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Interleukin 6 inhibition by triptolide prevents inflammation in a mouse model of ulcerative colitis
Haifeng Zhang1,2, Weichang Chen1
1Department of Gastroenterology, The First Affiliated Hospital of Soochow University, Soochow, Jiangsu 215006, P.R. China.
The present study aimed to assess interleukin (IL)-6 expression in a murine model of ulcerative colitis (UC) induced by dextran sulfate sodium (DSS) and its potential association with the anti-colitis effects of triptolide (TL). Serum IL-6 levels were measured by ELISA. IL-6 gene expression levels in colonic mucosa specimens were assessed by reverse-transcription quantitative PCR and protein expression was evaluated by western blot analysis and immunohistochemistry. The expression of IL-6 was weak in mucosa specimens from normal control animals and upregulated in DSS-induced mice. 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. There was no significant difference among TL (0.4 mg/kg and 0.6 mg/kg), mesalazine and dexamethasone treatments (P>0.05) in terms of IL-6 expression or histological score. The results of the present study indicated that IL-6 was overexpressed in a mouse model of UC and was involved in disease progression. In addition, TL exerted therapeutic effects in UC through inhibition of IL-6 expression.
The present study aimed to assess interleukin (IL)-6 expression in a murine model of ulcerative colitis (UC) induced by dextran sulfate sodium (DSS) and its potential association with the anti-colitis effects of triptolide (TL). Serum IL-6 levels were measured by ELISA. IL-6 gene expression levels in colonic mucosa specimens were assessed by reverse-transcription quantitative PCR and protein expression was evaluated by western blot analysis and immunohistochemistry. The expression of IL-6 was weak in mucosa specimens from normal control animals and upregulated in DSS-induced mice. 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. There was no significant difference among TL (0.4 mg/kg and 0.6 mg/kg), mesalazine and dexamethasone treatments (P>0.05) in terms of IL-6 expression or histological score. The results of the present study indicated that IL-6 was overexpressed in a mouse model of UC and was involved in disease progression. In addition, TL exerted therapeutic effects in UC through inhibition of IL-6 expression.
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