soybean lipoxygenase in a dose dependent and noncompetitive manner (Ki 3.0 X 10(-8) M, IC50 250 microM). Mesalamine 136-157 linoleate 9S-lipoxygenase-4 Glycine max 171-183 2867770-1 1985 Sulphasalazine (SASP), used in the treatment of inflammatory bowel disease, is split into sulphapyridine (SP) and 5-aminosalicylic acid (5-ASA) in the colon. Mesalamine 114-135 aspartic peptidase retroviral like 1 Homo sapiens 16-20 2867770-1 1985 Sulphasalazine (SASP), used in the treatment of inflammatory bowel disease, is split into sulphapyridine (SP) and 5-aminosalicylic acid (5-ASA) in the colon. Mesalamine 137-142 aspartic peptidase retroviral like 1 Homo sapiens 16-20 2867770-3 1985 In this study we determined the pK values of 5-ASA and its major metabolite, N-acetyl amino-salicylic acid (AcASA), by 13C-NMR spectroscopy and compared the pH dependent apparent benzene-water partition coefficients (Papp) of SASP, SP and 5-ASA with respect to their different plasma levels. Mesalamine 45-50 aspartic peptidase retroviral like 1 Homo sapiens 226-230 6428914-2 1984 In an extension of a recent study which showed that therapeutically active compounds, such as sulphasalazine and its colonic metabolite 5-aminosalicylic acid were soybean lipoxygenase inhibitors, it has now been shown that N-acetylaminosalicylic acid, the principal metabolite of 5-aminosalicylic acid, also inhibits soybean lipoxygenase in a dose dependent and noncompetitive manner (Ki 3.0 X 10(-8) M, IC50 250 microM). Mesalamine 136-157 linoleate 9S-lipoxygenase-4 Glycine max 325-337 6121576-6 1982 3 Most of the SASP reaches the colon and is there split by bacteria, forming sulphapyridine (SP) and 5-aminosalicylic acid (5-ASA). Mesalamine 101-122 aspartic peptidase retroviral like 1 Homo sapiens 14-18 6121576-6 1982 3 Most of the SASP reaches the colon and is there split by bacteria, forming sulphapyridine (SP) and 5-aminosalicylic acid (5-ASA). Mesalamine 124-129 aspartic peptidase retroviral like 1 Homo sapiens 14-18 33839254-7 2021 Molecular docking studies were conducted with four proteins (COX-2, MMP-9, TNF-alpha and MPO) to examine the interaction of mesalamine (MS) and mesalamine coumarin derivative (MS-CU). Mesalamine 124-134 tumor necrosis factor Rattus norvegicus 75-84 36326-2 1979 The role of the small bowel in absorption and metabolism of SASP was determined by the amount of administered SASP excreted in ileostomy effluents, and the concentration of serum and urinary SASP and its metabolites, sulfapyridine and 5-amino salicylic acid. Mesalamine 235-257 aspartic peptidase retroviral like 1 Homo sapiens 60-64 33839254-7 2021 Molecular docking studies were conducted with four proteins (COX-2, MMP-9, TNF-alpha and MPO) to examine the interaction of mesalamine (MS) and mesalamine coumarin derivative (MS-CU). Mesalamine 124-134 myeloperoxidase Rattus norvegicus 89-92 33984358-8 2021 The downregulation of miR-145 reduced the drug sensitivity of 5-aminosalicylic acid (5-ASA) and glucocorticoids in treating UC, indicating that miR-145 might be a potential therapeutic target for UC. Mesalamine 62-83 microRNA 145 Rattus norvegicus 22-29 33252129-12 2021 Notably, the commonly used anti-inflammatory 5-aminosalicylic acid (ie, mesalazine) and sodium salicylate ameliorated dextran sodium sulfate-induced colitis through the activation of macrophage AMPK targeting the beta1 subunit. Mesalamine 45-66 brain protein 1 Mus musculus 213-218 33252129-12 2021 Notably, the commonly used anti-inflammatory 5-aminosalicylic acid (ie, mesalazine) and sodium salicylate ameliorated dextran sodium sulfate-induced colitis through the activation of macrophage AMPK targeting the beta1 subunit. Mesalamine 72-82 brain protein 1 Mus musculus 213-218 33984358-8 2021 The downregulation of miR-145 reduced the drug sensitivity of 5-aminosalicylic acid (5-ASA) and glucocorticoids in treating UC, indicating that miR-145 might be a potential therapeutic target for UC. Mesalamine 62-83 microRNA 145 Rattus norvegicus 144-151 33984358-8 2021 The downregulation of miR-145 reduced the drug sensitivity of 5-aminosalicylic acid (5-ASA) and glucocorticoids in treating UC, indicating that miR-145 might be a potential therapeutic target for UC. Mesalamine 85-90 microRNA 145 Rattus norvegicus 22-29 33984358-8 2021 The downregulation of miR-145 reduced the drug sensitivity of 5-aminosalicylic acid (5-ASA) and glucocorticoids in treating UC, indicating that miR-145 might be a potential therapeutic target for UC. Mesalamine 85-90 microRNA 145 Rattus norvegicus 144-151 33835051-6 2021 At post-treatment week 4, IL-23 and IL-17 levels were significantly lower in the UDCA + Mesalazine group compared to those in the Mesalazine group (both P < 0.038). Mesalamine 88-98 interleukin 17A Homo sapiens 36-41 34012961-12 2021 Importantly, patients receiving mesalazine had significantly higher arpin levels than untreated patients. Mesalamine 32-42 actin related protein 2/3 complex inhibitor Homo sapiens 68-73 32676662-10 2021 Patients on anti-tumor necrosis factor (anti-TNF) medications had the lowest probability of hospitalizations (overall 5-year probability in patients with IBD stratified by maximal therapeutic step: 5-aminosalicylic acids 37% [SD = 0.6%]; anti-TNFs 31% [SD = 1.8%]; P < 0.0001). Mesalamine 198-220 tumor necrosis factor Homo sapiens 17-38 32676662-10 2021 Patients on anti-tumor necrosis factor (anti-TNF) medications had the lowest probability of hospitalizations (overall 5-year probability in patients with IBD stratified by maximal therapeutic step: 5-aminosalicylic acids 37% [SD = 0.6%]; anti-TNFs 31% [SD = 1.8%]; P < 0.0001). Mesalamine 198-220 tumor necrosis factor Homo sapiens 45-48 33785874-7 2021 RESULTS: 5-ASA was shown, in vitro, to inhibit the growth of adenoma cells and suppress beta-catenin transcriptional activity. Mesalamine 9-14 catenin beta 1 Homo sapiens 88-100 33835051-6 2021 At post-treatment week 4, IL-23 and IL-17 levels were significantly lower in the UDCA + Mesalazine group compared to those in the Mesalazine group (both P < 0.038). Mesalamine 88-98 interleukin 23 subunit alpha Homo sapiens 26-31 33064167-11 2021 Additionally, TGFbeta led to increased cell stiffness and adhesion, which were reversed by mesalazine treatment. Mesalamine 91-101 transforming growth factor alpha Homo sapiens 14-21 33465392-11 2021 And the percentages of Tim-4-expressing monocytes were significantly decreased in UC patients that received a 3-week treatment with mesalazine. Mesalamine 132-142 T cell immunoglobulin and mucin domain containing 4 Homo sapiens 23-28 33150655-11 2021 A dosage guideline for azathioprine was developed based on the PPK model that enables individualised azathioprine dosing in adult patients with different body weights, TPMT*3C genotypes and co-administration with mesalazine. Mesalamine 213-223 kallikrein B1 Homo sapiens 63-66 33522827-7 2021 Further in vivo activities and biodistribution experiments found that the GC-B-Que micelles tended to accumulate in intestinal inflammation sites and showed better therapeutic efficacy than the free drugs (quercetin and mesalazine) in a colitis mice model. Mesalamine 220-230 natriuretic peptide receptor 2 Mus musculus 74-78 33562228-4 2021 Under optimal conditions, the best analytical performance was obtained with CNT/PMBDES/GCE in 0.04 M BR buffer pH 7.0 in the range 5-100 microM 5-ASA using the DPV method, with an excellent sensitivity of 9.84 muA cm-2 muM-1 (4.9 % RSD, n = 5) and a detection limit (LOD) (3sigma/slope) of 7.7 nM, outclassing most similar sensors found in the literature. Mesalamine 144-149 PWWP domain containing 3A, DNA repair factor Homo sapiens 219-224 33470487-0 2021 Mesalazine formulations differentially affect thiopurine metabolism through thiopurine S-methyltransferase inhibition. Mesalamine 0-10 thiopurine S-methyltransferase Homo sapiens 76-106 33289917-0 2021 Targeting IL-10, ZO-1 gene expression and IL-6/STAT-3 trans-signaling by a combination of atorvastatin and mesalazine to enhance anti-inflammatory effects and attenuate progression of oxazolone induced colitis. Mesalamine 107-117 interleukin 6 Homo sapiens 42-46 33289917-0 2021 Targeting IL-10, ZO-1 gene expression and IL-6/STAT-3 trans-signaling by a combination of atorvastatin and mesalazine to enhance anti-inflammatory effects and attenuate progression of oxazolone induced colitis. Mesalamine 107-117 signal transducer and activator of transcription 3 Homo sapiens 47-53 32383169-0 2021 Targeting IL-10, ZO-1 genes expression and IL-6/STAT-3 trans-signaling by a combination of atorvastatin and mesalazine to enhance anti-inflammatory effects and attenuates progression of oxazolone induced colitis. Mesalamine 108-118 interleukin 6 Rattus norvegicus 43-47 32383169-0 2021 Targeting IL-10, ZO-1 genes expression and IL-6/STAT-3 trans-signaling by a combination of atorvastatin and mesalazine to enhance anti-inflammatory effects and attenuates progression of oxazolone induced colitis. Mesalamine 108-118 signal transducer and activator of transcription 3 Rattus norvegicus 48-54 33501934-9 2022 The genome-wide association studies and meta-analysis identified one significant association between rs144384547 (upstream of RGS17) and mesalamine-induced fever and diarrhea (P = 7.21e-09; odds ratio = 11.2). Mesalamine 137-147 regulator of G protein signaling 17 Homo sapiens 126-131 33470487-3 2021 5-ASA is known to inhibit thiopurine S-methyltransferase (TPMT) activity and to affect thiopurine metabolism. Mesalamine 0-5 thiopurine S-methyltransferase Homo sapiens 26-56 33470487-3 2021 5-ASA is known to inhibit thiopurine S-methyltransferase (TPMT) activity and to affect thiopurine metabolism. Mesalamine 0-5 thiopurine S-methyltransferase Homo sapiens 58-62 33470487-4 2021 There have been no studies comparing TPMT inhibition by multi-matrix mesalazine (MMX) with other formulations. Mesalamine 69-79 thiopurine S-methyltransferase Homo sapiens 37-41 33470487-5 2021 We investigated the difference in TPMT inhibition by different mesalazine formulations and prospectively confirmed the clinical relevance. Mesalamine 63-73 thiopurine S-methyltransferase Homo sapiens 34-38 33470487-9 2021 RESULTS: Plasma 5-ASA and N-Ac-5-ASA levels were significantly higher in patients receiving time-dependent mesalazine (n=12) compared to pH-dependent (n=12) and MMX (n=15), accompanied by greater TPMT inhibition. Mesalamine 16-21 thiopurine S-methyltransferase Homo sapiens 196-200 33470487-12 2021 CONCLUSIONS: Time-dependent mesalazine has higher plasma 5-ASA and N-Ac-5-ASA levels and greater TPMT inhibition than MMX. Mesalamine 28-38 thiopurine S-methyltransferase Homo sapiens 97-101 32856298-1 2020 BACKGROUND: Oral 5-aminosalicylic acid (5-ASA; also known as mesalazine or mesalamine) preparations were intended to avoid the adverse effects of sulfasalazine (SASP) while maintaining its therapeutic benefits. Mesalamine 17-38 aspartic peptidase retroviral like 1 Homo sapiens 161-165 32956646-7 2020 Also, the results indicated that mesalazine, reduced the tissue reactive oxygen species (ROS), malondialdehyde (MDA), and protein carbonyl (PCO) levels, serum nitric oxide (NO), and increased the level of tissue NO and glutathione (GSH) and activity of Catalase (CAT), Based on these results, it can be concluded that mesalazine strengthens the antioxidant defense system of gastric mucosal cells during oxidative damage caused by ethanol. Mesalamine 33-43 catalase Rattus norvegicus 253-261 32956646-7 2020 Also, the results indicated that mesalazine, reduced the tissue reactive oxygen species (ROS), malondialdehyde (MDA), and protein carbonyl (PCO) levels, serum nitric oxide (NO), and increased the level of tissue NO and glutathione (GSH) and activity of Catalase (CAT), Based on these results, it can be concluded that mesalazine strengthens the antioxidant defense system of gastric mucosal cells during oxidative damage caused by ethanol. Mesalamine 33-43 catalase Rattus norvegicus 263-266 33257796-4 2020 Despite the high binding percentage of 5-aminosalicylates for human serum albumin (> 61.44%), results have shown that folic acid binding to human serum albumin protein is far greater (69.40%) compared to alpha1-acid-glycoprotein (3.45%). Mesalamine 39-57 albumin Homo sapiens 68-81 33138176-8 2020 Intrarectal treatment of colitis with 30 mg/kg chitosan alone and with 30 mg/kg 5-ASA for 3 days led to a significant decrease in MPO, ALP, TNF-alpha, IL-6, IL-1beta and NF-kappaB in colitis mice compared to untreated mice. Mesalamine 80-85 myeloperoxidase Mus musculus 130-133 33138176-8 2020 Intrarectal treatment of colitis with 30 mg/kg chitosan alone and with 30 mg/kg 5-ASA for 3 days led to a significant decrease in MPO, ALP, TNF-alpha, IL-6, IL-1beta and NF-kappaB in colitis mice compared to untreated mice. Mesalamine 80-85 tumor necrosis factor Mus musculus 140-149 33138176-8 2020 Intrarectal treatment of colitis with 30 mg/kg chitosan alone and with 30 mg/kg 5-ASA for 3 days led to a significant decrease in MPO, ALP, TNF-alpha, IL-6, IL-1beta and NF-kappaB in colitis mice compared to untreated mice. Mesalamine 80-85 interleukin 6 Mus musculus 151-155 33138176-8 2020 Intrarectal treatment of colitis with 30 mg/kg chitosan alone and with 30 mg/kg 5-ASA for 3 days led to a significant decrease in MPO, ALP, TNF-alpha, IL-6, IL-1beta and NF-kappaB in colitis mice compared to untreated mice. Mesalamine 80-85 interleukin 1 alpha Mus musculus 157-165 33138176-8 2020 Intrarectal treatment of colitis with 30 mg/kg chitosan alone and with 30 mg/kg 5-ASA for 3 days led to a significant decrease in MPO, ALP, TNF-alpha, IL-6, IL-1beta and NF-kappaB in colitis mice compared to untreated mice. Mesalamine 80-85 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 170-179 33091174-1 2021 BACKGROUND: Limited data are available on the effects of fermentable fiber in altering intestinal pH and transit to predict efficacy-based delivery profiles of pH-dependent mesalamine coatings in ulcerative colitis (UC). Mesalamine 173-183 phenylalanine hydroxylase Homo sapiens 160-162 33091174-11 2021 These have potentially detrimental effects on predicted luminal release patterns of pH-dependent 5-aminosalicylic acid release systems. Mesalamine 97-118 phenylalanine hydroxylase Homo sapiens 84-86 33019698-4 2020 Results: 5-ASA ameliorated indomethacin-induced cell apoptosis and an increase in the intracellular ROS content while augmenting the indomethacin-induced suppression of SOD2 activity in IEC-6 cells. Mesalamine 9-14 superoxide dismutase 2 Rattus norvegicus 169-173 33019698-5 2020 Moreover, 5-ASA reversed the indomethacin-induced attenuation of occludin and ZO-1 expression and promoted faster wound healing effects in IEC-6 cells following an indomethacin-induced injury. Mesalamine 10-15 occludin Rattus norvegicus 65-73 33019698-5 2020 Moreover, 5-ASA reversed the indomethacin-induced attenuation of occludin and ZO-1 expression and promoted faster wound healing effects in IEC-6 cells following an indomethacin-induced injury. Mesalamine 10-15 tight junction protein 1 Rattus norvegicus 78-82 33468700-0 2021 5-Aminosalicylic Acid Ameliorates Colitis and Checks Dysbiotic Escherichia coli Expansion by Activating PPAR-gamma Signaling in the Intestinal Epithelium. Mesalamine 0-21 peroxisome proliferator activated receptor gamma Mus musculus 104-114 33468700-1 2021 5-Aminosalicylic acid (5-ASA), a peroxisome proliferator-activated receptor gamma (PPAR-gamma) agonist, is a widely used first-line medication for the treatment of ulcerative colitis, but its anti-inflammatory mechanism is not fully resolved. Mesalamine 0-21 peroxisome proliferator activated receptor gamma Mus musculus 83-93 33468700-1 2021 5-Aminosalicylic acid (5-ASA), a peroxisome proliferator-activated receptor gamma (PPAR-gamma) agonist, is a widely used first-line medication for the treatment of ulcerative colitis, but its anti-inflammatory mechanism is not fully resolved. Mesalamine 23-28 peroxisome proliferator activated receptor gamma Mus musculus 83-93 33468700-2 2021 Here, we show that 5-ASA ameliorates colitis in dextran sulfate sodium (DSS)-treated mice by activating PPAR-gamma signaling in the intestinal epithelium. Mesalamine 19-24 peroxisome proliferator activated receptor gamma Mus musculus 104-114 33468700-5 2021 These data suggest that the anti-inflammatory activity of 5-ASA requires activation of epithelial PPAR-gamma signaling, thus pointing to the intestinal epithelium as a potential target for therapeutic intervention in ulcerative colitis.IMPORTANCE An expansion of Enterobacterales in the fecal microbiota is a microbial signature of dysbiosis that is linked to many noncommunicable diseases, including ulcerative colitis. Mesalamine 58-63 peroxisome proliferator activated receptor gamma Mus musculus 98-108 33468700-8 2021 Activation of epithelial peroxisome proliferator-activated receptor gamma (PPAR-gamma) signaling with 5-aminosalicylic acid (5-ASA) was sufficient to restore mitochondrial activity and blunt a dysbiotic E. coli expansion. Mesalamine 102-123 peroxisome proliferator activated receptor gamma Mus musculus 75-85 33468700-8 2021 Activation of epithelial peroxisome proliferator-activated receptor gamma (PPAR-gamma) signaling with 5-aminosalicylic acid (5-ASA) was sufficient to restore mitochondrial activity and blunt a dysbiotic E. coli expansion. Mesalamine 125-130 peroxisome proliferator activated receptor gamma Mus musculus 75-85 33256292-9 2020 The expression of MGP mRNA in the colonic mucosa of UC patients treated with hormone and immunosuppressive agents or biological agents or surgery was higher than that of patients treated with mesalazine. Mesalamine 192-202 matrix Gla protein Homo sapiens 18-21 32047894-5 2020 Overall infectious complications were increased in patients who received anti-tumor necrosis factor (TNF) agents (odds ratio [OR] 1.26; 95% confidence interval [CI], 1.07-1.50) and corticosteroids (OR 1.34; 95% CI, 1.25-1.44) and decreased in those who received 5-aminosalicylic acid (OR 0.63; 95% CI, 0.46-0.87). Mesalamine 262-283 tumor necrosis factor Homo sapiens 73-99 32047894-5 2020 Overall infectious complications were increased in patients who received anti-tumor necrosis factor (TNF) agents (odds ratio [OR] 1.26; 95% confidence interval [CI], 1.07-1.50) and corticosteroids (OR 1.34; 95% CI, 1.25-1.44) and decreased in those who received 5-aminosalicylic acid (OR 0.63; 95% CI, 0.46-0.87). Mesalamine 262-283 tumor necrosis factor Homo sapiens 101-104 32047894-7 2020 Both corticosteroids and anti-TNF agents were associated with increased intra-abdominal infection risk (OR 1.63; 95% CI, 1.33-2.00 and OR 1.46; 95% CI, 1.08-1.97, respectively), whereas no impact was observed with 5-aminosalicylates, immunomodulators, or anti-integrin therapy. Mesalamine 214-232 tumor necrosis factor Homo sapiens 30-33 33092149-6 2020 Western blot analysis of colon tissues revealed that cyclooxygenase-2, tumor necrosis factor alpha (TNF-alpha), and phosphorylated signal transducer and activator of transcription-3 (p-STAT3) were significantly decreased in the colitis + 5-ASA group, whereas forkhead box P3 (FOXP3) was increased. Mesalamine 238-243 signal transducer and activator of transcription 3 Homo sapiens 131-181 32526285-0 2020 The protective effect of Lactobacillus versus 5-aminosalicylic acid in ulcerative colitis model by modulation of gut microbiota and Nrf2/Ho-1 pathway. Mesalamine 46-67 NFE2 like bZIP transcription factor 2 Rattus norvegicus 132-136 32526285-0 2020 The protective effect of Lactobacillus versus 5-aminosalicylic acid in ulcerative colitis model by modulation of gut microbiota and Nrf2/Ho-1 pathway. Mesalamine 46-67 heme oxygenase 1 Rattus norvegicus 137-141 32526285-14 2020 Both Lactobacillus and 5-ASA show significant increase of NrF2 and HO-1 and marked decrease of TNF-alpha. Mesalamine 23-28 NFE2 like bZIP transcription factor 2 Rattus norvegicus 58-62 32526285-14 2020 Both Lactobacillus and 5-ASA show significant increase of NrF2 and HO-1 and marked decrease of TNF-alpha. Mesalamine 23-28 heme oxygenase 1 Rattus norvegicus 67-71 32526285-14 2020 Both Lactobacillus and 5-ASA show significant increase of NrF2 and HO-1 and marked decrease of TNF-alpha. Mesalamine 23-28 tumor necrosis factor Rattus norvegicus 95-104 32856298-1 2020 BACKGROUND: Oral 5-aminosalicylic acid (5-ASA; also known as mesalazine or mesalamine) preparations were intended to avoid the adverse effects of sulfasalazine (SASP) while maintaining its therapeutic benefits. Mesalamine 40-45 aspartic peptidase retroviral like 1 Homo sapiens 161-165 32856298-1 2020 BACKGROUND: Oral 5-aminosalicylic acid (5-ASA; also known as mesalazine or mesalamine) preparations were intended to avoid the adverse effects of sulfasalazine (SASP) while maintaining its therapeutic benefits. Mesalamine 61-71 aspartic peptidase retroviral like 1 Homo sapiens 161-165 32856298-1 2020 BACKGROUND: Oral 5-aminosalicylic acid (5-ASA; also known as mesalazine or mesalamine) preparations were intended to avoid the adverse effects of sulfasalazine (SASP) while maintaining its therapeutic benefits. Mesalamine 75-85 aspartic peptidase retroviral like 1 Homo sapiens 161-165 32668218-5 2020 Restoring mitochondrial bioenergetics in the colonic epithelium with 5-amino salicylic acid, a PPAR-gamma (peroxisome proliferator-activated receptor gamma) agonist that stimulates mitochondrial activity, ameliorated pre-IBD symptoms. Mesalamine 69-91 peroxisome proliferator activated receptor gamma Homo sapiens 95-105 33319050-10 2020 In DSS-treated rats, 5-ASA, but not DKT, suppressed the MPO activity. Mesalamine 21-26 myeloperoxidase Rattus norvegicus 56-59 32668218-5 2020 Restoring mitochondrial bioenergetics in the colonic epithelium with 5-amino salicylic acid, a PPAR-gamma (peroxisome proliferator-activated receptor gamma) agonist that stimulates mitochondrial activity, ameliorated pre-IBD symptoms. Mesalamine 69-91 peroxisome proliferator activated receptor gamma Homo sapiens 107-155 33214334-7 2020 Studies have shown that activation of NF-kappaB is reduced by treatment with, among others, mesalazine and glucocorticoids. Mesalamine 92-102 nuclear factor kappa B subunit 1 Homo sapiens 38-47 32786164-1 2020 BACKGROUND: Oral 5-aminosalicylic acid (5-ASA) preparations were intended to avoid the adverse effects of sulfasalazine (SASP) while maintaining its therapeutic benefits. Mesalamine 17-38 aspartic peptidase retroviral like 1 Homo sapiens 121-125 32786164-1 2020 BACKGROUND: Oral 5-aminosalicylic acid (5-ASA) preparations were intended to avoid the adverse effects of sulfasalazine (SASP) while maintaining its therapeutic benefits. Mesalamine 40-45 aspartic peptidase retroviral like 1 Homo sapiens 121-125 32014250-0 2020 Transport characteristics of 5-aminosalicylic acid into colonic epithelium: Involvement of sodium-coupled monocarboxylate transporter SMCT1-mediated transport system. Mesalamine 29-50 sodium-coupled monocarboxylate transporter 1 Xenopus laevis 134-139 32329325-8 2020 The expressions of IL-6, TNF-alpha were significantly higher in roselle-treated group on day 7 and 14, but not on day 21 and 28, whereas, the expression of IL-10 was significantly lower only on day 7 compared with mesalazine-treated group. Mesalamine 214-224 tumor necrosis factor Mus musculus 25-34 32067935-0 2020 In vitro investigation of the effect of mesalazine on amyloid fibril formation of hen egg-white lysozyme and defibrillation lysozyme fibrils. Mesalamine 40-50 lysozyme Homo sapiens 96-104 32067935-3 2020 In this study, we investigated the in vitro effects of mesalazine drug on both preventions of lysozyme aggregation and the removal of lysozyme fibrils. Mesalamine 55-65 lysozyme Homo sapiens 94-102 32067935-3 2020 In this study, we investigated the in vitro effects of mesalazine drug on both preventions of lysozyme aggregation and the removal of lysozyme fibrils. Mesalamine 55-65 lysozyme Homo sapiens 134-142 32067935-8 2020 Based on the obtained results, we conclude that mesalazine can be used as a drug for the prevention of amyloid-fibrils formation in hereditary lysozyme amyloidosis and other systemic non-neuropathic hereditary amyloidosis. Mesalamine 48-58 lysozyme Homo sapiens 143-151 32014250-1 2020 5-Aminosalicylic acid (5-ASA) is conventionally used as a first line drug for inflammatory bowel disease (IBD). Mesalamine 0-21 anti-sarcolemmal autoantibodies Mus musculus 25-28 32238712-10 2020 Taken together, these results showed that these 5-ASA derivatives are transportable substrates for PEPT1. Mesalamine 48-53 solute carrier family 15 (oligopeptide transporter), member 1 L homeolog Xenopus laevis 99-104 31743034-7 2020 In murine macrophage and human colon carcinoma cells, activation of GPR109A by 5-ANA elevated the level of the anti-inflammatory cytokine IL-10, suppressed NF-kappaB activation, and potentiated the inhibitory activity of 5-ASA on NF-kappaB. Mesalamine 221-226 hydroxycarboxylic acid receptor 2 Homo sapiens 68-75 32395486-11 2020 6-gingerol could also inhibit the decrease of mRNA levels and serum and bowel levels of IL-10 induced by DSS, which is also similar to mesalazine. Mesalamine 135-145 interleukin 10 Mus musculus 88-93 32394929-0 2020 Mesalazine induced focal segmental glomerulosclerosis in a patient with ulcerative colitis. Mesalamine 0-10 actinin alpha 4 Homo sapiens 19-53 32394929-1 2020 Focal segmental glomerulosclerosis (FSGS) and other glomerulonephritis due to the use of 5-aminosalicylic acid derivatives have been reported in the literature. Mesalamine 89-110 actinin alpha 4 Homo sapiens 0-34 32394929-1 2020 Focal segmental glomerulosclerosis (FSGS) and other glomerulonephritis due to the use of 5-aminosalicylic acid derivatives have been reported in the literature. Mesalamine 89-110 actinin alpha 4 Homo sapiens 36-40 31743034-0 2020 5-Aminosalicylic Acid Azo-Coupled with a GPR109A Agonist Is a Colon-Targeted Anticolitic Codrug with a Reduced Risk of Skin Toxicity. Mesalamine 0-21 hydroxycarboxylic acid receptor 2 Rattus norvegicus 41-48 31743034-1 2020 To develop a 5-aminosalicylic acid (5-ASA)-based anticolitic drug with enhanced therapeutic activity, a colon-targeted codrug constituting 5-ASA and a GPR109A agonist was designed. Mesalamine 13-34 hydroxycarboxylic acid receptor 2 Rattus norvegicus 151-158 31743034-1 2020 To develop a 5-aminosalicylic acid (5-ASA)-based anticolitic drug with enhanced therapeutic activity, a colon-targeted codrug constituting 5-ASA and a GPR109A agonist was designed. Mesalamine 36-41 hydroxycarboxylic acid receptor 2 Rattus norvegicus 151-158 32238712-0 2020 Transport Characteristics of 5-Aminosalicylic Acid Derivatives Conjugated with Amino Acids via Human H+-Coupled Oligopeptide Transporter PEPT1. Mesalamine 29-50 solute carrier family 15 member 1 Homo sapiens 137-142 32238712-5 2020 Therefore, we considered that PEPT1 would be a target transporter to improve 5-ASA delivery efficiency to local colonic lesions. Mesalamine 77-82 solute carrier family 15 member 1 Homo sapiens 30-35 31687082-8 2019 Importantly, the efficacy of 45 mg/kg of AL-1 was higher than that of 100 mg/kg of the positive control drugs 5-aminosalicylic acid and mesalazine. Mesalamine 110-131 ephrin A5 Mus musculus 41-45 32017001-17 2020 CONCLUSIONS: Mesalazine combined with bifid triple viable is able to enhance the curative effect for UC, improve the composition of intestinal flora, weaken the immune response, and reduce levels of Cal and MMP-9 in the intestinal tract. Mesalamine 13-23 matrix metallopeptidase 9 Homo sapiens 207-212 31520133-6 2019 The combination of mesalazine and LAB mixture was the most effective to decrease the intestinal damage at macroscopic and histological levels and to reduce pro-inflammatory cytokines (IL-6 and TNF-alpha) in intestinal fluids. Mesalamine 19-29 interleukin 6 Mus musculus 184-188 31520133-6 2019 The combination of mesalazine and LAB mixture was the most effective to decrease the intestinal damage at macroscopic and histological levels and to reduce pro-inflammatory cytokines (IL-6 and TNF-alpha) in intestinal fluids. Mesalamine 19-29 tumor necrosis factor Mus musculus 193-202 31520133-7 2019 In animals instilled with ethanol, mesalazine produced a loss of body weight and intestinal damages with increased IL-6. Mesalamine 35-45 interleukin 6 Mus musculus 115-119 33328413-10 2020 He was also diagnosed with SLCO2A1-associated chronic enteropathy and thus was treated with 5-aminosalicylic acid, which temporarily improved the ileal ulcers, anemia, and hypoalbuminemia. Mesalamine 92-113 solute carrier organic anion transporter family member 2A1 Homo sapiens 27-34 31810227-11 2019 CONCLUSIONS: Switching from mesalazine to SASP was effective in more than half of cases. Mesalamine 28-38 aspartic peptidase retroviral like 1 Homo sapiens 42-46 31687082-8 2019 Importantly, the efficacy of 45 mg/kg of AL-1 was higher than that of 100 mg/kg of the positive control drugs 5-aminosalicylic acid and mesalazine. Mesalamine 136-146 ephrin A5 Mus musculus 41-45 31351432-7 2019 It was observed that separate and combined administrations of FO and mesalazine decreased the increase in the serum and tissue TNF-alpha and IL-6 levels caused by colitis (p < 0.05). Mesalamine 69-79 tumor necrosis factor Rattus norvegicus 127-136 31351432-7 2019 It was observed that separate and combined administrations of FO and mesalazine decreased the increase in the serum and tissue TNF-alpha and IL-6 levels caused by colitis (p < 0.05). Mesalamine 69-79 interleukin 6 Rattus norvegicus 141-145 30895635-2 2019 5-ASA acts locally in the colonic mucosa by numerous proposed mechanisms, and is metabolised by N-acetyltransferase (NAT). Mesalamine 0-5 bromodomain containing 2 Homo sapiens 96-115 31567972-6 2019 Levels of IL-6, IL-7, and monocyte chemoattractant protein 1 were higher with 5-aminosalicylic acid (5-ASA) + Azathioprine therapy than controls (P < .05). Mesalamine 78-99 interleukin 6 Homo sapiens 10-14 31567972-6 2019 Levels of IL-6, IL-7, and monocyte chemoattractant protein 1 were higher with 5-aminosalicylic acid (5-ASA) + Azathioprine therapy than controls (P < .05). Mesalamine 78-99 interleukin 7 Homo sapiens 16-20 31567972-6 2019 Levels of IL-6, IL-7, and monocyte chemoattractant protein 1 were higher with 5-aminosalicylic acid (5-ASA) + Azathioprine therapy than controls (P < .05). Mesalamine 78-99 C-C motif chemokine ligand 2 Homo sapiens 26-60 31567972-6 2019 Levels of IL-6, IL-7, and monocyte chemoattractant protein 1 were higher with 5-aminosalicylic acid (5-ASA) + Azathioprine therapy than controls (P < .05). Mesalamine 101-106 interleukin 6 Homo sapiens 10-14 31567972-6 2019 Levels of IL-6, IL-7, and monocyte chemoattractant protein 1 were higher with 5-aminosalicylic acid (5-ASA) + Azathioprine therapy than controls (P < .05). Mesalamine 101-106 interleukin 7 Homo sapiens 16-20 31567972-6 2019 Levels of IL-6, IL-7, and monocyte chemoattractant protein 1 were higher with 5-aminosalicylic acid (5-ASA) + Azathioprine therapy than controls (P < .05). Mesalamine 101-106 C-C motif chemokine ligand 2 Homo sapiens 26-60 31567972-7 2019 Combined therapy with 5-ASA + Adalimumab led to the strongest changes in marker modulation: IL-4, IL-5, IL-15, and PDGF-BB, were upregulated (P < .05).Elevated serum levels of G-CSF, IL-1Ra, and PDGF-BB were associated with IBD endoscopic activity, and of IP-10 with extraintestinal manifestations of IBD. Mesalamine 22-27 interleukin 4 Homo sapiens 92-96 31567972-7 2019 Combined therapy with 5-ASA + Adalimumab led to the strongest changes in marker modulation: IL-4, IL-5, IL-15, and PDGF-BB, were upregulated (P < .05).Elevated serum levels of G-CSF, IL-1Ra, and PDGF-BB were associated with IBD endoscopic activity, and of IP-10 with extraintestinal manifestations of IBD. Mesalamine 22-27 interleukin 5 Homo sapiens 98-102 31567972-7 2019 Combined therapy with 5-ASA + Adalimumab led to the strongest changes in marker modulation: IL-4, IL-5, IL-15, and PDGF-BB, were upregulated (P < .05).Elevated serum levels of G-CSF, IL-1Ra, and PDGF-BB were associated with IBD endoscopic activity, and of IP-10 with extraintestinal manifestations of IBD. Mesalamine 22-27 interleukin 15 Homo sapiens 104-109 31567972-7 2019 Combined therapy with 5-ASA + Adalimumab led to the strongest changes in marker modulation: IL-4, IL-5, IL-15, and PDGF-BB, were upregulated (P < .05).Elevated serum levels of G-CSF, IL-1Ra, and PDGF-BB were associated with IBD endoscopic activity, and of IP-10 with extraintestinal manifestations of IBD. Mesalamine 22-27 colony stimulating factor 3 Homo sapiens 179-184 31567972-7 2019 Combined therapy with 5-ASA + Adalimumab led to the strongest changes in marker modulation: IL-4, IL-5, IL-15, and PDGF-BB, were upregulated (P < .05).Elevated serum levels of G-CSF, IL-1Ra, and PDGF-BB were associated with IBD endoscopic activity, and of IP-10 with extraintestinal manifestations of IBD. Mesalamine 22-27 interleukin 1 receptor antagonist Homo sapiens 186-192 31567972-7 2019 Combined therapy with 5-ASA + Adalimumab led to the strongest changes in marker modulation: IL-4, IL-5, IL-15, and PDGF-BB, were upregulated (P < .05).Elevated serum levels of G-CSF, IL-1Ra, and PDGF-BB were associated with IBD endoscopic activity, and of IP-10 with extraintestinal manifestations of IBD. Mesalamine 22-27 C-X-C motif chemokine ligand 10 Homo sapiens 259-264 31567972-8 2019 Combined therapy of 5-ASA + Adalimumab produced significant upregulation of IL-4, IL-5, IL-15, and PDGF-BB. Mesalamine 20-25 interleukin 4 Homo sapiens 76-80 31567972-8 2019 Combined therapy of 5-ASA + Adalimumab produced significant upregulation of IL-4, IL-5, IL-15, and PDGF-BB. Mesalamine 20-25 interleukin 5 Homo sapiens 82-86 31567972-8 2019 Combined therapy of 5-ASA + Adalimumab produced significant upregulation of IL-4, IL-5, IL-15, and PDGF-BB. Mesalamine 20-25 interleukin 15 Homo sapiens 88-93 31378906-0 2019 Regulatory mechanism of mesalazine on TLR4/MyD88-dependent pathway in mouse ulcerative colitis model. Mesalamine 24-34 toll-like receptor 4 Mus musculus 38-42 31378906-0 2019 Regulatory mechanism of mesalazine on TLR4/MyD88-dependent pathway in mouse ulcerative colitis model. Mesalamine 24-34 myeloid differentiation primary response gene 88 Mus musculus 43-48 31378906-1 2019 OBJECTIVE: The aim of this study was to investigate the regulatory mechanism of mesalazine (MSLZ) on microRNA-21, microRNA-31 and Toll-like receptor 4/myeloid differentiation primary response 88 (TLR4/MyD88)-dependent pathway in 2,4,6-trinitrobenzene sulfonic acid (TNBS)/ethanol-induced ulcerative colitis (UC) model in mice. Mesalamine 80-90 toll-like receptor 4 Mus musculus 130-150 31378906-1 2019 OBJECTIVE: The aim of this study was to investigate the regulatory mechanism of mesalazine (MSLZ) on microRNA-21, microRNA-31 and Toll-like receptor 4/myeloid differentiation primary response 88 (TLR4/MyD88)-dependent pathway in 2,4,6-trinitrobenzene sulfonic acid (TNBS)/ethanol-induced ulcerative colitis (UC) model in mice. Mesalamine 80-90 toll-like receptor 4 Mus musculus 196-200 31378906-1 2019 OBJECTIVE: The aim of this study was to investigate the regulatory mechanism of mesalazine (MSLZ) on microRNA-21, microRNA-31 and Toll-like receptor 4/myeloid differentiation primary response 88 (TLR4/MyD88)-dependent pathway in 2,4,6-trinitrobenzene sulfonic acid (TNBS)/ethanol-induced ulcerative colitis (UC) model in mice. Mesalamine 80-90 myeloid differentiation primary response gene 88 Mus musculus 201-206 31378906-1 2019 OBJECTIVE: The aim of this study was to investigate the regulatory mechanism of mesalazine (MSLZ) on microRNA-21, microRNA-31 and Toll-like receptor 4/myeloid differentiation primary response 88 (TLR4/MyD88)-dependent pathway in 2,4,6-trinitrobenzene sulfonic acid (TNBS)/ethanol-induced ulcerative colitis (UC) model in mice. Mesalamine 92-96 toll-like receptor 4 Mus musculus 130-150 31378906-1 2019 OBJECTIVE: The aim of this study was to investigate the regulatory mechanism of mesalazine (MSLZ) on microRNA-21, microRNA-31 and Toll-like receptor 4/myeloid differentiation primary response 88 (TLR4/MyD88)-dependent pathway in 2,4,6-trinitrobenzene sulfonic acid (TNBS)/ethanol-induced ulcerative colitis (UC) model in mice. Mesalamine 92-96 toll-like receptor 4 Mus musculus 196-200 31378906-1 2019 OBJECTIVE: The aim of this study was to investigate the regulatory mechanism of mesalazine (MSLZ) on microRNA-21, microRNA-31 and Toll-like receptor 4/myeloid differentiation primary response 88 (TLR4/MyD88)-dependent pathway in 2,4,6-trinitrobenzene sulfonic acid (TNBS)/ethanol-induced ulcerative colitis (UC) model in mice. Mesalamine 92-96 myeloid differentiation primary response gene 88 Mus musculus 201-206 31378906-18 2019 Furthermore, MSLZ also inhibited the release of inflammatory factors by inhibiting the TLR4/MyD88-dependent pathway in UC mice. Mesalamine 13-17 toll-like receptor 4 Mus musculus 87-91 31378906-18 2019 Furthermore, MSLZ also inhibited the release of inflammatory factors by inhibiting the TLR4/MyD88-dependent pathway in UC mice. Mesalamine 13-17 myeloid differentiation primary response gene 88 Mus musculus 92-97 30867139-6 2019 Apoptotic endpoints were significantly increased by the 5-ASA/HT combined treatment, as evidenced by presence of Annexin V-FITC/PI positive cells, loss of MMP, Bcl-2/Bax ratio alteration, and increased Fas, cleaved Bid, and caspase expression. Mesalamine 56-61 annexin A5 Homo sapiens 113-122 30867139-6 2019 Apoptotic endpoints were significantly increased by the 5-ASA/HT combined treatment, as evidenced by presence of Annexin V-FITC/PI positive cells, loss of MMP, Bcl-2/Bax ratio alteration, and increased Fas, cleaved Bid, and caspase expression. Mesalamine 56-61 BCL2 apoptosis regulator Homo sapiens 160-165 30867139-6 2019 Apoptotic endpoints were significantly increased by the 5-ASA/HT combined treatment, as evidenced by presence of Annexin V-FITC/PI positive cells, loss of MMP, Bcl-2/Bax ratio alteration, and increased Fas, cleaved Bid, and caspase expression. Mesalamine 56-61 BCL2 associated X, apoptosis regulator Homo sapiens 166-169 30867139-6 2019 Apoptotic endpoints were significantly increased by the 5-ASA/HT combined treatment, as evidenced by presence of Annexin V-FITC/PI positive cells, loss of MMP, Bcl-2/Bax ratio alteration, and increased Fas, cleaved Bid, and caspase expression. Mesalamine 56-61 BH3 interacting domain death agonist Homo sapiens 215-218 30420398-1 2019 OBJECTIVE: The benefit of continuing 5-aminosalicylate (5-ASA) in patients with ulcerative colitis (UC) who initiate anti-tumour necrosis factor-alpha (anti-TNF) biologics is unknown. Mesalamine 37-54 tumor necrosis factor Homo sapiens 157-160 30420398-1 2019 OBJECTIVE: The benefit of continuing 5-aminosalicylate (5-ASA) in patients with ulcerative colitis (UC) who initiate anti-tumour necrosis factor-alpha (anti-TNF) biologics is unknown. Mesalamine 56-61 tumor necrosis factor Homo sapiens 157-160 30420398-6 2019 Patients were classified as stopping 5-ASA if therapy was discontinued within 90 days of starting anti-TNF. Mesalamine 37-42 tumor necrosis factor Homo sapiens 103-106 30420398-12 2019 CONCLUSION: In two national databases, stopping 5-ASA in patients with UC starting anti-TNF therapy did not increase the risk of adverse clinical events. Mesalamine 48-53 tumor necrosis factor Homo sapiens 88-91 31513295-31 2019 We found some evidence that adalimumab (HR 0.11, 95% Crl 0.02 to 0.33; low-certainty evidence) and 5-ASA may reduce the probability of clinical relapse compared to placebo (HR 0.69, 95% Crl 0.53 to 0.87; moderate-certainty evidence). Mesalamine 99-104 interleukin 31 receptor A Homo sapiens 186-189 31322753-6 2019 However, 5-ASA seems to induce a more robust reduction of NOS2 expression. Mesalamine 9-14 nitric oxide synthase 2 Homo sapiens 58-62 30895635-2 2019 5-ASA acts locally in the colonic mucosa by numerous proposed mechanisms, and is metabolised by N-acetyltransferase (NAT). Mesalamine 0-5 bromodomain containing 2 Homo sapiens 117-120 30478770-7 2019 Multiple linear regression models predicted significant association between transcript levels of Ki-67, NF-kB (p65), PPARgamma, COX-2 and IL-8, CDC25A, and CXCL10 with duration of drug (5-ASA) exposure (P <= 0.05). Mesalamine 186-191 C-X-C motif chemokine ligand 8 Homo sapiens 138-142 30826665-10 2019 RESULTS: At baseline, men who were on high-DBP mesalamine (H1B-Arm) had 72%, (95% confidence interval (CI): 18, 151) higher normalized-QA than men who were on background exposure and when high-DBP mesalamine was removed for four months, normalized-QA decreased with 32%, (95% CI: -45.0, -15.1). Mesalamine 47-57 H1.5 linker histone, cluster member Homo sapiens 59-62 30826665-10 2019 RESULTS: At baseline, men who were on high-DBP mesalamine (H1B-Arm) had 72%, (95% confidence interval (CI): 18, 151) higher normalized-QA than men who were on background exposure and when high-DBP mesalamine was removed for four months, normalized-QA decreased with 32%, (95% CI: -45.0, -15.1). Mesalamine 197-207 H1.5 linker histone, cluster member Homo sapiens 59-62 30975785-0 2019 Plasma N-terminal pro-B-type natriuretic peptide (BNP) in mesalazine-induced myopericarditis. Mesalamine 58-68 natriuretic peptide B Homo sapiens 18-48 30975785-0 2019 Plasma N-terminal pro-B-type natriuretic peptide (BNP) in mesalazine-induced myopericarditis. Mesalamine 58-68 natriuretic peptide B Homo sapiens 50-53 30329067-8 2019 Concomitant use of 5-aminosalicylate was associated with higher persistence of first-line anti-TNF treatment in the overall population (hazard ratio [HR] 0.5; 95% CI, 0.3-0.8; P = 0.002). Mesalamine 19-36 tumor necrosis factor Homo sapiens 95-98 30329067-13 2019 Concomitant use of 5-aminosalicylates was associated with higher persistence of first-line anti-TNF treatment. Mesalamine 19-37 tumor necrosis factor Homo sapiens 96-99 31443089-9 2019 The effect of treatment with liposomal suspensions of 5-ASA and CGA was evaluated macroscopically and by measuring myeloperoxidase (MPO) activity. Mesalamine 54-59 myeloperoxidase Mus musculus 115-130 31443089-9 2019 The effect of treatment with liposomal suspensions of 5-ASA and CGA was evaluated macroscopically and by measuring myeloperoxidase (MPO) activity. Mesalamine 54-59 myeloperoxidase Mus musculus 132-135 30478770-7 2019 Multiple linear regression models predicted significant association between transcript levels of Ki-67, NF-kB (p65), PPARgamma, COX-2 and IL-8, CDC25A, and CXCL10 with duration of drug (5-ASA) exposure (P <= 0.05). Mesalamine 186-191 C-X-C motif chemokine ligand 10 Homo sapiens 156-162 30804707-4 2019 As one of the first-line medications for the treatment of IBD, 5-aminosalicylic acid (5-ASA) activates peroxisome proliferator-activated receptor gamma (PPARgamma) to attenuate colitis. Mesalamine 63-84 peroxisome proliferator activated receptor gamma Homo sapiens 103-151 30820432-0 2019 The Detergent Effect of Mesalazine Interferes with Phosphatidylcholine Binding to Mucin 2. Mesalamine 24-34 mucin 2, oligomeric mucus/gel-forming Homo sapiens 82-89 30804707-4 2019 As one of the first-line medications for the treatment of IBD, 5-aminosalicylic acid (5-ASA) activates peroxisome proliferator-activated receptor gamma (PPARgamma) to attenuate colitis. Mesalamine 63-84 peroxisome proliferator activated receptor gamma Homo sapiens 153-162 30804707-4 2019 As one of the first-line medications for the treatment of IBD, 5-aminosalicylic acid (5-ASA) activates peroxisome proliferator-activated receptor gamma (PPARgamma) to attenuate colitis. Mesalamine 86-91 peroxisome proliferator activated receptor gamma Homo sapiens 103-151 30804707-4 2019 As one of the first-line medications for the treatment of IBD, 5-aminosalicylic acid (5-ASA) activates peroxisome proliferator-activated receptor gamma (PPARgamma) to attenuate colitis. Mesalamine 86-91 peroxisome proliferator activated receptor gamma Homo sapiens 153-162 30204869-0 2019 miR-206 as a Biomarker for Response to Mesalamine Treatment in Ulcerative Colitis. Mesalamine 39-49 microRNA 206 Homo sapiens 0-7 30204869-4 2019 This study correlates expression levels of miR-206 with histologic remission in patients treated via long-term mesalamine treatment to identify a possible mode of action for this mainstay drug for UC. Mesalamine 111-121 microRNA 206 Homo sapiens 43-50 30204869-5 2019 Methods: Expression of miR-206 and its target A3AR were analyzed in HT29 cell line before and after mesalamine treatment (2 mM) at different time points (0, 4, 12, and 24 hours) by qRT-PCR and western blot analysis. Mesalamine 100-110 microRNA 206 Homo sapiens 23-30 30204869-7 2019 Results: miR-206 transcripts decreased 2.23-fold (P = 0.0001) 4 hours after 2 mM mesalamine treatment in HT29 colon cells compared with untreated controls. Mesalamine 81-91 microRNA 206 Homo sapiens 9-16 30204869-9 2019 miR-206 relative expression decreased significantly in patients treated with 4.8 g of mesalamine (P = 0.002) but not with 2.4 g (P = 0.35). Mesalamine 86-96 microRNA 206 Homo sapiens 0-7 30204869-10 2019 Tissue assessment of sequential mesalamine-treated colonoscopic biopsies indicate a strong correlation between downregulation of miR-206 and histologic improvement (R = 0.9111). Mesalamine 32-42 microRNA 206 Homo sapiens 129-136 30204869-12 2019 Downregulation of miR-206 by long-term mesalamine treatment may confer a protective effect in inducing and maintaining histologic remission. Mesalamine 39-49 microRNA 206 Homo sapiens 18-25 30204869-13 2019 Thus, miR-206 expression levels can be utilized as a possible biomarker for therapeutic response to mesalamine treatment. Mesalamine 100-110 microRNA 206 Homo sapiens 6-13 30688941-1 2018 OBJECTIVE: In this study, the effect of mesalazine was studied on TNF alpha IL-1 beta, IL-6, and C-reactive protein (CRP) levels and inflammatory changes in rat lungs with experimental peritonitis. Mesalamine 40-50 tumor necrosis factor Rattus norvegicus 66-75 30848228-0 2019 Mesalazine Activates Adenosine Monophosphate-activated Protein Kinase: Implication in the Anti-inflammatory Activity of this Anti-colitic Drug. Mesalamine 0-10 protein kinase AMP-activated catalytic subunit alpha 2 Rattus norvegicus 21-69 30848228-5 2019 RESULTS: 5-ASA induced phosphorylation of adenosine monophosphate-activated protein kinase (AMPK) and its substrate acetyl-CoA carboxylase in cells. Mesalamine 9-14 protein kinase AMP-activated catalytic subunit alpha 2 Rattus norvegicus 42-90 30848228-5 2019 RESULTS: 5-ASA induced phosphorylation of adenosine monophosphate-activated protein kinase (AMPK) and its substrate acetyl-CoA carboxylase in cells. Mesalamine 9-14 protein kinase AMP-activated catalytic subunit alpha 2 Rattus norvegicus 92-96 30848228-6 2019 5-ASA activation of AMPK occurred regardless of the presence of the pro-inflammatory mediators, Tumor Necrosis Factor Alpha (TNF-alpha) and lipopolysaccharide. Mesalamine 0-5 protein kinase AMP-activated catalytic subunit alpha 2 Rattus norvegicus 20-24 30848228-7 2019 5-ASA inhibits TNF-alpha-dependent Nuclear Factor-Kappa B (NF-kappaB) activation, which was dampened by AMPK inhibition. Mesalamine 0-5 tumor necrosis factor Rattus norvegicus 15-24 30848228-7 2019 5-ASA inhibits TNF-alpha-dependent Nuclear Factor-Kappa B (NF-kappaB) activation, which was dampened by AMPK inhibition. Mesalamine 0-5 protein kinase AMP-activated catalytic subunit alpha 2 Rattus norvegicus 104-108 30848228-9 2019 Rectal co-administration of 5-ASA and an AMPK inhibitor undermined 5-ASA-mediated activation of AMPK and its anti-colitic effects. Mesalamine 28-33 protein kinase AMP-activated catalytic subunit alpha 2 Rattus norvegicus 96-100 30848228-9 2019 Rectal co-administration of 5-ASA and an AMPK inhibitor undermined 5-ASA-mediated activation of AMPK and its anti-colitic effects. Mesalamine 67-72 protein kinase AMP-activated catalytic subunit alpha 2 Rattus norvegicus 41-45 30848228-9 2019 Rectal co-administration of 5-ASA and an AMPK inhibitor undermined 5-ASA-mediated activation of AMPK and its anti-colitic effects. Mesalamine 67-72 protein kinase AMP-activated catalytic subunit alpha 2 Rattus norvegicus 96-100 30848228-10 2019 CONCLUSION: These findings suggest that the activation of AMPK is involved in 5-ASA-mediated anticolitic effects at least partly via interference with pro-inflammatory NF-kappaB signaling. Mesalamine 78-83 protein kinase AMP-activated catalytic subunit alpha 2 Rattus norvegicus 58-62 30630805-1 2018 Present investigation is conducted to investigate the clinical efficacy of mesalazine in combination with the Bifid Triple Viable Capsules on the ulcerative colitis (UC) and the resultant effect on the inflammatory factors (TNF-alpha, IL-8 and IL-10) of UC patients. Mesalamine 75-85 tumor necrosis factor Homo sapiens 224-233 30630805-1 2018 Present investigation is conducted to investigate the clinical efficacy of mesalazine in combination with the Bifid Triple Viable Capsules on the ulcerative colitis (UC) and the resultant effect on the inflammatory factors (TNF-alpha, IL-8 and IL-10) of UC patients. Mesalamine 75-85 C-X-C motif chemokine ligand 8 Homo sapiens 235-239 30630805-1 2018 Present investigation is conducted to investigate the clinical efficacy of mesalazine in combination with the Bifid Triple Viable Capsules on the ulcerative colitis (UC) and the resultant effect on the inflammatory factors (TNF-alpha, IL-8 and IL-10) of UC patients. Mesalamine 75-85 interleukin 10 Homo sapiens 244-249 30341279-6 2018 Treatment of skin cultures lacking Grhl3 with the broad spectrum anti-inflammatory 5-aminosalicylic acid (5ASA) partially restored epidermal differentiation, indicating that abnormal keratinocyte proliferation/differentiation balance is a key driver of barrier dysfunction following loss of Grhl3, and providing a promising therapeutic avenue in the treatment of GRHL3-mediated epidermal disorders. Mesalamine 83-104 grainyhead like transcription factor 3 Homo sapiens 35-40 30341279-6 2018 Treatment of skin cultures lacking Grhl3 with the broad spectrum anti-inflammatory 5-aminosalicylic acid (5ASA) partially restored epidermal differentiation, indicating that abnormal keratinocyte proliferation/differentiation balance is a key driver of barrier dysfunction following loss of Grhl3, and providing a promising therapeutic avenue in the treatment of GRHL3-mediated epidermal disorders. Mesalamine 83-104 grainyhead like transcription factor 3 Homo sapiens 291-296 30341279-6 2018 Treatment of skin cultures lacking Grhl3 with the broad spectrum anti-inflammatory 5-aminosalicylic acid (5ASA) partially restored epidermal differentiation, indicating that abnormal keratinocyte proliferation/differentiation balance is a key driver of barrier dysfunction following loss of Grhl3, and providing a promising therapeutic avenue in the treatment of GRHL3-mediated epidermal disorders. Mesalamine 83-104 grainyhead like transcription factor 3 Homo sapiens 363-368 30341279-6 2018 Treatment of skin cultures lacking Grhl3 with the broad spectrum anti-inflammatory 5-aminosalicylic acid (5ASA) partially restored epidermal differentiation, indicating that abnormal keratinocyte proliferation/differentiation balance is a key driver of barrier dysfunction following loss of Grhl3, and providing a promising therapeutic avenue in the treatment of GRHL3-mediated epidermal disorders. Mesalamine 106-110 grainyhead like transcription factor 3 Homo sapiens 35-40 30341279-6 2018 Treatment of skin cultures lacking Grhl3 with the broad spectrum anti-inflammatory 5-aminosalicylic acid (5ASA) partially restored epidermal differentiation, indicating that abnormal keratinocyte proliferation/differentiation balance is a key driver of barrier dysfunction following loss of Grhl3, and providing a promising therapeutic avenue in the treatment of GRHL3-mediated epidermal disorders. Mesalamine 106-110 grainyhead like transcription factor 3 Homo sapiens 291-296 30341279-6 2018 Treatment of skin cultures lacking Grhl3 with the broad spectrum anti-inflammatory 5-aminosalicylic acid (5ASA) partially restored epidermal differentiation, indicating that abnormal keratinocyte proliferation/differentiation balance is a key driver of barrier dysfunction following loss of Grhl3, and providing a promising therapeutic avenue in the treatment of GRHL3-mediated epidermal disorders. Mesalamine 106-110 grainyhead like transcription factor 3 Homo sapiens 363-368 30688941-1 2018 OBJECTIVE: In this study, the effect of mesalazine was studied on TNF alpha IL-1 beta, IL-6, and C-reactive protein (CRP) levels and inflammatory changes in rat lungs with experimental peritonitis. Mesalamine 40-50 interleukin 1 beta Rattus norvegicus 76-85 30688941-1 2018 OBJECTIVE: In this study, the effect of mesalazine was studied on TNF alpha IL-1 beta, IL-6, and C-reactive protein (CRP) levels and inflammatory changes in rat lungs with experimental peritonitis. Mesalamine 40-50 interleukin 6 Rattus norvegicus 87-91 30688941-1 2018 OBJECTIVE: In this study, the effect of mesalazine was studied on TNF alpha IL-1 beta, IL-6, and C-reactive protein (CRP) levels and inflammatory changes in rat lungs with experimental peritonitis. Mesalamine 40-50 C-reactive protein Rattus norvegicus 97-115 30688941-1 2018 OBJECTIVE: In this study, the effect of mesalazine was studied on TNF alpha IL-1 beta, IL-6, and C-reactive protein (CRP) levels and inflammatory changes in rat lungs with experimental peritonitis. Mesalamine 40-50 C-reactive protein Rattus norvegicus 117-120 30688941-10 2018 CONCLUSION: TNF alpha, IL-1 beta, and CRP levels and leucocyte infiltration in the lung were found to be low in rats that were administered peritoneal irrigation using mesalazine after the development of secondary peritonitis. Mesalamine 168-178 tumor necrosis factor Rattus norvegicus 12-21 30688941-10 2018 CONCLUSION: TNF alpha, IL-1 beta, and CRP levels and leucocyte infiltration in the lung were found to be low in rats that were administered peritoneal irrigation using mesalazine after the development of secondary peritonitis. Mesalamine 168-178 interleukin 1 beta Rattus norvegicus 23-32 30688941-10 2018 CONCLUSION: TNF alpha, IL-1 beta, and CRP levels and leucocyte infiltration in the lung were found to be low in rats that were administered peritoneal irrigation using mesalazine after the development of secondary peritonitis. Mesalamine 168-178 C-reactive protein Rattus norvegicus 38-41 29550533-1 2018 Three new series of 5-aminosalicylic acid derivatives; series I (14, 16-18), series II (19-30) and series III (31-41) were synthesized as potential dual COX-2/5-LOX inhibitors. Mesalamine 20-41 mitochondrially encoded cytochrome c oxidase II Homo sapiens 153-158 29550533-1 2018 Three new series of 5-aminosalicylic acid derivatives; series I (14, 16-18), series II (19-30) and series III (31-41) were synthesized as potential dual COX-2/5-LOX inhibitors. Mesalamine 20-41 arachidonate 5-lipoxygenase Homo sapiens 159-164 29794245-1 2018 Mesalazine (5-ASA) is an aminosalicylate anti-inflammatory drug capable of inducing mu-protocadherin, a protein expressed by colorectal epithelial cells that is downregulated upon malignant transformation. Mesalamine 0-10 cadherin related family member 5 Homo sapiens 84-100 30111058-5 2018 High dose of BAEB group and Mesalazine group could improve the colonic pathology, decrease IL-6, IL-8, IL-1beta, HBD-2, HBD-3 expression level. Mesalamine 28-38 interleukin 6 Mus musculus 91-95 30001434-0 2018 Retraction: 5-aminosalicylic acid improves lipid profile in mice fed a high-fat cholesterol diet through its dual effects on intestinal PPARgamma and PPARalpha. Mesalamine 12-33 peroxisome proliferator activated receptor gamma Mus musculus 136-145 30001434-0 2018 Retraction: 5-aminosalicylic acid improves lipid profile in mice fed a high-fat cholesterol diet through its dual effects on intestinal PPARgamma and PPARalpha. Mesalamine 12-33 peroxisome proliferator activated receptor alpha Mus musculus 150-159 30111058-5 2018 High dose of BAEB group and Mesalazine group could improve the colonic pathology, decrease IL-6, IL-8, IL-1beta, HBD-2, HBD-3 expression level. Mesalamine 28-38 chemokine (C-X-C motif) ligand 15 Mus musculus 97-101 30111058-5 2018 High dose of BAEB group and Mesalazine group could improve the colonic pathology, decrease IL-6, IL-8, IL-1beta, HBD-2, HBD-3 expression level. Mesalamine 28-38 interleukin 1 beta Mus musculus 103-111 29352300-0 2018 5-aminosalicylic acid improves lipid profile in mice fed a high-fat cholesterol diet through its dual effects on intestinal PPARgamma and PPARalpha. Mesalamine 0-21 peroxisome proliferator activated receptor gamma Mus musculus 124-133 29350433-3 2018 In the present work, we aim to access the effect of two drugs, that is, acetylsalicylic acid and 5-amino salicylic acid on insulin amyloids by using various biophysical, imaging, cell viability assay, and computational approaches. Mesalamine 97-119 insulin Homo sapiens 123-130 29407223-1 2018 To develop a new strategy for inflamed site-specific drug delivery in the colon for the treatment of ulcerative colitis (UC), we leveraged on the interaction between myeloperoxidase (MPO) and human serum albumin (HSA) and prepared nanoparticles (HSA NPs) conjugated with 5-aminosalicylic acid (5-ASA). Mesalamine 271-292 myeloperoxidase Mus musculus 166-181 29407223-1 2018 To develop a new strategy for inflamed site-specific drug delivery in the colon for the treatment of ulcerative colitis (UC), we leveraged on the interaction between myeloperoxidase (MPO) and human serum albumin (HSA) and prepared nanoparticles (HSA NPs) conjugated with 5-aminosalicylic acid (5-ASA). Mesalamine 271-292 myeloperoxidase Mus musculus 183-186 29407223-1 2018 To develop a new strategy for inflamed site-specific drug delivery in the colon for the treatment of ulcerative colitis (UC), we leveraged on the interaction between myeloperoxidase (MPO) and human serum albumin (HSA) and prepared nanoparticles (HSA NPs) conjugated with 5-aminosalicylic acid (5-ASA). Mesalamine 271-292 albumin Mus musculus 198-211 29407223-1 2018 To develop a new strategy for inflamed site-specific drug delivery in the colon for the treatment of ulcerative colitis (UC), we leveraged on the interaction between myeloperoxidase (MPO) and human serum albumin (HSA) and prepared nanoparticles (HSA NPs) conjugated with 5-aminosalicylic acid (5-ASA). Mesalamine 294-299 myeloperoxidase Mus musculus 166-181 29407223-1 2018 To develop a new strategy for inflamed site-specific drug delivery in the colon for the treatment of ulcerative colitis (UC), we leveraged on the interaction between myeloperoxidase (MPO) and human serum albumin (HSA) and prepared nanoparticles (HSA NPs) conjugated with 5-aminosalicylic acid (5-ASA). Mesalamine 294-299 myeloperoxidase Mus musculus 183-186 29407223-1 2018 To develop a new strategy for inflamed site-specific drug delivery in the colon for the treatment of ulcerative colitis (UC), we leveraged on the interaction between myeloperoxidase (MPO) and human serum albumin (HSA) and prepared nanoparticles (HSA NPs) conjugated with 5-aminosalicylic acid (5-ASA). Mesalamine 294-299 albumin Mus musculus 198-211 29407223-4 2018 The specific interaction between the 5-ASA-HSA NPs and MPO was observed using quartz crystal microbalance analysis in vitro. Mesalamine 37-42 myeloperoxidase Mus musculus 55-58 29407223-8 2018 Therefore, these data demonstrated that an HSA NP formulation has the potential to specifically deliver 5-ASA to an inflamed site where MPO is highly expressed. Mesalamine 104-109 myeloperoxidase Mus musculus 136-139 29579042-13 2018 Genome-wide variants demonstrating a trend towards mesalamine response included ST8SIA5 (p = 1x10-5). Mesalamine 51-61 ST8 alpha-N-acetyl-neuraminide alpha-2,8-sialyltransferase 5 Homo sapiens 80-87 29080069-9 2018 5-ASA treatment decreased ex vivo Be-stimulated BAL cell TNF-alpha levels within the 5-ASA group and when compared to placebo. Mesalamine 0-5 tumor necrosis factor Homo sapiens 57-66 29080069-11 2018 CONCLUSIONS: 5-ASA"s ability to decrease BAL cell BeLPT and Be-stimulated BAL cell TNF-alpha levels suggests that 5-ASA may impact the beryllium-specific immune response in CBD. Mesalamine 13-18 tumor necrosis factor Homo sapiens 83-92 29080069-11 2018 CONCLUSIONS: 5-ASA"s ability to decrease BAL cell BeLPT and Be-stimulated BAL cell TNF-alpha levels suggests that 5-ASA may impact the beryllium-specific immune response in CBD. Mesalamine 114-119 tumor necrosis factor Homo sapiens 83-92 29738702-0 2018 Mesalazine, an osteopontin inhibitor: The potential prophylactic and remedial roles in induced liver fibrosis in rats. Mesalamine 0-10 secreted phosphoprotein 1 Rattus norvegicus 15-26 29738702-11 2018 Furthermore, mesalazine could suppress the expression of both alpha-SMA and caspase-3 in immunohistochemical sections. Mesalamine 13-23 caspase 3 Rattus norvegicus 76-85 29738702-12 2018 In conclusion, mesalazine could have a potential new indication as anti-fibrotic agent through limiting the oxidative damage and altering TNF-alpha pathway as an anti-inflammatory drug with down-regulating TGF-beta1, OPN, alpha-SMA and caspase-3 signaling pathways. Mesalamine 15-25 tumor necrosis factor Rattus norvegicus 138-147 29738702-12 2018 In conclusion, mesalazine could have a potential new indication as anti-fibrotic agent through limiting the oxidative damage and altering TNF-alpha pathway as an anti-inflammatory drug with down-regulating TGF-beta1, OPN, alpha-SMA and caspase-3 signaling pathways. Mesalamine 15-25 transforming growth factor, beta 1 Rattus norvegicus 206-215 29738702-12 2018 In conclusion, mesalazine could have a potential new indication as anti-fibrotic agent through limiting the oxidative damage and altering TNF-alpha pathway as an anti-inflammatory drug with down-regulating TGF-beta1, OPN, alpha-SMA and caspase-3 signaling pathways. Mesalamine 15-25 secreted phosphoprotein 1 Rattus norvegicus 217-220 29738702-12 2018 In conclusion, mesalazine could have a potential new indication as anti-fibrotic agent through limiting the oxidative damage and altering TNF-alpha pathway as an anti-inflammatory drug with down-regulating TGF-beta1, OPN, alpha-SMA and caspase-3 signaling pathways. Mesalamine 15-25 caspase 3 Rattus norvegicus 236-245 29030981-10 2018 This study shows that mesalazine is as effective as GFD in reducing oxidative burst and inducing PPARgamma expression; moreover it resulted more effective than GFD in decreasing NF-kB and NOS2 to the levels of controls. Mesalamine 22-32 peroxisome proliferator activated receptor gamma Homo sapiens 97-106 29030981-10 2018 This study shows that mesalazine is as effective as GFD in reducing oxidative burst and inducing PPARgamma expression; moreover it resulted more effective than GFD in decreasing NF-kB and NOS2 to the levels of controls. Mesalamine 22-32 nitric oxide synthase 2 Homo sapiens 188-192 29352300-0 2018 5-aminosalicylic acid improves lipid profile in mice fed a high-fat cholesterol diet through its dual effects on intestinal PPARgamma and PPARalpha. Mesalamine 0-21 peroxisome proliferator activated receptor alpha Mus musculus 138-147 29352300-7 2018 5-ASA also enhanced cholesterol translocation by elevating genes expression of Npc1l1 and Abcg5/8. Mesalamine 0-5 NPC1 like intracellular cholesterol transporter 1 Mus musculus 79-85 29352300-7 2018 5-ASA also enhanced cholesterol translocation by elevating genes expression of Npc1l1 and Abcg5/8. Mesalamine 0-5 ATP binding cassette subfamily G member 5 Mus musculus 90-95 29352300-8 2018 Moreover, mice fed HFC 5-ASA expressed increased Pparalpha in small intestinal and its target genes function in lipid oxidation and hydrolysis were remarkable elevated. Mesalamine 23-28 peroxisome proliferator activated receptor alpha Mus musculus 49-58 28473247-0 2017 Oxidized 5-aminosalicylic acid activates Nrf2-HO-1 pathway by covalently binding to Keap1: Implication in anti-inflammatory actions of 5-aminosalicylic acid. Mesalamine 9-30 NFE2 like bZIP transcription factor 2 Homo sapiens 41-45 28962154-5 2017 In model mice treated with TL (0.4 and 0.6 mg/kg), dexamethasone or mesalazine, IL-6 expression was significantly reduced compared with that in model mice treated with normal saline or propylene glycol (P<0.05), while TL at 0.2 mg/kg did not elicit any significant inhibitory effect. Mesalamine 68-78 interleukin 6 Mus musculus 80-84 29151408-0 2017 [Protective effect of 5-aminosalicylic acid on the kidney of paraquat poisoning rats by Nrf2-ARE signal pathway]. Mesalamine 22-43 NFE2 like bZIP transcription factor 2 Rattus norvegicus 88-92 29151408-12 2017 Only 5-ASA intervention had no significant effect on behavior, pathology, renal injury markers and oxidative stress parameters, but it could induce the expressions of Nrf2 and HO-1 protein in renal tissue, which were significantly higher than those of NS control group [Nrf2 protein (gray value): 0.78+-0.02 vs. 0.41+-0.04, HO-1 protein (gray value): 0.51+-0.03 vs. 0.23+-0.01, both P < 0.01]. Mesalamine 5-10 heme oxygenase 1 Rattus norvegicus 176-180 29151408-13 2017 CONCLUSIONS: 5-ASA attenuates the damage of acute renal injury (AKI) caused by PQ, which mechanism may be related with the activation of Nrf2-antioxidant response element (ARE) signaling pathway. Mesalamine 13-18 NFE2 like bZIP transcription factor 2 Rattus norvegicus 137-141 28979689-5 2017 The FOXP3+ cells and IL-4+ cells decreased, but IL-17A+ cells and IFN-gamma+ cells increased in the peripheral blood and colonic mucosa after DSS induced colitis, and these phenomena were reversed by MSC or mesalazine treatment. Mesalamine 207-217 forkhead box P3 Rattus norvegicus 4-9 28979689-5 2017 The FOXP3+ cells and IL-4+ cells decreased, but IL-17A+ cells and IFN-gamma+ cells increased in the peripheral blood and colonic mucosa after DSS induced colitis, and these phenomena were reversed by MSC or mesalazine treatment. Mesalamine 207-217 interleukin 17A Rattus norvegicus 48-54 28979689-5 2017 The FOXP3+ cells and IL-4+ cells decreased, but IL-17A+ cells and IFN-gamma+ cells increased in the peripheral blood and colonic mucosa after DSS induced colitis, and these phenomena were reversed by MSC or mesalazine treatment. Mesalamine 207-217 interleukin 18 Rattus norvegicus 66-75 28979689-7 2017 The expressions of Ki67 and LGR5 were significantly elevated in MSC treatment groups as compared with normal control group, DSS group, and mesalazine group. Mesalamine 139-149 leucine rich repeat containing G protein coupled receptor 5 Rattus norvegicus 28-32 28473247-0 2017 Oxidized 5-aminosalicylic acid activates Nrf2-HO-1 pathway by covalently binding to Keap1: Implication in anti-inflammatory actions of 5-aminosalicylic acid. Mesalamine 9-30 heme oxygenase 1 Homo sapiens 46-50 28473247-0 2017 Oxidized 5-aminosalicylic acid activates Nrf2-HO-1 pathway by covalently binding to Keap1: Implication in anti-inflammatory actions of 5-aminosalicylic acid. Mesalamine 9-30 kelch like ECH associated protein 1 Homo sapiens 84-89 28473247-0 2017 Oxidized 5-aminosalicylic acid activates Nrf2-HO-1 pathway by covalently binding to Keap1: Implication in anti-inflammatory actions of 5-aminosalicylic acid. Mesalamine 135-156 NFE2 like bZIP transcription factor 2 Homo sapiens 41-45 28473247-0 2017 Oxidized 5-aminosalicylic acid activates Nrf2-HO-1 pathway by covalently binding to Keap1: Implication in anti-inflammatory actions of 5-aminosalicylic acid. Mesalamine 135-156 heme oxygenase 1 Homo sapiens 46-50 28473247-0 2017 Oxidized 5-aminosalicylic acid activates Nrf2-HO-1 pathway by covalently binding to Keap1: Implication in anti-inflammatory actions of 5-aminosalicylic acid. Mesalamine 135-156 kelch like ECH associated protein 1 Homo sapiens 84-89 28473247-4 2017 Oxidized 5-ASA activated Nrf2 while 5-ASA itself was not effective. Mesalamine 9-14 NFE2 like bZIP transcription factor 2 Homo sapiens 25-29 28473247-6 2017 Western blot analysis of Keap1, a cytosolic repressor of Nrf2, following precipitation of biotin-labeled proteins in cell lysates treated with biotin-tagged 5-ASA, revealed a much greater amount of Keap1 when biotin-tagged 5-ASA was oxidized with HOCl. Mesalamine 157-162 kelch like ECH associated protein 1 Homo sapiens 25-30 28473247-6 2017 Western blot analysis of Keap1, a cytosolic repressor of Nrf2, following precipitation of biotin-labeled proteins in cell lysates treated with biotin-tagged 5-ASA, revealed a much greater amount of Keap1 when biotin-tagged 5-ASA was oxidized with HOCl. Mesalamine 157-162 NFE2 like bZIP transcription factor 2 Homo sapiens 57-61 28473247-6 2017 Western blot analysis of Keap1, a cytosolic repressor of Nrf2, following precipitation of biotin-labeled proteins in cell lysates treated with biotin-tagged 5-ASA, revealed a much greater amount of Keap1 when biotin-tagged 5-ASA was oxidized with HOCl. Mesalamine 157-162 kelch like ECH associated protein 1 Homo sapiens 198-203 28473247-6 2017 Western blot analysis of Keap1, a cytosolic repressor of Nrf2, following precipitation of biotin-labeled proteins in cell lysates treated with biotin-tagged 5-ASA, revealed a much greater amount of Keap1 when biotin-tagged 5-ASA was oxidized with HOCl. Mesalamine 223-228 NFE2 like bZIP transcription factor 2 Homo sapiens 57-61 28473247-6 2017 Western blot analysis of Keap1, a cytosolic repressor of Nrf2, following precipitation of biotin-labeled proteins in cell lysates treated with biotin-tagged 5-ASA, revealed a much greater amount of Keap1 when biotin-tagged 5-ASA was oxidized with HOCl. Mesalamine 223-228 kelch like ECH associated protein 1 Homo sapiens 198-203 28473247-7 2017 Precipitation of Keap1 was attenuated markedly by pretreatment with oxidized 5-ASA or a sulfhydryl donor. Mesalamine 77-82 kelch like ECH associated protein 1 Homo sapiens 17-22 28473247-8 2017 In addition, treatment with oxidized 5-ASA in cell lysates reduced the Keap1 amount that coimmunoprecipitated with Nrf2. Mesalamine 37-42 kelch like ECH associated protein 1 Homo sapiens 71-76 28473247-8 2017 In addition, treatment with oxidized 5-ASA in cell lysates reduced the Keap1 amount that coimmunoprecipitated with Nrf2. Mesalamine 37-42 NFE2 like bZIP transcription factor 2 Homo sapiens 115-119 28473247-9 2017 In parallel, rectal administration of 5-ASA increased the level of HO-1 and nuclear Nrf2 in the inflamed colonic tissues, but not in normal colonic tissues. Mesalamine 38-43 heme oxygenase 1 Homo sapiens 67-71 28473247-9 2017 In parallel, rectal administration of 5-ASA increased the level of HO-1 and nuclear Nrf2 in the inflamed colonic tissues, but not in normal colonic tissues. Mesalamine 38-43 NFE2 like bZIP transcription factor 2 Homo sapiens 84-88 28473247-10 2017 Moreover, oral gavage of sulfasalazine, a colon-specific prodrug of 5-ASA currently used clinically, activated the Nrf2-HO-1 pathway in the colonic tissues where inflammation was in progress, which was not observed when inflammation subsided. Mesalamine 68-73 NFE2 like bZIP transcription factor 2 Homo sapiens 115-119 28473247-10 2017 Moreover, oral gavage of sulfasalazine, a colon-specific prodrug of 5-ASA currently used clinically, activated the Nrf2-HO-1 pathway in the colonic tissues where inflammation was in progress, which was not observed when inflammation subsided. Mesalamine 68-73 heme oxygenase 1 Homo sapiens 120-124 28473247-11 2017 Collectively, our data suggest that Nrf2-HO-1 pathway is involved in the anti-inflammatory pharmacology of 5-ASA, which was likely being exerted exclusively in the inflammatory state. Mesalamine 107-112 NFE2 like bZIP transcription factor 2 Homo sapiens 36-40 28473247-11 2017 Collectively, our data suggest that Nrf2-HO-1 pathway is involved in the anti-inflammatory pharmacology of 5-ASA, which was likely being exerted exclusively in the inflammatory state. Mesalamine 107-112 heme oxygenase 1 Homo sapiens 41-45 28275298-11 2017 The expression levels of IL-1beta, IL-8 and TNF-alpha in the DSS group were higher than those in the control group (P < 0.05), and the expression levels of IL-1beta, IL-8 and TNF-alpha in the JPQCD and 5-ASA groups were lower than those in the DSS group after treating with JPQCD and 5-ASA. Mesalamine 205-210 interleukin 1 beta Mus musculus 159-167 28213866-0 2017 5-Aminosalicylic Acid Attenuates Monocrotaline-Induced Pulmonary Arterial Hypertension in Rats by Increasing the Expression of Nur77. Mesalamine 0-21 nuclear receptor subfamily 4, group A, member 1 Rattus norvegicus 127-132 28213866-5 2017 5-ASA attenuates PAH in MCT-injected rats, reducing pulmonary arterial pressures and right ventricular hypertrophy and improving survival rates, via the Nur77-NF-kappaB/IkappaBalpha pathway involved in modulating the pulmonary vascular remodeling. Mesalamine 0-5 nuclear receptor subfamily 4, group A, member 1 Rattus norvegicus 153-158 28213866-5 2017 5-ASA attenuates PAH in MCT-injected rats, reducing pulmonary arterial pressures and right ventricular hypertrophy and improving survival rates, via the Nur77-NF-kappaB/IkappaBalpha pathway involved in modulating the pulmonary vascular remodeling. Mesalamine 0-5 NFKB inhibitor alpha Rattus norvegicus 169-181 28329021-6 2017 The strong inhibition of COX-2 expression seems to be a crucial anti-inflammatory mechanism common to both ARF and 5-ASA, but the additional higher abilities of anthocyanins to downregulate iNOS and to decrease leukocytes infiltration and to increase antioxidant defenses in colon may account for the much higher anti-inflammatory action of anthocyanins. Mesalamine 115-120 prostaglandin-endoperoxide synthase 2 Rattus norvegicus 25-30 28138699-10 2017 Expression of IL-6 and TNF-alpha mRNA in colonic mucosa in the normal dosage, high dosage and 5-ASA-SiO2 NP group was significantly lower than that in the model group. Mesalamine 94-99 interleukin 6 Mus musculus 14-18 28138699-10 2017 Expression of IL-6 and TNF-alpha mRNA in colonic mucosa in the normal dosage, high dosage and 5-ASA-SiO2 NP group was significantly lower than that in the model group. Mesalamine 94-99 tumor necrosis factor Mus musculus 23-32 28138699-11 2017 Colonic mucosal IL-6 and TNF-alpha mRNA expression in the high dosage and 5-ASA-SiO2 NP groups was significantly lower than that in the normal dosage group (P<0.05). Mesalamine 74-79 interleukin 6 Mus musculus 16-20 28138699-11 2017 Colonic mucosal IL-6 and TNF-alpha mRNA expression in the high dosage and 5-ASA-SiO2 NP groups was significantly lower than that in the normal dosage group (P<0.05). Mesalamine 74-79 tumor necrosis factor Mus musculus 25-34 28063246-11 2017 Besides the challenge test, elevation of CRP and positive DLST appeared to support the diagnosis of 5-ASA intolerance. Mesalamine 100-105 C-reactive protein Homo sapiens 41-44 28593185-0 2017 Induction of Colonic Regulatory T Cells by Mesalamine by Activating the Aryl Hydrocarbon Receptor. Mesalamine 43-53 aryl-hydrocarbon receptor Mus musculus 72-97 28593185-7 2017 RESULTS: Treatment of wild-type mice with mesalamine increased the accumulation of Tregs in the colon and up-regulated the AhR target gene Cyp1A1, but this effect was not observed in AhR-/- or BM-AhR-/- mice. Mesalamine 42-52 aryl-hydrocarbon receptor Mus musculus 123-126 28593185-7 2017 RESULTS: Treatment of wild-type mice with mesalamine increased the accumulation of Tregs in the colon and up-regulated the AhR target gene Cyp1A1, but this effect was not observed in AhR-/- or BM-AhR-/- mice. Mesalamine 42-52 cytochrome P450, family 1, subfamily a, polypeptide 1 Mus musculus 139-145 28593185-7 2017 RESULTS: Treatment of wild-type mice with mesalamine increased the accumulation of Tregs in the colon and up-regulated the AhR target gene Cyp1A1, but this effect was not observed in AhR-/- or BM-AhR-/- mice. Mesalamine 42-52 aryl-hydrocarbon receptor Mus musculus 183-186 28593185-7 2017 RESULTS: Treatment of wild-type mice with mesalamine increased the accumulation of Tregs in the colon and up-regulated the AhR target gene Cyp1A1, but this effect was not observed in AhR-/- or BM-AhR-/- mice. Mesalamine 42-52 aryl-hydrocarbon receptor Mus musculus 183-186 28593185-8 2017 In addition, mesalamine promoted in vitro differentiation of naive T cells to Tregs, concomitant with AhR activation. Mesalamine 13-23 aryl-hydrocarbon receptor Mus musculus 102-105 28593185-9 2017 Mice treated with mesalamine exhibited increased levels of the active form of TGF-beta in the colon in an AhR-dependent manner and blockade of TGF-beta signaling suppressed induction of Tregs by mesalamine in the colon. Mesalamine 18-28 transforming growth factor, beta 1 Mus musculus 78-86 28593185-9 2017 Mice treated with mesalamine exhibited increased levels of the active form of TGF-beta in the colon in an AhR-dependent manner and blockade of TGF-beta signaling suppressed induction of Tregs by mesalamine in the colon. Mesalamine 18-28 aryl-hydrocarbon receptor Mus musculus 106-109 28593185-9 2017 Mice treated with mesalamine exhibited increased levels of the active form of TGF-beta in the colon in an AhR-dependent manner and blockade of TGF-beta signaling suppressed induction of Tregs by mesalamine in the colon. Mesalamine 18-28 transforming growth factor, beta 1 Mus musculus 143-151 28593185-9 2017 Mice treated with mesalamine exhibited increased levels of the active form of TGF-beta in the colon in an AhR-dependent manner and blockade of TGF-beta signaling suppressed induction of Tregs by mesalamine in the colon. Mesalamine 195-205 transforming growth factor, beta 1 Mus musculus 143-151 28593185-11 2017 CONCLUSIONS: We propose a novel anti-inflammatory mechanism of mesalamine for colitis: induction of Tregs in the colon via the AhR pathway, followed by TGF-beta activation. Mesalamine 63-73 aryl-hydrocarbon receptor Mus musculus 127-130 28593185-11 2017 CONCLUSIONS: We propose a novel anti-inflammatory mechanism of mesalamine for colitis: induction of Tregs in the colon via the AhR pathway, followed by TGF-beta activation. Mesalamine 63-73 transforming growth factor, beta 1 Mus musculus 152-160 28138699-5 2017 The therapeutic effect of 5-ASA-SiO2 NPs was assessed based on their disease activity index (DAI), colon histopathology, myeloperoxidase (MPO) and levels of tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6). Mesalamine 26-31 myeloperoxidase Mus musculus 121-136 28138699-5 2017 The therapeutic effect of 5-ASA-SiO2 NPs was assessed based on their disease activity index (DAI), colon histopathology, myeloperoxidase (MPO) and levels of tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6). Mesalamine 26-31 tumor necrosis factor Mus musculus 157-184 28138699-5 2017 The therapeutic effect of 5-ASA-SiO2 NPs was assessed based on their disease activity index (DAI), colon histopathology, myeloperoxidase (MPO) and levels of tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6). Mesalamine 26-31 tumor necrosis factor Mus musculus 186-195 28138699-5 2017 The therapeutic effect of 5-ASA-SiO2 NPs was assessed based on their disease activity index (DAI), colon histopathology, myeloperoxidase (MPO) and levels of tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6). Mesalamine 26-31 interleukin 6 Mus musculus 201-214 28138699-5 2017 The therapeutic effect of 5-ASA-SiO2 NPs was assessed based on their disease activity index (DAI), colon histopathology, myeloperoxidase (MPO) and levels of tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6). Mesalamine 26-31 interleukin 6 Mus musculus 216-220 28275298-11 2017 The expression levels of IL-1beta, IL-8 and TNF-alpha in the DSS group were higher than those in the control group (P < 0.05), and the expression levels of IL-1beta, IL-8 and TNF-alpha in the JPQCD and 5-ASA groups were lower than those in the DSS group after treating with JPQCD and 5-ASA. Mesalamine 287-292 interleukin 1 beta Mus musculus 159-167 28275298-12 2017 Comparing with the DSS group, the mRNA level of IL-1beta, IL-8, TNF-alpha and NF-kappaB was significantly reduced by 5-ASA and JPQCD. Mesalamine 117-122 interleukin 1 beta Mus musculus 48-56 28275298-12 2017 Comparing with the DSS group, the mRNA level of IL-1beta, IL-8, TNF-alpha and NF-kappaB was significantly reduced by 5-ASA and JPQCD. Mesalamine 117-122 chemokine (C-X-C motif) ligand 15 Mus musculus 58-62 28275298-12 2017 Comparing with the DSS group, the mRNA level of IL-1beta, IL-8, TNF-alpha and NF-kappaB was significantly reduced by 5-ASA and JPQCD. Mesalamine 117-122 tumor necrosis factor Mus musculus 64-73 28275298-12 2017 Comparing with the DSS group, the mRNA level of IL-1beta, IL-8, TNF-alpha and NF-kappaB was significantly reduced by 5-ASA and JPQCD. Mesalamine 117-122 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 78-87 27388883-8 2016 Treatment with 5-ASA after burn injury prevented the burn-induced increase in permeability, partially restored normal intestinal transit, normalized the levels of the proinflammatory cytokines IL-6 and IL-18, and restored tight junction protein expression of claudin-4 and occludin compared with that of sham levels. Mesalamine 15-20 interleukin 6 Homo sapiens 193-197 28867741-2 2017 The uptake transport of glycylsarcosine, a typical substrate for PEPT1, was reduced to 60% only by 5-aminosalicylate at the clinically relevant concentration among tested marketed drugs in PEPT1 transfected HEK293 cell lines. Mesalamine 99-116 solute carrier family 15 member 1 Homo sapiens 65-70 28867741-2 2017 The uptake transport of glycylsarcosine, a typical substrate for PEPT1, was reduced to 60% only by 5-aminosalicylate at the clinically relevant concentration among tested marketed drugs in PEPT1 transfected HEK293 cell lines. Mesalamine 99-116 solute carrier family 15 member 1 Homo sapiens 189-194 27294352-7 2017 Significant depression was found in the luminal appearance of PNP metabolites by giving of indomethacin and these alterations could not be compensated by mesalazine.Hepatic elimination of PNP (biliary excretion of PNP and its metabolites) was decreased definitely by indomethacin which was - at least partly - compensated by mesalazine.The findings of the present study suggest that the indomethacin-induced inflammation in the small intestine represents a useful rat model of Crohn"s disease. Mesalamine 325-335 purine nucleoside phosphorylase Rattus norvegicus 188-191 27294352-7 2017 Significant depression was found in the luminal appearance of PNP metabolites by giving of indomethacin and these alterations could not be compensated by mesalazine.Hepatic elimination of PNP (biliary excretion of PNP and its metabolites) was decreased definitely by indomethacin which was - at least partly - compensated by mesalazine.The findings of the present study suggest that the indomethacin-induced inflammation in the small intestine represents a useful rat model of Crohn"s disease. Mesalamine 325-335 purine nucleoside phosphorylase Rattus norvegicus 188-191 27818126-3 2016 Unlike cyanidin-3-glucoside, resveratrol and 5-ASA also increased nuclear levels of PPAR-gamma in cytokine-stimulated cells. Mesalamine 45-50 peroxisome proliferator activated receptor gamma Homo sapiens 84-94 27416043-2 2016 N-acetyltransferase (NAT) enzymes convert 5-ASA to its metabolite N-acetyl-5-ASA, and it is unresolved whether 5-ASA or N-acetyl-5-ASA is the effective therapeutic molecule. Mesalamine 42-47 bromodomain containing 2 Homo sapiens 0-19 27416043-2 2016 N-acetyltransferase (NAT) enzymes convert 5-ASA to its metabolite N-acetyl-5-ASA, and it is unresolved whether 5-ASA or N-acetyl-5-ASA is the effective therapeutic molecule. Mesalamine 42-47 bromodomain containing 2 Homo sapiens 21-24 27416043-2 2016 N-acetyltransferase (NAT) enzymes convert 5-ASA to its metabolite N-acetyl-5-ASA, and it is unresolved whether 5-ASA or N-acetyl-5-ASA is the effective therapeutic molecule. Mesalamine 75-80 bromodomain containing 2 Homo sapiens 0-19 27416043-2 2016 N-acetyltransferase (NAT) enzymes convert 5-ASA to its metabolite N-acetyl-5-ASA, and it is unresolved whether 5-ASA or N-acetyl-5-ASA is the effective therapeutic molecule. Mesalamine 75-80 bromodomain containing 2 Homo sapiens 21-24 27416043-4 2016 Our hypothesis is that 5-ASA is the therapeutic molecule to improve colitis, with the corollary that altered NAT activity affects drug efficacy. Mesalamine 23-28 bromodomain containing 2 Homo sapiens 109-112 26033966-8 2016 Treatment with 5-ASA suppressed BCL-3 expression in colorectal cancer cells. Mesalamine 15-20 BCL3 transcription coactivator Homo sapiens 32-37 28071183-0 2017 5-Aminosalicylic acid inhibits inflammatory responses by suppressing JNK and p38 activity in murine macrophages. Mesalamine 0-21 mitogen-activated protein kinase 14 Mus musculus 77-80 28071183-6 2017 RESULTS: 5-ASA suppressed the production of NO and IL-6, and also decreased the expression of iNOS in LPS-induced RAW264.7 cells. Mesalamine 9-14 interleukin 6 Mus musculus 51-55 28071183-6 2017 RESULTS: 5-ASA suppressed the production of NO and IL-6, and also decreased the expression of iNOS in LPS-induced RAW264.7 cells. Mesalamine 9-14 nitric oxide synthase 2, inducible Mus musculus 94-98 28071183-7 2017 5-ASA inhibited the phosphorylation of JNKs and p38, but did not block NF-kappaB activation at all doses tested. Mesalamine 0-5 mitogen-activated protein kinase 14 Mus musculus 48-51 28071183-8 2017 DISCUSSION AND CONCLUSION: The results indicated that the anti-inflammatory effect of 5-ASA was mainly regulated by the inhibition of the JNKs, p38 pathways rather than NF-kappaB pathway. Mesalamine 86-91 mitogen-activated protein kinase 14 Mus musculus 144-147 27294352-6 2017 Disappearance of PNP from the luminal perfusion solution was diminished by indomethacin which was corrected by administration of mesalazine. Mesalamine 129-139 purine nucleoside phosphorylase Rattus norvegicus 17-20 27185300-5 2016 VEGF, a potent angiogenic growth factor, over expressed during UC was down-regulated by collagen hydrolysate (1.06+-0.25) and collagen (1.76+-0.45) to a greater extent than by mesalamine (2.59+-0.51) and untreated control (4.17+-0.15). Mesalamine 176-186 vascular endothelial growth factor A Mus musculus 0-4 27648296-2 2016 Sulfasalazine (SASP) could deliver a high concentration of 5-aminosalicylic acid to the colon. Mesalamine 59-80 aspartic peptidase retroviral like 1 Homo sapiens 15-19 27648296-10 2016 In 9 (64.3%) of 14 patients with UC treated with mesalazine enemas, mesalazine enemas could be discontinued with SASP. Mesalamine 49-59 aspartic peptidase retroviral like 1 Homo sapiens 113-117 27648296-10 2016 In 9 (64.3%) of 14 patients with UC treated with mesalazine enemas, mesalazine enemas could be discontinued with SASP. Mesalamine 68-78 aspartic peptidase retroviral like 1 Homo sapiens 113-117 27416043-10 2016 In the setting of colitis, 5-ASA significantly restored colon length and decreased myeloperoxidase activity in NAT knockout but not in WT mice. Mesalamine 27-32 myeloperoxidase Mus musculus 83-98 27416043-10 2016 In the setting of colitis, 5-ASA significantly restored colon length and decreased myeloperoxidase activity in NAT knockout but not in WT mice. Mesalamine 27-32 solute carrier family 38, member 3 Mus musculus 111-114 27416043-13 2016 Decreased NAT activity enhances the therapeutic effect of 5-ASA in mice. Mesalamine 58-63 solute carrier family 38, member 3 Mus musculus 10-13 27416043-14 2016 A NAT activity assay could be useful to help predict the efficacy of 5-ASA therapy. Mesalamine 69-74 bromodomain containing 2 Homo sapiens 2-5 27388883-8 2016 Treatment with 5-ASA after burn injury prevented the burn-induced increase in permeability, partially restored normal intestinal transit, normalized the levels of the proinflammatory cytokines IL-6 and IL-18, and restored tight junction protein expression of claudin-4 and occludin compared with that of sham levels. Mesalamine 15-20 interleukin 18 Homo sapiens 202-207 27388883-8 2016 Treatment with 5-ASA after burn injury prevented the burn-induced increase in permeability, partially restored normal intestinal transit, normalized the levels of the proinflammatory cytokines IL-6 and IL-18, and restored tight junction protein expression of claudin-4 and occludin compared with that of sham levels. Mesalamine 15-20 claudin 4 Homo sapiens 259-268 27388883-8 2016 Treatment with 5-ASA after burn injury prevented the burn-induced increase in permeability, partially restored normal intestinal transit, normalized the levels of the proinflammatory cytokines IL-6 and IL-18, and restored tight junction protein expression of claudin-4 and occludin compared with that of sham levels. Mesalamine 15-20 occludin Homo sapiens 273-281 27101467-1 2016 BACKGROUND: Oral 5-aminosalicylic acid (5-ASA) preparations were intended to avoid the adverse effects of sulfasalazine (SASP) while maintaining its therapeutic benefits. Mesalamine 17-38 aspartic peptidase retroviral like 1 Homo sapiens 121-125 27112518-7 2016 Furthermore, combined treatment with 5-ASA and PA additively inhibited nuclear factor-kappaB (NFkappaB) activity in human colon carcinoma cells and inflamed colonic tissues. Mesalamine 37-42 nuclear factor kappa B subunit 1 Homo sapiens 71-92 27112518-7 2016 Furthermore, combined treatment with 5-ASA and PA additively inhibited nuclear factor-kappaB (NFkappaB) activity in human colon carcinoma cells and inflamed colonic tissues. Mesalamine 37-42 nuclear factor kappa B subunit 1 Homo sapiens 94-102 27112518-9 2016 5-ASA-azo-PA may be a colon-specific mutual prodrug acting against colitis, and the mutual anticolitic effects occurred at least partly through the cooperative inhibition of NFkappaB activity. Mesalamine 0-5 nuclear factor kappa B subunit 1 Homo sapiens 174-182 27310872-2 2016 Notably, treatment of colorectal cancer (CRC) cells with mesalazine lead to increased expression of MUCDHL, and is associated with sequestration of beta-catenin on the plasma membrane and inhibition of its transcriptional activity. Mesalamine 57-67 cadherin related family member 5 Homo sapiens 100-106 27310872-2 2016 Notably, treatment of colorectal cancer (CRC) cells with mesalazine lead to increased expression of MUCDHL, and is associated with sequestration of beta-catenin on the plasma membrane and inhibition of its transcriptional activity. Mesalamine 57-67 catenin beta 1 Homo sapiens 148-160 26800315-9 2016 Following treatment with mesalazine, the numbers of circulating IgG(+) IgD(-) CD27(+) CD19(+) memory B cells were significantly increased, while the numbers of CD138(+) CD38(+) CD20(-) CD19(+) and IgG(+) CD38(+) CD20(-) CD19(+) plasmablasts were reduced in UC patients. Mesalamine 25-35 CD27 molecule Homo sapiens 78-82 26800315-9 2016 Following treatment with mesalazine, the numbers of circulating IgG(+) IgD(-) CD27(+) CD19(+) memory B cells were significantly increased, while the numbers of CD138(+) CD38(+) CD20(-) CD19(+) and IgG(+) CD38(+) CD20(-) CD19(+) plasmablasts were reduced in UC patients. Mesalamine 25-35 CD19 molecule Homo sapiens 86-90 26800315-9 2016 Following treatment with mesalazine, the numbers of circulating IgG(+) IgD(-) CD27(+) CD19(+) memory B cells were significantly increased, while the numbers of CD138(+) CD38(+) CD20(-) CD19(+) and IgG(+) CD38(+) CD20(-) CD19(+) plasmablasts were reduced in UC patients. Mesalamine 25-35 CD38 molecule Homo sapiens 169-173 26800315-9 2016 Following treatment with mesalazine, the numbers of circulating IgG(+) IgD(-) CD27(+) CD19(+) memory B cells were significantly increased, while the numbers of CD138(+) CD38(+) CD20(-) CD19(+) and IgG(+) CD38(+) CD20(-) CD19(+) plasmablasts were reduced in UC patients. Mesalamine 25-35 keratin 20 Homo sapiens 177-181 26800315-9 2016 Following treatment with mesalazine, the numbers of circulating IgG(+) IgD(-) CD27(+) CD19(+) memory B cells were significantly increased, while the numbers of CD138(+) CD38(+) CD20(-) CD19(+) and IgG(+) CD38(+) CD20(-) CD19(+) plasmablasts were reduced in UC patients. Mesalamine 25-35 CD19 molecule Homo sapiens 185-189 26800315-9 2016 Following treatment with mesalazine, the numbers of circulating IgG(+) IgD(-) CD27(+) CD19(+) memory B cells were significantly increased, while the numbers of CD138(+) CD38(+) CD20(-) CD19(+) and IgG(+) CD38(+) CD20(-) CD19(+) plasmablasts were reduced in UC patients. Mesalamine 25-35 CD38 molecule Homo sapiens 204-208 26800315-9 2016 Following treatment with mesalazine, the numbers of circulating IgG(+) IgD(-) CD27(+) CD19(+) memory B cells were significantly increased, while the numbers of CD138(+) CD38(+) CD20(-) CD19(+) and IgG(+) CD38(+) CD20(-) CD19(+) plasmablasts were reduced in UC patients. Mesalamine 25-35 keratin 20 Homo sapiens 212-216 26800315-9 2016 Following treatment with mesalazine, the numbers of circulating IgG(+) IgD(-) CD27(+) CD19(+) memory B cells were significantly increased, while the numbers of CD138(+) CD38(+) CD20(-) CD19(+) and IgG(+) CD38(+) CD20(-) CD19(+) plasmablasts were reduced in UC patients. Mesalamine 25-35 CD19 molecule Homo sapiens 185-189 26739837-0 2016 Reduced Plasma Levels of sCD14 and I-FABP in HIV-infected Patients with Mesalazine-treated Ulcerative Colitis. Mesalamine 72-82 fatty acid binding protein 2 Homo sapiens 35-41 27087958-6 2016 RESULTS: In the multivariate regression analysis a delay of 5-ASA treatment by at least two months (odds ratio (OR) 6.21 (95% confidence interval (CI) 2.13-18.14), p = 0.001) as well as a delay with other medication with thiopurines (OR 6.48 (95% CI 2.01-20.91), p = 0.002) were associated with a higher risk for complications. Mesalamine 60-65 olfactory receptor family 2 subfamily H member 4 pseudogene Homo sapiens 100-120 27101467-1 2016 BACKGROUND: Oral 5-aminosalicylic acid (5-ASA) preparations were intended to avoid the adverse effects of sulfasalazine (SASP) while maintaining its therapeutic benefits. Mesalamine 40-45 aspartic peptidase retroviral like 1 Homo sapiens 121-125 26377354-4 2016 Oral administration of Dex-5-ESA (equivalent to 10 mg 5-ASA/kg, twice a day) alleviated colonic injury and reduced MPO activity in the inflamed colon. Mesalamine 54-59 myeloperoxidase Rattus norvegicus 115-118 26896068-9 2016 Moreover, metformin enhanced the anti-inflammatory effect of 5-ASA by decreasing the gene expression of IL-1beta, IL-6, COX-2 and TNF-alpha and its receptors; TNF-R1 and TNF-R2. Mesalamine 61-66 interleukin 1 beta Homo sapiens 104-112 26896068-9 2016 Moreover, metformin enhanced the anti-inflammatory effect of 5-ASA by decreasing the gene expression of IL-1beta, IL-6, COX-2 and TNF-alpha and its receptors; TNF-R1 and TNF-R2. Mesalamine 61-66 interleukin 6 Homo sapiens 114-118 26896068-9 2016 Moreover, metformin enhanced the anti-inflammatory effect of 5-ASA by decreasing the gene expression of IL-1beta, IL-6, COX-2 and TNF-alpha and its receptors; TNF-R1 and TNF-R2. Mesalamine 61-66 mitochondrially encoded cytochrome c oxidase II Homo sapiens 120-125 26896068-9 2016 Moreover, metformin enhanced the anti-inflammatory effect of 5-ASA by decreasing the gene expression of IL-1beta, IL-6, COX-2 and TNF-alpha and its receptors; TNF-R1 and TNF-R2. Mesalamine 61-66 tumor necrosis factor Homo sapiens 130-139 26896068-9 2016 Moreover, metformin enhanced the anti-inflammatory effect of 5-ASA by decreasing the gene expression of IL-1beta, IL-6, COX-2 and TNF-alpha and its receptors; TNF-R1 and TNF-R2. Mesalamine 61-66 TNF receptor superfamily member 1A Homo sapiens 159-165 26896068-9 2016 Moreover, metformin enhanced the anti-inflammatory effect of 5-ASA by decreasing the gene expression of IL-1beta, IL-6, COX-2 and TNF-alpha and its receptors; TNF-R1 and TNF-R2. Mesalamine 61-66 TNF receptor superfamily member 1B Homo sapiens 170-176 26896068-11 2016 Metformin also enhanced the inhibitory effect of 5-ASA on MMP-2 and MMP-9 enzyme activity, indicating a decrease in metastasis. Mesalamine 49-54 matrix metallopeptidase 2 Homo sapiens 58-63 26896068-11 2016 Metformin also enhanced the inhibitory effect of 5-ASA on MMP-2 and MMP-9 enzyme activity, indicating a decrease in metastasis. Mesalamine 49-54 matrix metallopeptidase 9 Homo sapiens 68-73 26643666-4 2016 5-aminosalicylic acid (5-ASA) and sodium salicylate are known to suppress NFkappaB activation by inhibiting inhibitor of kappa B kinase (IKkappaB). Mesalamine 0-21 nuclear factor kappa B subunit 1 Homo sapiens 74-82 26643666-4 2016 5-aminosalicylic acid (5-ASA) and sodium salicylate are known to suppress NFkappaB activation by inhibiting inhibitor of kappa B kinase (IKkappaB). Mesalamine 23-28 nuclear factor kappa B subunit 1 Homo sapiens 74-82 25429050-0 2015 Mesalazine and thymoquinone attenuate intestinal tumour development in Msh2(loxP/loxP) Villin-Cre mice. Mesalamine 0-10 mutS homolog 2 Mus musculus 71-75 26630041-3 2016 While on steroid treatment, the patients maintained clinical and laboratory remission, but with the initiation of mesalamine treatment, they had abdominal pain and bloody mucoid diarrhoea and/or elevation of white blood cell count, C-reactive protein level and erythrocyte sedimentation rate. Mesalamine 114-124 C-reactive protein Homo sapiens 232-250 26630041-5 2016 Within 3-7 days after the mesalamine treatment had been stopped, the patients showed improvement of colitis symptoms and normalisation of white blood cell count, C-reactive protein level and erythrocyte sedimentation rate. Mesalamine 26-36 C-reactive protein Homo sapiens 162-180 26642326-8 2015 Further, the up-regulation in mRNA level of colonic TNF-alpha as well as NFkappaB and JAK2 phosphorylation caused by DSS were more pronouncedly reversed in animals treated with the combination therapy than those treated with 5-ASA alone. Mesalamine 225-230 tumor necrosis factor Mus musculus 52-61 26642326-8 2015 Further, the up-regulation in mRNA level of colonic TNF-alpha as well as NFkappaB and JAK2 phosphorylation caused by DSS were more pronouncedly reversed in animals treated with the combination therapy than those treated with 5-ASA alone. Mesalamine 225-230 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 73-81 26642326-8 2015 Further, the up-regulation in mRNA level of colonic TNF-alpha as well as NFkappaB and JAK2 phosphorylation caused by DSS were more pronouncedly reversed in animals treated with the combination therapy than those treated with 5-ASA alone. Mesalamine 225-230 Janus kinase 2 Mus musculus 86-90 26642326-9 2015 Moreover, the addition of berberine to 5-ASA more significantly inhibited lymphocyte TNF-alpha secretion of DSS mice than 5-ASA alone. Mesalamine 39-44 tumor necrosis factor Mus musculus 85-94 26718757-6 2015 Treatment with 5-ASA or 1,25(OH)D3 ameliorated colitis by lowering CMDI (P=0.049, P=0.040, respectively), histological colonic damage score (P=0.010, P=0.005, respectively), and MPO activity (P=0.0003, P=0.0013, respectively) compared with the TNBS group. Mesalamine 15-20 myeloperoxidase Rattus norvegicus 178-181 26718757-7 2015 Combined treatment with 5-ASA and 1,25(OH)D3 significantly decreased MPO activity (P=0.003). Mesalamine 24-29 myeloperoxidase Rattus norvegicus 69-72 26304465-2 2015 PAK1 is a target of mesalamine [5-aminosylicylic acid (5-ASA)], a common drug for the treatment of ulcerative colitis with prospective chemopreventive properties. Mesalamine 20-30 p21 (RAC1) activated kinase 1 Mus musculus 0-4 26270730-6 2015 Furthermore, both NCI-H716 and GLUTag cells pretreated with TNFalpha for 24 hours no longer responded to known GLP-1 secretagogues, an effect that was reversed by coincubation with the Nuclear Factor Kappa B inhibitor, 5-aminosalicylic acid, in the NCI-H716 cells. Mesalamine 219-240 tumor necrosis factor Mus musculus 60-68 26270730-6 2015 Furthermore, both NCI-H716 and GLUTag cells pretreated with TNFalpha for 24 hours no longer responded to known GLP-1 secretagogues, an effect that was reversed by coincubation with the Nuclear Factor Kappa B inhibitor, 5-aminosalicylic acid, in the NCI-H716 cells. Mesalamine 219-240 glucagon Mus musculus 111-116 26036343-12 2015 Moreover, PAK1 overexpression downregulated PPARgamma and mesalamine recovered PPARgamma through PAK1 inhibition. Mesalamine 58-68 p21 (RAC1) activated kinase 1 Mus musculus 10-14 26036343-12 2015 Moreover, PAK1 overexpression downregulated PPARgamma and mesalamine recovered PPARgamma through PAK1 inhibition. Mesalamine 58-68 peroxisome proliferator activated receptor gamma Mus musculus 79-88 25429050-9 2015 In Msh2(loxP/loxP) Villin-Cre mice, tumour incidence was reduced by mesalazine from 94% to 69% (p=0.04) and to 56% (p=0.003) by thymoquinone. Mesalamine 68-78 mutS homolog 2 Mus musculus 3-7 25429050-13 2015 CONCLUSIONS: Mesalazine and thymoquinone reduce tumour incidence and multiplicity in Msh2(loxP/loxP) Villin-Cre mice by reduction of MSI independent of a functional mismatch repair system. Mesalamine 13-23 mutS homolog 2 Mus musculus 85-89 26665398-0 2015 THE EFFECT OF SULFASALAZINE AND 5-AMINOSALICYLIC ACID ON THE SECRETION OF INTERLEUKIN 8 BY HUMAN COLON MYOFIBROBLASTS. Mesalamine 32-53 C-X-C motif chemokine ligand 8 Homo sapiens 74-87 25569743-3 2015 p21 activated kinase 1 (PAK1) mediates 5-ASA activity by orchestrating MAPK signaling, Wnt-beta catenin pathway, and cell adhesion; all implicated in the colon carcinogenesis. Mesalamine 39-44 p21 (RAC1) activated kinase 1 Homo sapiens 0-22 26336590-0 2015 Measurement of Human Cytochrome P450 Enzyme Induction Based on Mesalazine and Mosapride Citrate Treatments Using a Luminescent Assay. Mesalamine 63-73 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 21-36 26336590-9 2015 The results showed that mesalazine promotes CYP2B6 and 3A4 activities, while mosapride citrate promotes CYP1A2, 2B6, and 3A4 activities. Mesalamine 24-34 cytochrome P450 family 2 subfamily B member 6 Homo sapiens 44-50 26069953-18 2015 R. tanguticum polysaccharide 1 and 5-amino salicylic acid had no effect on cyclooxygenase 1 protein expression, but inhibited the overexpression of the cyclooxygenase 2 protein. Mesalamine 35-57 prostaglandin-endoperoxide synthase 2 Rattus norvegicus 152-168 26467144-12 2015 There is also a potential for pharmacological stimulation of HSP70 expression, linked (for example) to geranylgeranylacetone, polaprezinc and mesalazine. Mesalamine 142-152 heat shock protein family A (Hsp70) member 4 Homo sapiens 61-66 25945013-13 2015 MESA significantly increased the expression of ZO-1 (P = 0.016) and occludin (P = 0.026). Mesalamine 0-4 tight junction protein 1 Homo sapiens 47-51 25945013-13 2015 MESA significantly increased the expression of ZO-1 (P = 0.016) and occludin (P = 0.026). Mesalamine 0-4 occludin Homo sapiens 68-76 25945013-18 2015 MESA significantly increased the expression of ZO-1 mRNA (P = 0.000), occludin mRNA (P = 0.042), and claudin-1 mRNA (P = 0.041). Mesalamine 0-4 tight junction protein 1 Homo sapiens 47-51 25945013-18 2015 MESA significantly increased the expression of ZO-1 mRNA (P = 0.000), occludin mRNA (P = 0.042), and claudin-1 mRNA (P = 0.041). Mesalamine 0-4 occludin Homo sapiens 70-78 25945013-18 2015 MESA significantly increased the expression of ZO-1 mRNA (P = 0.000), occludin mRNA (P = 0.042), and claudin-1 mRNA (P = 0.041). Mesalamine 0-4 claudin 1 Homo sapiens 101-110 25488057-9 2015 CONCLUSION: Anti-TNF agents may be more effective in preventing clinical and endoscopic postoperative Crohn"s disease recurrence than control treatment (thiopurines or mesalamine). Mesalamine 168-178 tumor necrosis factor Homo sapiens 17-20 26622660-8 2015 The expression level of PPAR-gamma in the intestinal tissue was also increased in the AOM/DSS/5-ASA group compared with AOM/DSS group (P<0.001). Mesalamine 94-99 peroxisome proliferator activated receptor gamma Homo sapiens 24-34 26622660-10 2015 The present study found that 5-ASA significantly alleviates the colitis and tumor burden in a mouse model of AOM/DSS-induced colitis-associated neoplasia, and promotes the expression of PPAR-gamma in the intestinal tract. Mesalamine 29-34 peroxisome proliferator activated receptor gamma Mus musculus 186-196 26032070-17 2015 4) The TNF-alpha expression was significantly down-regulated in the novaferon groups (at low-dose, middle-dose or high-dose), the mesalazine group and the prednisone group compared with model group (all P<0.01); but there was no significant difference between the mesalazine group and the prednisone group (P>0.05); the decrease of TNF-alpha expression by novaferon displayed a dose-dependent manner. Mesalamine 130-140 tumor necrosis factor Mus musculus 7-16 26032070-17 2015 4) The TNF-alpha expression was significantly down-regulated in the novaferon groups (at low-dose, middle-dose or high-dose), the mesalazine group and the prednisone group compared with model group (all P<0.01); but there was no significant difference between the mesalazine group and the prednisone group (P>0.05); the decrease of TNF-alpha expression by novaferon displayed a dose-dependent manner. Mesalamine 267-277 tumor necrosis factor Mus musculus 7-16 25834322-9 2015 NAT1 genotypes corresponding to fast enzymatic activity were associated with reduced TGN concentration (P value linear mixed effects model 0.033), putatively because of increased 5-ASA inactivation and consequent reduced inhibition of thiopurine metabolism. Mesalamine 179-184 N-acetyltransferase 1 Homo sapiens 0-4 25569743-3 2015 p21 activated kinase 1 (PAK1) mediates 5-ASA activity by orchestrating MAPK signaling, Wnt-beta catenin pathway, and cell adhesion; all implicated in the colon carcinogenesis. Mesalamine 39-44 p21 (RAC1) activated kinase 1 Homo sapiens 24-28 25569743-3 2015 p21 activated kinase 1 (PAK1) mediates 5-ASA activity by orchestrating MAPK signaling, Wnt-beta catenin pathway, and cell adhesion; all implicated in the colon carcinogenesis. Mesalamine 39-44 mitogen-activated protein kinase 1 Homo sapiens 71-75 25569743-11 2015 In colorectal cancer cell lines, PAK1, and beta-catenin expression correlated and inhibition of PAK1 and addition of 5-ASA elicited similar molecular affects by reducing ERK and AKT activation. Mesalamine 117-122 mitogen-activated protein kinase 1 Homo sapiens 170-173 25973010-7 2015 Treatment of mesalazine, an anti-ulcerative colitis drug, down-regulated Foxp3 and IL-17 expression in BTLA positive T cells along with attenuated severity for colitis. Mesalamine 13-23 forkhead box P3 Mus musculus 73-78 25973010-7 2015 Treatment of mesalazine, an anti-ulcerative colitis drug, down-regulated Foxp3 and IL-17 expression in BTLA positive T cells along with attenuated severity for colitis. Mesalamine 13-23 interleukin 17A Mus musculus 83-88 25973010-7 2015 Treatment of mesalazine, an anti-ulcerative colitis drug, down-regulated Foxp3 and IL-17 expression in BTLA positive T cells along with attenuated severity for colitis. Mesalamine 13-23 B and T lymphocyte associated Mus musculus 103-107 25569743-11 2015 In colorectal cancer cell lines, PAK1, and beta-catenin expression correlated and inhibition of PAK1 and addition of 5-ASA elicited similar molecular affects by reducing ERK and AKT activation. Mesalamine 117-122 AKT serine/threonine kinase 1 Homo sapiens 178-181 25569743-12 2015 Moreover, 5-ASA disrupted PAK1 interaction and colocalization with beta-catenin. Mesalamine 10-15 p21 (RAC1) activated kinase 1 Homo sapiens 26-30 25569743-12 2015 Moreover, 5-ASA disrupted PAK1 interaction and colocalization with beta-catenin. Mesalamine 10-15 catenin beta 1 Homo sapiens 67-79 25947923-2 2015 We hypothesized that the absorption of 5-ASA is mediated by the polyspecific carnitine/organic cation transporter (OCTN1/SLC22A4), based on the similarity of chemical structure between 5-ASA and other OCTN1 substrates. Mesalamine 185-190 solute carrier family 22 (organic cation transporter), member 4 Mus musculus 115-120 25947923-0 2015 Gene ablation of carnitine/organic cation transporter 1 reduces gastrointestinal absorption of 5-aminosalicylate in mice. Mesalamine 95-112 solute carrier family 22 (organic cation transporter), member 1 Mus musculus 27-55 25947923-2 2015 We hypothesized that the absorption of 5-ASA is mediated by the polyspecific carnitine/organic cation transporter (OCTN1/SLC22A4), based on the similarity of chemical structure between 5-ASA and other OCTN1 substrates. Mesalamine 39-44 solute carrier family 22 (organic cation transporter), member 4 Mus musculus 115-120 25947923-2 2015 We hypothesized that the absorption of 5-ASA is mediated by the polyspecific carnitine/organic cation transporter (OCTN1/SLC22A4), based on the similarity of chemical structure between 5-ASA and other OCTN1 substrates. Mesalamine 39-44 solute carrier family 22 (organic cation transporter), member 4 Mus musculus 121-128 25947923-2 2015 We hypothesized that the absorption of 5-ASA is mediated by the polyspecific carnitine/organic cation transporter (OCTN1/SLC22A4), based on the similarity of chemical structure between 5-ASA and other OCTN1 substrates. Mesalamine 39-44 solute carrier family 22 (organic cation transporter), member 4 Mus musculus 201-206 26027988-4 2015 The esophageal ulcer, which was intractable to conventional therapy, improved with the administration of 5-aminosalicylate, a drug known to inhibit IL-1beta. Mesalamine 105-122 interleukin 1 beta Homo sapiens 148-156 25445696-15 2015 Furthermore, real-time PCR analysis indicated increased activation of the target receptor PPAR-gamma and the HMGCS2 gene in rats upon administration of 5-ASA loaded Nutriose:EC- and peas starch:EC pellets compared to the commercial product. Mesalamine 152-157 peroxisome proliferator-activated receptor gamma Rattus norvegicus 90-100 25445696-15 2015 Furthermore, real-time PCR analysis indicated increased activation of the target receptor PPAR-gamma and the HMGCS2 gene in rats upon administration of 5-ASA loaded Nutriose:EC- and peas starch:EC pellets compared to the commercial product. Mesalamine 152-157 3-hydroxy-3-methylglutaryl-CoA synthase 2 Rattus norvegicus 109-115 25445696-17 2015 In addition to the rat study, in vivo imaging of transgenic mice expressing the luciferase gene evidenced much more pronounced PPAR-gamma activation upon 5-ASA administration in the form of Nutriose:EC-coated pellets versus Pentasa pellets. Mesalamine 154-159 peroxisome proliferator activated receptor gamma Mus musculus 127-137 25574095-9 2015 In multivariate analyses adjusting for gender, IBD type and duration of disease, these associations with mesalamine and anti-TNF remained significant [(adjusted values for mesalamine (OR = 0.43, 95%CI: 0.19-0.86) and anti-TNFs (OR = 0.28, 95%CI: 0.08-0.98)]. Mesalamine 172-182 tumor necrosis factor Homo sapiens 125-128 25947923-2 2015 We hypothesized that the absorption of 5-ASA is mediated by the polyspecific carnitine/organic cation transporter (OCTN1/SLC22A4), based on the similarity of chemical structure between 5-ASA and other OCTN1 substrates. Mesalamine 185-190 solute carrier family 22 (organic cation transporter), member 4 Mus musculus 121-128 25947923-4 2015 After oral administration of 5-ASA, the plasma concentrations of 5-ASA and its primary metabolite, N-acetyl-5-aminosalicylate (Ac-5-ASA), in octn1(-/-) mice were much lower than those in wild-type mice. Mesalamine 29-34 solute carrier family 22 (organic cation transporter), member 4 Mus musculus 141-146 25947923-4 2015 After oral administration of 5-ASA, the plasma concentrations of 5-ASA and its primary metabolite, N-acetyl-5-aminosalicylate (Ac-5-ASA), in octn1(-/-) mice were much lower than those in wild-type mice. Mesalamine 65-70 solute carrier family 22 (organic cation transporter), member 4 Mus musculus 141-146 25947923-7 2015 Uptake of 5-ASA from the apical to the basal side of isolated small-intestinal tissues of octn1(-/-) mice, determined in an Ussing-type chamber, was lower than that in wild-type mice. Mesalamine 10-15 solute carrier family 22 (organic cation transporter), member 4 Mus musculus 90-95 25947923-8 2015 Further, uptake of 5-ASA in HEK293 cells stably transfected with the OCTN1 gene, assessed as the sum of cell-associated 5-ASA and Ac-5-ASA, was higher than that in HEK293 cells transfected with the vector alone. Mesalamine 19-24 solute carrier family 22 member 4 Homo sapiens 69-74 25947923-8 2015 Further, uptake of 5-ASA in HEK293 cells stably transfected with the OCTN1 gene, assessed as the sum of cell-associated 5-ASA and Ac-5-ASA, was higher than that in HEK293 cells transfected with the vector alone. Mesalamine 120-125 solute carrier family 22 member 4 Homo sapiens 69-74 25947923-9 2015 Overall, these results indicate that OCTN1 is involved, at least in part, in the gastrointestinal absorption of 5-ASA. Mesalamine 112-117 solute carrier family 22 (organic cation transporter), member 4 Mus musculus 37-42 25545673-0 2014 The immunologic effects of mesalamine in treated HIV-infected individuals with incomplete CD4+ T cell recovery: a randomized crossover trial. Mesalamine 27-37 CD4 molecule Homo sapiens 90-93 25545673-3 2014 We randomized 33 HIV-infected subjects with CD4 counts <350 cells/mm3 and plasma HIV RNA levels <40 copies/ml on antiretroviral therapy (ART) to add mesalamine vs. placebo to their existing regimen for 12 weeks followed by a 12 week crossover to the other arm. Mesalamine 155-165 CD4 molecule Homo sapiens 44-47 25550915-12 2014 Baicalin and mesalazine treatment suppressed the expression of TNF-alpha, IL-6 and IL-13 mRNA (P < 0.05), yet up-regulated the expression of IL-10 mRNA (P < 0.05), compared to the DDS and control groups. Mesalamine 13-23 tumor necrosis factor Mus musculus 63-72 25101553-5 2014 In the present study 5-aminosalicylic acid (5-ASA), a salicylic acid derivative, was evaluated, in vivo for its potential to suppress TNF-alpha, IL-6 and IL-13 using ovalbumin (OVA) induced allergic asthma in Balb/C mice. Mesalamine 21-42 tumor necrosis factor Mus musculus 134-143 25101553-5 2014 In the present study 5-aminosalicylic acid (5-ASA), a salicylic acid derivative, was evaluated, in vivo for its potential to suppress TNF-alpha, IL-6 and IL-13 using ovalbumin (OVA) induced allergic asthma in Balb/C mice. Mesalamine 21-42 interleukin 6 Mus musculus 145-149 25101553-5 2014 In the present study 5-aminosalicylic acid (5-ASA), a salicylic acid derivative, was evaluated, in vivo for its potential to suppress TNF-alpha, IL-6 and IL-13 using ovalbumin (OVA) induced allergic asthma in Balb/C mice. Mesalamine 21-42 interleukin 13 Mus musculus 154-159 25101553-5 2014 In the present study 5-aminosalicylic acid (5-ASA), a salicylic acid derivative, was evaluated, in vivo for its potential to suppress TNF-alpha, IL-6 and IL-13 using ovalbumin (OVA) induced allergic asthma in Balb/C mice. Mesalamine 44-49 tumor necrosis factor Mus musculus 134-143 25101553-5 2014 In the present study 5-aminosalicylic acid (5-ASA), a salicylic acid derivative, was evaluated, in vivo for its potential to suppress TNF-alpha, IL-6 and IL-13 using ovalbumin (OVA) induced allergic asthma in Balb/C mice. Mesalamine 44-49 interleukin 6 Mus musculus 145-149 25101553-5 2014 In the present study 5-aminosalicylic acid (5-ASA), a salicylic acid derivative, was evaluated, in vivo for its potential to suppress TNF-alpha, IL-6 and IL-13 using ovalbumin (OVA) induced allergic asthma in Balb/C mice. Mesalamine 44-49 interleukin 13 Mus musculus 154-159 25101553-6 2014 Oral administration of 65, 130 and 195 mg/kg 5-ASA significantly reduced the OVA induced total and differential leucocyte count, TNF-alpha, IL-6, IL-13, nitrite, nitrate, MDA, MPO and TPL levels in the lung lavage samples. Mesalamine 45-50 tumor necrosis factor Mus musculus 129-138 25101553-6 2014 Oral administration of 65, 130 and 195 mg/kg 5-ASA significantly reduced the OVA induced total and differential leucocyte count, TNF-alpha, IL-6, IL-13, nitrite, nitrate, MDA, MPO and TPL levels in the lung lavage samples. Mesalamine 45-50 interleukin 6 Mus musculus 140-144 25101553-6 2014 Oral administration of 65, 130 and 195 mg/kg 5-ASA significantly reduced the OVA induced total and differential leucocyte count, TNF-alpha, IL-6, IL-13, nitrite, nitrate, MDA, MPO and TPL levels in the lung lavage samples. Mesalamine 45-50 interleukin 13 Mus musculus 146-151 25101553-6 2014 Oral administration of 65, 130 and 195 mg/kg 5-ASA significantly reduced the OVA induced total and differential leucocyte count, TNF-alpha, IL-6, IL-13, nitrite, nitrate, MDA, MPO and TPL levels in the lung lavage samples. Mesalamine 45-50 myeloperoxidase Mus musculus 176-179 25101553-6 2014 Oral administration of 65, 130 and 195 mg/kg 5-ASA significantly reduced the OVA induced total and differential leucocyte count, TNF-alpha, IL-6, IL-13, nitrite, nitrate, MDA, MPO and TPL levels in the lung lavage samples. Mesalamine 45-50 BPI fold containing family A, member 5 Mus musculus 184-187 25550915-12 2014 Baicalin and mesalazine treatment suppressed the expression of TNF-alpha, IL-6 and IL-13 mRNA (P < 0.05), yet up-regulated the expression of IL-10 mRNA (P < 0.05), compared to the DDS and control groups. Mesalamine 13-23 interleukin 6 Mus musculus 74-78 25550915-12 2014 Baicalin and mesalazine treatment suppressed the expression of TNF-alpha, IL-6 and IL-13 mRNA (P < 0.05), yet up-regulated the expression of IL-10 mRNA (P < 0.05), compared to the DDS and control groups. Mesalamine 13-23 interleukin 13 Mus musculus 83-88 25550915-12 2014 Baicalin and mesalazine treatment suppressed the expression of TNF-alpha, IL-6 and IL-13 mRNA (P < 0.05), yet up-regulated the expression of IL-10 mRNA (P < 0.05), compared to the DDS and control groups. Mesalamine 13-23 interleukin 10 Mus musculus 144-149 25320942-6 2014 Interstitial lung disease is a rare side effect of mesalazine probably underdiagnosed by physicians especially in patients treated with TNF alpha inhibitors. Mesalamine 51-61 tumor necrosis factor Homo sapiens 136-145 24056767-11 2014 CONCLUSIONS: Parallel to an increasing use of thiopurines and TNF-alpha blockers in IBD over time, a persistent significant decrease in surgery rates was observed along with a significant decrease in use of 5-ASA and corticosteroids. Mesalamine 207-212 tumor necrosis factor Homo sapiens 62-71 24982311-9 2014 CONCLUSIONS: Combination therapy with TNF-alpha inhibitors appears to be associated with a lower risk of pancreatitis in IBD patients on mesalamine, thiopurines, or a combination of both. Mesalamine 137-147 tumor necrosis factor Homo sapiens 38-47 24467436-16 2014 NAT inhibitors for co-administration with 5-aminosalicylate (5-AS) in inflammatory bowel disease has prompted ongoing investigations of azoreductases in gut bacteria which release 5-AS from prodrugs including balsalazide. Mesalamine 42-59 bromodomain containing 2 Homo sapiens 0-3 25509254-15 2014 CONCLUSION: QHR combined Mesalazine could synergically enhance the effect and effectively inhibit intestinal inflammation through down-regulating the expression of IL-17. Mesalamine 25-35 interleukin 17A Homo sapiens 164-169 25285021-1 2014 In 1977, 5-aminosalicylic acid (5-ASA) was discovered as a therapeutically active moiety of sulfasalazine (SASP) and was launched for topical and oral therapy of ulcerative colitis (UC) in 1984. Mesalamine 9-30 aspartic peptidase retroviral like 1 Homo sapiens 107-111 25285021-1 2014 In 1977, 5-aminosalicylic acid (5-ASA) was discovered as a therapeutically active moiety of sulfasalazine (SASP) and was launched for topical and oral therapy of ulcerative colitis (UC) in 1984. Mesalamine 32-37 aspartic peptidase retroviral like 1 Homo sapiens 107-111 25144293-0 2014 Distinct kinetics in the frequency of peripheral CD4+ T cells in patients with ulcerative colitis experiencing a flare during treatment with mesalazine or with a herbal preparation of myrrh, chamomile, and coffee charcoal. Mesalamine 141-151 CD4 molecule Homo sapiens 49-52 25144293-16 2014 CONCLUSIONS: In patients with UC experiencing acute flare, the CD4+ T compartment demonstrates a distinctly different pattern during treatment with myrrh, chamomile extract, and coffee charcoal than during treatment with mesalazine. Mesalamine 221-231 CD4 molecule Homo sapiens 63-66 24742986-0 2014 Acute murine colitis reduces colonic 5-aminosalicylic acid metabolism by regulation of N-acetyltransferase-2. Mesalamine 37-58 N-acetyltransferase 2 (arylamine N-acetyltransferase) Mus musculus 87-108 24742986-2 2014 Inflammation can affect therapeutic outcomes by regulating the expression and activity of drug-metabolizing enzymes; its effect on 5-ASA metabolism by the colonic arylamine N-acetyltransferase (NAT) enzyme isoforms is not firmly established. Mesalamine 131-136 solute carrier family 38, member 3 Mus musculus 194-197 24742986-5 2014 5-ASA metabolism reported by the assay was dependent on Ac-CoA, inhibited by alternative NAT substrates (isoniazid, p-aminobenzoylglutamate), and saturable with Km (5-ASA) = 5.8 muM. Mesalamine 0-5 solute carrier family 38, member 3 Mus musculus 89-92 24742986-8 2014 Use of selective substrates of NAT isoforms to inhibit 5-ASA metabolism suggested that mNAT2 mediated 5-ASA metabolism in normal and colitis conditions. Mesalamine 55-60 solute carrier family 38, member 3 Mus musculus 31-34 24742986-8 2014 Use of selective substrates of NAT isoforms to inhibit 5-ASA metabolism suggested that mNAT2 mediated 5-ASA metabolism in normal and colitis conditions. Mesalamine 55-60 N-acetyltransferase 2 (arylamine N-acetyltransferase) Mus musculus 87-92 24742986-8 2014 Use of selective substrates of NAT isoforms to inhibit 5-ASA metabolism suggested that mNAT2 mediated 5-ASA metabolism in normal and colitis conditions. Mesalamine 102-107 solute carrier family 38, member 3 Mus musculus 31-34 24742986-8 2014 Use of selective substrates of NAT isoforms to inhibit 5-ASA metabolism suggested that mNAT2 mediated 5-ASA metabolism in normal and colitis conditions. Mesalamine 102-107 N-acetyltransferase 2 (arylamine N-acetyltransferase) Mus musculus 87-92 24742986-10 2014 In conclusion, an acute colonic inflammation impairs the expression and function of mNAT2 enzyme, thereby diminishing the capacity for 5-ASA metabolism by colonic mucosa. Mesalamine 135-140 N-acetyltransferase 2 (arylamine N-acetyltransferase) Mus musculus 84-89 24637189-20 2014 In contrast to the model group, the expressions of DOR, beta-arrestin1 and Bcl-2 were significantly decreased in the mesalazine group and the groups that received different doses of QRZSLXF (P<0.05), and there were no statistically significant differences among the mesalazine and QRZSLXF-treated groups (P>0.05). Mesalamine 117-127 arrestin, beta 1 Rattus norvegicus 56-70 24637189-20 2014 In contrast to the model group, the expressions of DOR, beta-arrestin1 and Bcl-2 were significantly decreased in the mesalazine group and the groups that received different doses of QRZSLXF (P<0.05), and there were no statistically significant differences among the mesalazine and QRZSLXF-treated groups (P>0.05). Mesalamine 117-127 BCL2, apoptosis regulator Rattus norvegicus 75-80 24467436-16 2014 NAT inhibitors for co-administration with 5-aminosalicylate (5-AS) in inflammatory bowel disease has prompted ongoing investigations of azoreductases in gut bacteria which release 5-AS from prodrugs including balsalazide. Mesalamine 61-65 bromodomain containing 2 Homo sapiens 0-3 24467436-16 2014 NAT inhibitors for co-administration with 5-aminosalicylate (5-AS) in inflammatory bowel disease has prompted ongoing investigations of azoreductases in gut bacteria which release 5-AS from prodrugs including balsalazide. Mesalamine 180-184 bromodomain containing 2 Homo sapiens 0-3 24508089-3 2014 The synthesized graft copolymer (Ag-g-PAM) has been investigated (in vitro) for controlled and colon targeted release of 5-amino salicylic acid (5-ASA). Mesalamine 121-143 peptidylglycine alpha-amidating monooxygenase Homo sapiens 38-41 24762746-3 2014 It has also been reported that 5-aminosalicylic acid (5-ASA) inhibits TPMT activity, and that increased 6-thioguanine nucleotide (6-TGN, a metabolite of AZA) blood concentrations result in an increased number of ADRs. Mesalamine 31-52 thiopurine S-methyltransferase Homo sapiens 70-74 24762746-3 2014 It has also been reported that 5-aminosalicylic acid (5-ASA) inhibits TPMT activity, and that increased 6-thioguanine nucleotide (6-TGN, a metabolite of AZA) blood concentrations result in an increased number of ADRs. Mesalamine 54-59 thiopurine S-methyltransferase Homo sapiens 70-74 24508089-3 2014 The synthesized graft copolymer (Ag-g-PAM) has been investigated (in vitro) for controlled and colon targeted release of 5-amino salicylic acid (5-ASA). Mesalamine 145-150 peptidylglycine alpha-amidating monooxygenase Homo sapiens 38-41 24375143-11 2014 The enzyme showed low activity for 5-aminosalicylic acid and 5-hydroxytryptamine, which are reported as good substrates of a known arylamine N-acetyltransferase and an arylalkylamine N-acetyltransferase. Mesalamine 35-56 aralkylamine N-acetyltransferase Homo sapiens 168-202 24492313-0 2014 DUOX2 and DUOXA2 form the predominant enzyme system capable of producing the reactive oxygen species H2O2 in active ulcerative colitis and are modulated by 5-aminosalicylic acid. Mesalamine 156-177 dual oxidase 2 Homo sapiens 0-5 24492313-0 2014 DUOX2 and DUOXA2 form the predominant enzyme system capable of producing the reactive oxygen species H2O2 in active ulcerative colitis and are modulated by 5-aminosalicylic acid. Mesalamine 156-177 dual oxidase maturation factor 2 Homo sapiens 10-16 24492313-7 2014 5-ASA upregulated DUOX2 and DUOXA2 levels in the setting of active versus quiescent disease and altered DUOX2 expression in cultured biopsies. Mesalamine 0-5 dual oxidase 2 Homo sapiens 18-23 24492313-7 2014 5-ASA upregulated DUOX2 and DUOXA2 levels in the setting of active versus quiescent disease and altered DUOX2 expression in cultured biopsies. Mesalamine 0-5 dual oxidase maturation factor 2 Homo sapiens 28-34 24492313-7 2014 5-ASA upregulated DUOX2 and DUOXA2 levels in the setting of active versus quiescent disease and altered DUOX2 expression in cultured biopsies. Mesalamine 0-5 dual oxidase 2 Homo sapiens 104-109 24492313-8 2014 Ingenuity pathway analysis confirmed that inflammation status and 5-ASA increase expression of DUOX2 and DUOXA2. Mesalamine 66-71 dual oxidase 2 Homo sapiens 95-100 24492313-8 2014 Ingenuity pathway analysis confirmed that inflammation status and 5-ASA increase expression of DUOX2 and DUOXA2. Mesalamine 66-71 dual oxidase maturation factor 2 Homo sapiens 105-111 25045574-9 2014 Inhibition of 5-LO by 5-ASA disrupts this pathway and supports the concept that LTB4 activation of TRPV1 plays a role in toxin A colitis. Mesalamine 22-27 transient receptor potential cation channel, subfamily V, member 1 Rattus norvegicus 99-104 24168842-10 2014 Carriers of the mutant allele for IL23R SNPs had a significantly higher probability of developing EIMs (P<0.05), a higher probability of being refractory to 5-ASA (P<0.03), but a higher likelihood of responding to AZT (P=0.05). Mesalamine 160-165 interleukin 23 receptor Homo sapiens 34-39 24168842-11 2014 A significant synergism was observed between IL23R C2370A and EIMs with respect to nonresponse to 5-ASA (P=0.03). Mesalamine 98-103 interleukin 23 receptor Homo sapiens 45-50 24168842-13 2014 IL23R SNPs are associated both with EIMs and with nonresponse to 5-ASA and corticosteroids. Mesalamine 65-70 interleukin 23 receptor Homo sapiens 0-5 24496680-13 2014 The colonic mucosal damage, both macroscopical and histological, was significantly relieved and the myeloperoxidase activity was markedly decreased in rats topically treated with 5-ASA compared with those treated with oral 5-ASA or Etiasa. Mesalamine 179-184 myeloperoxidase Rattus norvegicus 100-115 24496680-14 2014 The mRNA and protein expression of IL-1beta, IL-6, and TNF-alpha was down-regulated in the colonic tissue of rats topically treated with 5-ASA, significantly lower than those from rats treated with oral 5-ASA or Etiasa. Mesalamine 137-142 interleukin 1 beta Rattus norvegicus 35-43 24496680-14 2014 The mRNA and protein expression of IL-1beta, IL-6, and TNF-alpha was down-regulated in the colonic tissue of rats topically treated with 5-ASA, significantly lower than those from rats treated with oral 5-ASA or Etiasa. Mesalamine 137-142 interleukin 6 Rattus norvegicus 45-49 24496680-14 2014 The mRNA and protein expression of IL-1beta, IL-6, and TNF-alpha was down-regulated in the colonic tissue of rats topically treated with 5-ASA, significantly lower than those from rats treated with oral 5-ASA or Etiasa. Mesalamine 137-142 tumor necrosis factor Rattus norvegicus 55-64 24496680-14 2014 The mRNA and protein expression of IL-1beta, IL-6, and TNF-alpha was down-regulated in the colonic tissue of rats topically treated with 5-ASA, significantly lower than those from rats treated with oral 5-ASA or Etiasa. Mesalamine 203-208 interleukin 1 beta Rattus norvegicus 35-43 24496680-14 2014 The mRNA and protein expression of IL-1beta, IL-6, and TNF-alpha was down-regulated in the colonic tissue of rats topically treated with 5-ASA, significantly lower than those from rats treated with oral 5-ASA or Etiasa. Mesalamine 203-208 interleukin 6 Rattus norvegicus 45-49 24496680-14 2014 The mRNA and protein expression of IL-1beta, IL-6, and TNF-alpha was down-regulated in the colonic tissue of rats topically treated with 5-ASA, significantly lower than those from rats treated with oral 5-ASA or Etiasa. Mesalamine 203-208 tumor necrosis factor Rattus norvegicus 55-64 24076458-0 2014 Molecular modeling and multispectroscopic studies of the interaction of mesalamine with bovine serum albumin. Mesalamine 72-82 albumin Homo sapiens 95-108 24076458-1 2014 The interaction of mesalamine (5-aminosalicylic acid (5-ASA)) with bovine serum albumin (BSA) was investigated by fluorescence quenching, absorption spectroscopy, circular dichroism (CD) techniques, and molecular docking. Mesalamine 19-29 albumin Homo sapiens 74-87 24076458-1 2014 The interaction of mesalamine (5-aminosalicylic acid (5-ASA)) with bovine serum albumin (BSA) was investigated by fluorescence quenching, absorption spectroscopy, circular dichroism (CD) techniques, and molecular docking. Mesalamine 31-52 albumin Homo sapiens 74-87 24076458-1 2014 The interaction of mesalamine (5-aminosalicylic acid (5-ASA)) with bovine serum albumin (BSA) was investigated by fluorescence quenching, absorption spectroscopy, circular dichroism (CD) techniques, and molecular docking. Mesalamine 54-59 albumin Homo sapiens 74-87 24184502-0 2014 Modulation of N-glycosylation by mesalamine facilitates membranous E-cadherin expression in colon epithelial cells. Mesalamine 33-43 cadherin 1 Mus musculus 67-77 24184502-4 2014 We have recently demonstrated that mesalamine (5-ASA); the anti-inflammatory drug used to treat ulcerative colitis, induces membranous expression of E-cadherin and increases intercellular adhesion. Mesalamine 35-45 cadherin 1 Mus musculus 149-159 24184502-4 2014 We have recently demonstrated that mesalamine (5-ASA); the anti-inflammatory drug used to treat ulcerative colitis, induces membranous expression of E-cadherin and increases intercellular adhesion. Mesalamine 47-52 cadherin 1 Mus musculus 149-159 24184502-10 2014 5-ASA activity modulated E-cadherin glycosylation and increased both mRNA and protein levels of GnT-III and its activity as detected by increased E4-lectin reactivity. Mesalamine 0-5 cadherin 1 Mus musculus 25-35 24184502-10 2014 5-ASA activity modulated E-cadherin glycosylation and increased both mRNA and protein levels of GnT-III and its activity as detected by increased E4-lectin reactivity. Mesalamine 0-5 mannoside acetylglucosaminyltransferase 3 Mus musculus 96-103 24184502-12 2014 The data demonstrated that remodeling of glycans by GnT-III mediated bisect glycosylation, contributes to the membranous retention of E-cadherin by 5-ASA; facilitating intercellular adhesion. Mesalamine 148-153 mannoside acetylglucosaminyltransferase 3 Mus musculus 52-59 24184502-12 2014 The data demonstrated that remodeling of glycans by GnT-III mediated bisect glycosylation, contributes to the membranous retention of E-cadherin by 5-ASA; facilitating intercellular adhesion. Mesalamine 148-153 cadherin 1 Mus musculus 134-144 24184502-13 2014 Induction of membranous expression of E-cadherin by 5-ASA is a novel mechanism for mucosal healing in colitis that might impede tumor progression by modulation of GnT-III expression. Mesalamine 52-57 cadherin 1 Mus musculus 38-48 24184502-13 2014 Induction of membranous expression of E-cadherin by 5-ASA is a novel mechanism for mucosal healing in colitis that might impede tumor progression by modulation of GnT-III expression. Mesalamine 52-57 mannoside acetylglucosaminyltransferase 3 Mus musculus 163-170 25548431-6 2014 We observed an increase of PPARalpha expression in patients with UC who were treated with 5-aminosalicylates compared with those who received any other combined therapy (P = 0.03, OR = 0.08). Mesalamine 90-108 peroxisome proliferator activated receptor alpha Homo sapiens 27-36 24379584-10 2013 Consistent with this observation, mesalazine and azathioprine induced, in primary fibroblasts, IL10RB and TNFRII over-expression and TNFRI and TNFalpha under-expression. Mesalamine 34-44 interleukin 10 receptor subunit beta Homo sapiens 95-101 24379584-10 2013 Consistent with this observation, mesalazine and azathioprine induced, in primary fibroblasts, IL10RB and TNFRII over-expression and TNFRI and TNFalpha under-expression. Mesalamine 34-44 TNF receptor superfamily member 1B Homo sapiens 106-112 24379584-10 2013 Consistent with this observation, mesalazine and azathioprine induced, in primary fibroblasts, IL10RB and TNFRII over-expression and TNFRI and TNFalpha under-expression. Mesalamine 34-44 TNF receptor superfamily member 1A Homo sapiens 106-111 24379584-10 2013 Consistent with this observation, mesalazine and azathioprine induced, in primary fibroblasts, IL10RB and TNFRII over-expression and TNFRI and TNFalpha under-expression. Mesalamine 34-44 tumor necrosis factor Homo sapiens 143-151 23832232-0 2013 Novel solid-phase extractor based on functionalization of multi-walled carbon nano tubes with 5-aminosalicylic acid for preconcentration of Pb(II) in water samples prior to determination by ICP-OES. Mesalamine 94-115 submaxillary gland androgen regulated protein 3B Homo sapiens 140-146 23832232-3 2013 Batch experiments were conducted as a function of pH to explore MWCNTs-5-ASA efficiency to extract several metal ions viz., Cr(III), Fe(III), Co(II), Ni(II), Cu(II), Zn(II), Cd(II) and Pb(II). Mesalamine 71-76 submaxillary gland androgen regulated protein 3B Homo sapiens 185-191 23843037-0 2013 The 5-aminosalicylic acid antineoplastic effect in the intestine is mediated by PPARgamma. Mesalamine 4-25 peroxisome proliferator activated receptor gamma Homo sapiens 80-89 23843037-2 2013 Our aim is to investigate whether peroxisome proliferator-activated receptor-gamma (PPARgamma) mediates the antineoplastic effects of 5-ASA. Mesalamine 134-139 peroxisome proliferator activated receptor gamma Homo sapiens 34-82 23843037-2 2013 Our aim is to investigate whether peroxisome proliferator-activated receptor-gamma (PPARgamma) mediates the antineoplastic effects of 5-ASA. Mesalamine 134-139 peroxisome proliferator activated receptor gamma Homo sapiens 84-93 23843037-12 2013 In conclusion, 5-ASA exerts potent antineoplastic effects that are mediated through PPARgamma. Mesalamine 15-20 peroxisome proliferator activated receptor gamma Homo sapiens 84-93 23651165-8 2013 By the demonstration that the anti-inflammatory effects of 5- aminosalicylic acid (5-ASA) in patients with ulcerative colitis were mediated by PPARgamma activation, several molecules having 5-ASA similarities have been developed and screened leading to the selection of a aminophenyl-alpha-methoxypropionic acids named GED-0507-34-Levo (GED). Mesalamine 59-81 peroxisome proliferator activated receptor gamma Homo sapiens 143-152 23651165-8 2013 By the demonstration that the anti-inflammatory effects of 5- aminosalicylic acid (5-ASA) in patients with ulcerative colitis were mediated by PPARgamma activation, several molecules having 5-ASA similarities have been developed and screened leading to the selection of a aminophenyl-alpha-methoxypropionic acids named GED-0507-34-Levo (GED). Mesalamine 83-88 peroxisome proliferator activated receptor gamma Homo sapiens 143-152 23651165-8 2013 By the demonstration that the anti-inflammatory effects of 5- aminosalicylic acid (5-ASA) in patients with ulcerative colitis were mediated by PPARgamma activation, several molecules having 5-ASA similarities have been developed and screened leading to the selection of a aminophenyl-alpha-methoxypropionic acids named GED-0507-34-Levo (GED). Mesalamine 190-195 peroxisome proliferator activated receptor gamma Homo sapiens 143-152 23651165-9 2013 This compound activating PPARgamma has 100-to 150-fold higher anti-inflammatory activity than 5-ASA. Mesalamine 94-99 peroxisome proliferator activated receptor gamma Homo sapiens 25-34 23529546-6 2013 The presence of 5-ASA at 0.1 and 1.0 mM was found to significantly inhibit SIN-1-induced DNA strand breaks in a concentration-dependent manner. Mesalamine 16-21 MAPK associated protein 1 Homo sapiens 75-80 23732799-1 2013 In the present study, hydroxypropyl methyl cellulose grafted with polyacrylamide (HPMC-g-PAM) hydrogel was evaluated in vitro as a potential carrier for controlled release of 5-amino salicylic acid (5-ASA). Mesalamine 175-197 peptidylglycine alpha-amidating monooxygenase Homo sapiens 89-92 23867870-0 2013 Antioxidant properties of mesalamine in colitis inhibit phosphoinositide 3-kinase signaling in progenitor cells. Mesalamine 26-36 phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit gamma Homo sapiens 56-81 23867870-1 2013 BACKGROUND: Mesalamine, 5-aminosalicylic acid (5-ASA), is a potent antioxidant and is known to enhance peroxisome proliferator-activated receptor gamma activity in the intestine. Mesalamine 12-22 peroxisome proliferator activated receptor gamma Homo sapiens 103-151 23867870-1 2013 BACKGROUND: Mesalamine, 5-aminosalicylic acid (5-ASA), is a potent antioxidant and is known to enhance peroxisome proliferator-activated receptor gamma activity in the intestine. Mesalamine 24-45 peroxisome proliferator activated receptor gamma Homo sapiens 103-151 23867870-1 2013 BACKGROUND: Mesalamine, 5-aminosalicylic acid (5-ASA), is a potent antioxidant and is known to enhance peroxisome proliferator-activated receptor gamma activity in the intestine. Mesalamine 47-52 peroxisome proliferator activated receptor gamma Homo sapiens 103-151 23867870-2 2013 Our previous studies suggested reduced Phosphoinositide 3-Kinase (PI3K)/beta-catenin signaling as a mechanism for 5-ASA chemoprevention in chronic ulcerative colitis (CUC). Mesalamine 114-119 phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit gamma Homo sapiens 39-64 23867870-2 2013 Our previous studies suggested reduced Phosphoinositide 3-Kinase (PI3K)/beta-catenin signaling as a mechanism for 5-ASA chemoprevention in chronic ulcerative colitis (CUC). Mesalamine 114-119 catenin beta 1 Homo sapiens 72-84 23867870-3 2013 We now hypothesize that 5-ASA mediates changes in intestinal epithelial cell (IEC) reactive oxygen species during colitis to affect phosphatase and tensin homolog (PTEN), PI3K, and beta-catenin signaling. Mesalamine 24-29 phosphatase and tensin homolog Homo sapiens 164-168 23867870-3 2013 We now hypothesize that 5-ASA mediates changes in intestinal epithelial cell (IEC) reactive oxygen species during colitis to affect phosphatase and tensin homolog (PTEN), PI3K, and beta-catenin signaling. Mesalamine 24-29 catenin beta 1 Homo sapiens 181-193 23867870-8 2013 Also, 5-ASA increased nuclear peroxisome proliferator-activated receptor gamma protein and target gene expression. Mesalamine 6-11 peroxisome proliferator activated receptor gamma Homo sapiens 30-78 23867870-9 2013 Data showed 5-ASA-induced peroxisome proliferator-activated receptor gamma DNA binding to the PTEN promoter (chromatin immunoprecipitation) and reduced both phosphorylated and oxidized (inactive) PTEN protein levels. Mesalamine 12-17 peroxisome proliferator activated receptor gamma Homo sapiens 26-74 23867870-9 2013 Data showed 5-ASA-induced peroxisome proliferator-activated receptor gamma DNA binding to the PTEN promoter (chromatin immunoprecipitation) and reduced both phosphorylated and oxidized (inactive) PTEN protein levels. Mesalamine 12-17 phosphatase and tensin homolog Homo sapiens 94-98 23867870-9 2013 Data showed 5-ASA-induced peroxisome proliferator-activated receptor gamma DNA binding to the PTEN promoter (chromatin immunoprecipitation) and reduced both phosphorylated and oxidized (inactive) PTEN protein levels. Mesalamine 12-17 phosphatase and tensin homolog Homo sapiens 196-200 23867870-10 2013 Analysis of patient samples revealed 5-ASA that also reduced levels of active phosphorylated Akt in inflamed colitis tissue. Mesalamine 37-42 AKT serine/threonine kinase 1 Homo sapiens 93-96 23867870-11 2013 Reduced PI3K/Akt signaling and expression of beta-catenin target genes in 5-ASA-treated CUC patients additionally suggests enhanced PTEN activity as well. Mesalamine 74-79 AKT serine/threonine kinase 1 Homo sapiens 13-16 23867870-11 2013 Reduced PI3K/Akt signaling and expression of beta-catenin target genes in 5-ASA-treated CUC patients additionally suggests enhanced PTEN activity as well. Mesalamine 74-79 catenin beta 1 Homo sapiens 45-57 23867870-11 2013 Reduced PI3K/Akt signaling and expression of beta-catenin target genes in 5-ASA-treated CUC patients additionally suggests enhanced PTEN activity as well. Mesalamine 74-79 phosphatase and tensin homolog Homo sapiens 132-136 23867870-12 2013 CONCLUSIONS: Therefore, 5-ASA reduces CUC-induced reactive oxygen species in colonic progenitor cells and enhances PTEN activity, thus attenuating PI3K/Akt signaling. Mesalamine 24-29 phosphatase and tensin homolog Homo sapiens 115-119 23867870-12 2013 CONCLUSIONS: Therefore, 5-ASA reduces CUC-induced reactive oxygen species in colonic progenitor cells and enhances PTEN activity, thus attenuating PI3K/Akt signaling. Mesalamine 24-29 AKT serine/threonine kinase 1 Homo sapiens 152-155 22841543-10 2013 5-ASA also reduces mRNA levels of tumor necrosis factor alpha (P<.05). Mesalamine 0-5 tumor necrosis factor Rattus norvegicus 34-61 22841543-12 2013 The dual therapy n-3 PUFA plus 5-ASA also inhibited inflammatory response by lowering NF-kappaB activation (P<.01) or inducing peroxisome proliferator-activated receptor-gamma (PPARgamma) expression (P<.05). Mesalamine 31-36 peroxisome proliferator-activated receptor gamma Rattus norvegicus 130-178 22841543-12 2013 The dual therapy n-3 PUFA plus 5-ASA also inhibited inflammatory response by lowering NF-kappaB activation (P<.01) or inducing peroxisome proliferator-activated receptor-gamma (PPARgamma) expression (P<.05). Mesalamine 31-36 peroxisome proliferator-activated receptor gamma Rattus norvegicus 180-189 22841543-13 2013 These results indicate that 5-ASA plus n-3 PUFAs are more effective than a higher dose of 5-ASA alone to reduce NF-kappaB activation and to induce PPARgamma. Mesalamine 28-33 peroxisome proliferator-activated receptor gamma Rattus norvegicus 147-156 22841543-13 2013 These results indicate that 5-ASA plus n-3 PUFAs are more effective than a higher dose of 5-ASA alone to reduce NF-kappaB activation and to induce PPARgamma. Mesalamine 90-95 peroxisome proliferator-activated receptor gamma Rattus norvegicus 147-156 24039842-6 2013 Interestingly, cyanidin-3-glucoside and 5-aminosalicylic acid neither prevented IkB-alpha degradation nor the activation of NF-kB, but significantly reduced cytokine-induced levels of activated STAT1 accumulated in the cell nucleus. Mesalamine 40-61 NFKB inhibitor alpha Homo sapiens 80-89 24039842-6 2013 Interestingly, cyanidin-3-glucoside and 5-aminosalicylic acid neither prevented IkB-alpha degradation nor the activation of NF-kB, but significantly reduced cytokine-induced levels of activated STAT1 accumulated in the cell nucleus. Mesalamine 40-61 signal transducer and activator of transcription 1 Homo sapiens 194-199 23640018-0 2013 Novel NaCS-CS-PPS microcapsules as a potential enzyme-triggered release carrier for highly-loading 5-ASA. Mesalamine 99-104 inositol polyphosphate-5-phosphatase K Homo sapiens 14-17 24030235-5 2013 A systematic review including 48 studies linked 5-ASA chemopreventive properties to five distinct pathways: cell cycle progression, scavenging of reactive oxygen- or nitrogen-derived metabolites, TNF-alpha/TGF-ss signaling, WNT/beta-catenin signaling and antibacterial properties. Mesalamine 48-53 catenin beta 1 Homo sapiens 228-240 22937971-0 2013 Design, synthesis, and evaluation of novel cyclic phosphates of 5-aminosalicylic acid as cytochrome p450-activated prodrugs. Mesalamine 64-85 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 89-104 22937971-1 2013 Four novel cyclic phosphates of the anti-inflammatory agent 5-aminosalicylic acid (5-ASA) were designed and synthesized as cytochrome P450 (CYP)-activated prodrugs. Mesalamine 60-81 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 123-138 22937971-1 2013 Four novel cyclic phosphates of the anti-inflammatory agent 5-aminosalicylic acid (5-ASA) were designed and synthesized as cytochrome P450 (CYP)-activated prodrugs. Mesalamine 60-81 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 140-143 22937971-1 2013 Four novel cyclic phosphates of the anti-inflammatory agent 5-aminosalicylic acid (5-ASA) were designed and synthesized as cytochrome P450 (CYP)-activated prodrugs. Mesalamine 83-88 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 123-138 22937971-1 2013 Four novel cyclic phosphates of the anti-inflammatory agent 5-aminosalicylic acid (5-ASA) were designed and synthesized as cytochrome P450 (CYP)-activated prodrugs. Mesalamine 83-88 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 140-143 23146664-5 2013 Filtering and analysis of data identified three oncogenic pathways interfered by 5-ASA: MAPK/ERK pathway, cell adhesion and beta-catenin/Wnt signaling. Mesalamine 81-86 catenin beta 1 Homo sapiens 124-136 23146664-6 2013 PAK1 emerged as a consensus target of 5-ASA, orchestrating these pathways. Mesalamine 38-43 p21 (RAC1) activated kinase 1 Homo sapiens 0-4 23146664-9 2013 Moreover, 5-ASA treatment restored membranous expression of adhesion molecules E-cadherin and beta-catenin. Mesalamine 10-15 cadherin 1 Homo sapiens 79-89 23146664-9 2013 Moreover, 5-ASA treatment restored membranous expression of adhesion molecules E-cadherin and beta-catenin. Mesalamine 10-15 catenin beta 1 Homo sapiens 94-106 23146664-10 2013 Role of PAK1 as a mediator of mesalamine activity was validated in vitro and in vivo. Mesalamine 30-40 p21 (RAC1) activated kinase 1 Homo sapiens 8-12 23146664-13 2013 Our data demonstrates novel pharmacological mechanism of mesalamine in modulation of cell adhesion and role of PAK1 in APC(min) polyposis. Mesalamine 57-67 p21 (RAC1) activated kinase 1 Homo sapiens 111-115 23146664-14 2013 We propose that inhibition of PAK1 expression by 5-ASA can impede with neoplastic progression in colorectal carcinogenesis. Mesalamine 49-54 p21 (RAC1) activated kinase 1 Homo sapiens 30-34 23146664-15 2013 The mechanism of PAK1 inhibition and induction of membranous translocation of adhesion proteins by 5-ASA might be independent of its known anti-inflammatory action. Mesalamine 99-104 p21 (RAC1) activated kinase 1 Homo sapiens 17-21 22187071-11 2012 CONCLUSION: 5-ASA interferes with proliferation of colorectal cancer cells via inhibition of PLD-dependent generation of PA and loss of mTOR signalling. Mesalamine 12-17 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 93-96 22187071-11 2012 CONCLUSION: 5-ASA interferes with proliferation of colorectal cancer cells via inhibition of PLD-dependent generation of PA and loss of mTOR signalling. Mesalamine 12-17 mechanistic target of rapamycin kinase Homo sapiens 136-140 22772914-14 2012 Compared with the model group, the expression of NF-kappa Bp65 was significantly decreased in the mesalazine group (P<0.01) and oxymatrine treatment group (P<0.01) while the expressions of beta2AR and beta-arrestin2 were significantly increased (P<0.01). Mesalamine 98-108 adrenoceptor beta 2 Rattus norvegicus 195-202 22187071-0 2012 5-Aminosalicylic acid inhibits cell cycle progression in a phospholipase D dependent manner in colorectal cancer. Mesalamine 0-21 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 59-74 22187071-4 2012 METHODS: The influence of 5-ASA on mTOR signalling was examined in a panel of colorectal cancer cell lines. Mesalamine 26-31 mechanistic target of rapamycin kinase Homo sapiens 35-39 22187071-5 2012 The effects of 5-ASA on the pathways that control mTOR activity were studied in detail in two different colorectal cancer cell lines, using western blot, siRNA, a phospholipase D (PLD) activity assay, proliferation assays and cell cycle analysis. Mesalamine 15-20 mechanistic target of rapamycin kinase Homo sapiens 50-54 22187071-6 2012 The phosphorylation status of mTOR and its downstream target, ribosomal protein S6, was studied in colorectal cancers before and after topical 5-ASA treatment. Mesalamine 143-148 mechanistic target of rapamycin kinase Homo sapiens 30-34 22187071-7 2012 RESULTS: Treatment of colorectal cancer with 5-ASA inhibited mTOR signalling in vitro and in vivo. Mesalamine 45-50 mechanistic target of rapamycin kinase Homo sapiens 61-65 22187071-10 2012 5-ASA treatment inhibited PLD activity and proliferation; these effects could be rescued with exogenous PA. Mesalamine 0-5 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 26-29 23076889-1 2012 BACKGROUND: Oral 5-aminosalicylic acid (5-ASA) preparations were intended to avoid the adverse effects of sulfasalazine (SASP) while maintaining its therapeutic benefits. Mesalamine 17-38 aspartic peptidase retroviral like 1 Homo sapiens 121-125 23076889-1 2012 BACKGROUND: Oral 5-aminosalicylic acid (5-ASA) preparations were intended to avoid the adverse effects of sulfasalazine (SASP) while maintaining its therapeutic benefits. Mesalamine 40-45 aspartic peptidase retroviral like 1 Homo sapiens 121-125 22772914-14 2012 Compared with the model group, the expression of NF-kappa Bp65 was significantly decreased in the mesalazine group (P<0.01) and oxymatrine treatment group (P<0.01) while the expressions of beta2AR and beta-arrestin2 were significantly increased (P<0.01). Mesalamine 98-108 arrestin, beta 2, pseudogene Rattus norvegicus 207-221 22493349-0 2012 5-aminosalicylic acid mediates expression of cyclooxygenase-2 and 15-hydroxyprostaglandin dehydrogenase to suppress colorectal tumorigenesis. Mesalamine 0-21 prostaglandin-endoperoxide synthase 2 Mus musculus 45-61 22493349-0 2012 5-aminosalicylic acid mediates expression of cyclooxygenase-2 and 15-hydroxyprostaglandin dehydrogenase to suppress colorectal tumorigenesis. Mesalamine 0-21 hydroxyprostaglandin dehydrogenase 15 (NAD) Mus musculus 66-103 22493349-3 2012 Here we determined the effect of 5-aminosalicylic acid (5-ASA) on COX-2 and 15-PGDH expression and investigated its preventive effect for colorectal cancer (CRC). Mesalamine 33-54 prostaglandin-endoperoxide synthase 2 Mus musculus 66-71 22493349-3 2012 Here we determined the effect of 5-aminosalicylic acid (5-ASA) on COX-2 and 15-PGDH expression and investigated its preventive effect for colorectal cancer (CRC). Mesalamine 33-54 hydroxyprostaglandin dehydrogenase 15 (NAD) Mus musculus 76-83 22493349-3 2012 Here we determined the effect of 5-aminosalicylic acid (5-ASA) on COX-2 and 15-PGDH expression and investigated its preventive effect for colorectal cancer (CRC). Mesalamine 56-61 prostaglandin-endoperoxide synthase 2 Mus musculus 66-71 22493349-3 2012 Here we determined the effect of 5-aminosalicylic acid (5-ASA) on COX-2 and 15-PGDH expression and investigated its preventive effect for colorectal cancer (CRC). Mesalamine 56-61 hydroxyprostaglandin dehydrogenase 15 (NAD) Mus musculus 76-83 22493349-7 2012 RESULTS: 5-ASA significantly suppressed COX-2 expression and induced 15-PGDH expression in HT-29 cells. Mesalamine 9-14 prostaglandin-endoperoxide synthase 2 Mus musculus 40-45 22493349-7 2012 RESULTS: 5-ASA significantly suppressed COX-2 expression and induced 15-PGDH expression in HT-29 cells. Mesalamine 9-14 15-hydroxyprostaglandin dehydrogenase Homo sapiens 69-76 22493349-10 2012 CONCLUSION: 5-ASA exerts a preventive effect against colorectal tumor development through mediation of COX-2 and 15-PGDH expression. Mesalamine 12-17 prostaglandin-endoperoxide synthase 2 Mus musculus 103-108 22493349-10 2012 CONCLUSION: 5-ASA exerts a preventive effect against colorectal tumor development through mediation of COX-2 and 15-PGDH expression. Mesalamine 12-17 hydroxyprostaglandin dehydrogenase 15 (NAD) Mus musculus 113-120 22198215-0 2012 The influence of 5-aminosalicylic acid on the progression of colorectal adenomas via the beta-catenin signaling pathway. Mesalamine 17-38 catenin beta 1 Homo sapiens 89-101 20923254-1 2012 Novel "beads-in-a-tablet" formulations (total weight ~740-780 mg) have been prepared that meet USP 31 requirements for Delayed Release of mesalamine. Mesalamine 138-148 ubiquitin specific peptidase 31 Homo sapiens 95-101 22662201-9 2012 NAE-PPARalpha signaling system is impaired during active UC and 5-ASA/glucocorticoids treatment restored its normal expression. Mesalamine 64-69 peroxisome proliferator activated receptor alpha Homo sapiens 4-13 22662201-10 2012 Since 5-ASA actions may work through PPARalpha and glucocorticoids through NAE-producing/degrading enzymes, the use of PPARalpha agonists or FAAH/NAAA blockers that increases endogenous PPARalpha ligands may yield similar therapeutics advantages. Mesalamine 6-11 peroxisome proliferator activated receptor alpha Homo sapiens 37-46 22662201-10 2012 Since 5-ASA actions may work through PPARalpha and glucocorticoids through NAE-producing/degrading enzymes, the use of PPARalpha agonists or FAAH/NAAA blockers that increases endogenous PPARalpha ligands may yield similar therapeutics advantages. Mesalamine 6-11 peroxisome proliferator activated receptor alpha Homo sapiens 119-128 22412841-9 2012 However, 5-aminosalicylic acid (5-ASA) inhibited 5-FU-induced NF-kappaB activation and proinflammatory cytokine production. Mesalamine 9-30 nuclear factor kappa B subunit 1 Homo sapiens 62-71 22412841-9 2012 However, 5-aminosalicylic acid (5-ASA) inhibited 5-FU-induced NF-kappaB activation and proinflammatory cytokine production. Mesalamine 32-37 nuclear factor kappa B subunit 1 Homo sapiens 62-71 21441812-6 2011 Amelioration of symptoms was associated with reduction of both inflammation and Hsp60, a reduction that was most marked in the group treated with 5-ASA and probiotics. Mesalamine 146-151 heat shock protein family D (Hsp60) member 1 Homo sapiens 80-85 22888278-7 2012 Mesalamine with Multi-Matrix System( ) (MMX) technology (Cosmo SpA, Milan, Italy) is an oral (1.2 g), once-daily tablet formulation of mesalamine used for the treatment of UC (Lialda( ) or Mezavant( ), Shire Pharmaceuticals Inc, Wayne, PA). Mesalamine 0-10 surfactant protein A2 Homo sapiens 63-66 22754377-0 2012 A novel preparation method for 5-aminosalicylic acid loaded Eudragit S100 nanoparticles. Mesalamine 31-52 S100 calcium binding protein A1 Homo sapiens 69-73 22754377-1 2012 In this study, solution enhanced dispersion by supercritical fluids (SEDS) technique was applied for the preparation of 5-aminosalicylic acid (5-ASA) loaded Eudragit S100 (EU S100) nanoparticles. Mesalamine 120-141 S100 calcium binding protein A1 Homo sapiens 166-170 22754377-1 2012 In this study, solution enhanced dispersion by supercritical fluids (SEDS) technique was applied for the preparation of 5-aminosalicylic acid (5-ASA) loaded Eudragit S100 (EU S100) nanoparticles. Mesalamine 120-141 S100 calcium binding protein A1 Homo sapiens 175-179 22754377-1 2012 In this study, solution enhanced dispersion by supercritical fluids (SEDS) technique was applied for the preparation of 5-aminosalicylic acid (5-ASA) loaded Eudragit S100 (EU S100) nanoparticles. Mesalamine 143-148 S100 calcium binding protein A1 Homo sapiens 166-170 22754377-1 2012 In this study, solution enhanced dispersion by supercritical fluids (SEDS) technique was applied for the preparation of 5-aminosalicylic acid (5-ASA) loaded Eudragit S100 (EU S100) nanoparticles. Mesalamine 143-148 S100 calcium binding protein A1 Homo sapiens 175-179 22754377-5 2012 The results showed that 5-ASA was imbedded into EU S100 in an amorphous state after SEDS processing and the SEDS process did not induce degradation of 5-ASA. Mesalamine 24-29 S100 calcium binding protein A1 Homo sapiens 51-55 24349903-3 2012 The use of 2,5-DHB and 5-ASA leads to "hydrogen-abundant" peptide radicals and subsequent radical-induced N-Calpha bonds cleavage. Mesalamine 23-28 CEA cell adhesion molecule 6 Homo sapiens 106-114 22662201-10 2012 Since 5-ASA actions may work through PPARalpha and glucocorticoids through NAE-producing/degrading enzymes, the use of PPARalpha agonists or FAAH/NAAA blockers that increases endogenous PPARalpha ligands may yield similar therapeutics advantages. Mesalamine 6-11 fatty acid amide hydrolase Homo sapiens 141-145 22662201-10 2012 Since 5-ASA actions may work through PPARalpha and glucocorticoids through NAE-producing/degrading enzymes, the use of PPARalpha agonists or FAAH/NAAA blockers that increases endogenous PPARalpha ligands may yield similar therapeutics advantages. Mesalamine 6-11 peroxisome proliferator activated receptor alpha Homo sapiens 119-128