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[Rosiglitazone ameliorates TNBS-induced colitis in mice by inhibiting inflammation of the mesenteric adipose tissues].

Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi; 34(9): 787-793, 2018 Sep.
Artigo em Chinês | MEDLINE | ID: mdl-30463649
Objective To evaluate the therapeutic effect and possible mechanism of PPARγ agonist rosiglitazone on 2, 4, 6-trinitrobenzenesulfonic acid (TNBS)-induced colitis in mice. Methods Twenty male BALB/c mice were selected to establish TNBS-induced colitis model and were randomly divided into rosiglitazone treated group and model group with 10 rats in each group. Rosiglitazone group was treated with rosiglitazone(0.2 mL, [20 mg/(kg.d)])and model group with normal saline(0.2 mL/d). After 6 weeks of administration, the mice were sacrificed. Inflammatory bowel disease disease activity index (DAI) and HE staining combined with Spencer colitis histological score were used to evaluate the degree of intestinal inflammation and histological changes in the two groups. ELISA was used to detect the levels of interleukin-1ß (IL-1ß), tumor necrosis factor alpha(TNF-α) and IL-10 in the intestinal mucosa, the levels of IL-6 and monocyte chemoattractant protein 1 (MCP-1) in the mesenteric adipose tissues. The mean diameter of adipocytes in the mesenteric adipose tissues was calculated under light microscope after HE staining.The number of F4/80 macrophages and the expressions of peripherin, adiponectin and leptin in mesenteric adipose tissues were detected by immunohistochemical staining. The phosphorylation of NF-κBp65, IKK, IκB proteins in the mesenteric adipose tissues was detected by Western blot analysis. Results The DAI score of rosiglitazone group was significantly lower than that of model group at 5 and 6 weeks after rosiglitazone treatment. At the same time, the levels of IL-1ß and TNF-α in the intestinal mucosa of the treated group were significantly lower than those in the model group, while the IL-10 levels were significantly higher in the treated group than in the model group. Compared with the model group, the mesenteric adipocyte diameter and the perilipin level of adipocyte maturation markers in rosiglitazone treated mice were significantly higher than those in model group. Meanwhile, the number of infiltration of macrophages in mesenteric adipose tissues of mice treated with rosiglitazone and the levels of inflammatory mediators IL-6 and MCP-1 were significantly lower than that of the model group. Rosiglitazone significantly promoted the expression of adiponectin and inhibited the expression of leptin in mesenteric adipocytes. The phosphorylation of NF-κBp65, IKK and IκB proteins in mesenteric adipose tissues of rosiglitazone treated mice was significantly lower than those of model group. Conclusion Rosiglitazone significantly inhibites intestinal inflammation in TNBS-induced colitis in mice, which may be related to the inhibition of NF-κBp65 pathway in mesenteric adipose tissues.