PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 28619075-10 2017 Further, the CAS treatment also significantly suppressed the mRNA and protein levels of pro-inflammatory cytokines, namely interleukin-1beta and tumor necrosis factor-alpha while enhancing the level of anti-inflammatory cytokine IL-10 in the TNBS-treated rats. Trinitrobenzenesulfonic Acid 242-246 interleukin 10 Rattus norvegicus 229-234 30735453-8 2019 Chronic TNBS induced 1) a visceral hypersensitivity (P = 0.03), 2) an increased colon weight-to-length ratio (P = 0.01), 3) higher inflammatory and fibrosis scores (P = 0.0390 and P = 0.0016, respectively), and 4) a higher colonic IL-6 and IL-10 production (P = 0.008 and P = 0.005, respectively) compared with control rats. Trinitrobenzenesulfonic Acid 8-12 interleukin 10 Rattus norvegicus 240-245 27478078-10 2016 Similar results were obtained in TNBS-induced colitis at 24 h. Intestinal IL-10 mRNA expression significantly decreased at 12 h and then increased by 6-43 times (p<0.05 to p<0.001) 48h after IA administration. Trinitrobenzenesulfonic Acid 33-37 interleukin 10 Rattus norvegicus 74-79 27822176-10 2016 Up-regulated mRNA expression of TNF-alpha, IL-1beta, IL-6, COX-2, and iNOs, as well as down-regulated IL-10 mRNA expressions after TNBS administration, were significantly inhibited by FA (20 and 40 mg/kg) treatment. Trinitrobenzenesulfonic Acid 131-135 interleukin 10 Rattus norvegicus 102-107 27478078-12 2016 In the TNBS group, there was 4-12- and 4-7-fold increases in small intestinal IL-10 mRNA expression at 1 and 21 days after colitis induction, respectively (both p<0.01). Trinitrobenzenesulfonic Acid 7-11 interleukin 10 Rattus norvegicus 78-83 26019800-7 2015 RESULTS: The results showed that the oral RJ treatment inhibited proinflammatory cytokines, IL-1beta and TNF-alpha secretion, while increasing anti-inflammatory cytokine IL-10 production in the TNBS-induced colitis+RJ group compared with the colitis group not treated with RJ. Trinitrobenzenesulfonic Acid 194-198 interleukin 10 Rattus norvegicus 170-175 24931258-25 2014 In the TNBS model group, the IL-10 expression peaked later than in the thalidomide treatment group. Trinitrobenzenesulfonic Acid 7-11 interleukin 10 Rattus norvegicus 29-34 17517520-2 2007 This study describes the changes in the expression of nerve growth factor (NGF) and interleukin-10 (IL-10) in the colon and in various segments of the small intestine in two rat models of experimental colitis induced by iodoacetamide or 2,4,6-trinitrobenzene sulfonic acid (TNBS). Trinitrobenzenesulfonic Acid 237-272 interleukin 10 Rattus norvegicus 100-105 22234755-5 2011 The relief of trinitrobenzene sulfonic acid-induced colitis was accompanied by significantly decreased production of tumor necrosis factor-alpha in both serum and intra-colon (p<0.05) and by significantly increased production of interleukin-10 in both serum and intra-colon (p<0.05). Trinitrobenzenesulfonic Acid 14-43 interleukin 10 Rattus norvegicus 232-246 17517520-2 2007 This study describes the changes in the expression of nerve growth factor (NGF) and interleukin-10 (IL-10) in the colon and in various segments of the small intestine in two rat models of experimental colitis induced by iodoacetamide or 2,4,6-trinitrobenzene sulfonic acid (TNBS). Trinitrobenzenesulfonic Acid 274-278 interleukin 10 Rattus norvegicus 100-105 17517520-4 2007 NGF and IL-10 increased significantly in homogenates of strips isolated from all small intestinal segments, 3-6h after iodoacetamide or TNBS administration and remained elevated until the colonic inflammation subsided. Trinitrobenzenesulfonic Acid 136-140 interleukin 10 Rattus norvegicus 8-13 20469967-0 2010 Exosomes derived from interleukin-10-treated dendritic cells can inhibit trinitrobenzene sulfonic acid-induced rat colitis. Trinitrobenzenesulfonic Acid 73-102 interleukin 10 Rattus norvegicus 22-36 20469967-3 2010 Based on the essential role of IL-10 in the development of normal mucosal immunity, we investigated whether exosomes derived from DCs treated with IL-10 (known as IL-10-exosomes) can suppress the trinitrobenzene sulfonic acid (TNBS)-induced colitis. Trinitrobenzenesulfonic Acid 196-225 interleukin 10 Rattus norvegicus 163-177 20469967-3 2010 Based on the essential role of IL-10 in the development of normal mucosal immunity, we investigated whether exosomes derived from DCs treated with IL-10 (known as IL-10-exosomes) can suppress the trinitrobenzene sulfonic acid (TNBS)-induced colitis. Trinitrobenzenesulfonic Acid 227-231 interleukin 10 Rattus norvegicus 163-177