Tripterygium Glycosides Protects Mice against Colonic Inflammation by Inhibiting TLR4/NF-κB Signaling Pathway
10.3969/j.issn.1008-7125.2015.10.007
- VernacularTitle:雷公藤多苷通过抑制 TLR4/NF-κB信号通路抑制小鼠结肠炎症
- Author:
Ling ZHU
;
Jun ZHOU
;
Haijun CAO
;
Jihong ZHONG
;
Jun LIU
;
Huajun HU
;
Shangao LI
- Publication Type:Journal Article
- Keywords:
Tripterygium Glycosides;
Colitis,Ulcerative;
Toll-Like Receptor 4;
NF-kappa B
- From:
Chinese Journal of Gastroenterology
2015;(10):606-611
- CountryChina
- Language:Chinese
-
Abstract:
Background:Tripterygium glycosides(TG)is effective for treatment of ulcerative colitis(UC)in clinical practice, however,the underlying mechanism has not been clarified yet. Aims:To investigate the therapeutic effect of TG on dextran sulfate sodium(DSS)-induced experimental colitis in mice and its possible mechanisms. Methods:Sixty healthy male BALB/ c mice were randomly divided into six groups:model control group,low,medium and high-dose TG group,blank control group and normal control group. Mice in the first four groups drank 5% DSS freely for 7 days to induce experimental colitis;simultaneously,distilled water,9. 01,27. 03 or 81. 09 mg/(kg·d)TG were given intragastrically for 21 days in these four groups,respectively. Histopathological changes of colonic mucosal tissues were observed;expressions of TLR4 mRNA and protein were determined by RT-PCR and Western blotting;expression of NF-κB p65 was detected by immunohistochemistry;concentrations of IL-1α,TNF-α and IL-13 were measured by ELISA. Results:Tissue damage and inflammation in varying degrees were observed in colonic mucosal tissues in TG groups with different dosage,but all were less severe than those in model control group. Expressions of TLR4 mRNA,TLR4 protein,and NF-κB p65 in colonic mucosal tissues,as well as concentrations of IL-1α and TNF-α in supernatant of colonic homogenate were significantly lower in TG groups than those in model control group(P < 0. 01). These parameters in medium and high-dose TG groups were significantly lower than those in low-dose TG group(P < 0. 05),but higher than those in blank control group and normal control group(P < 0. 05). Except for TNF-α,no significant differences were seen between medium and high-dose TG groups(P > 0. 05). Conclusions:TG exerts a protective effect on DSS-induced experimental colitis in mice. The underlying mechanism of its anti-inflammatory effect might be related with the inhibition of TLR4 / NF-κB signaling pathway activation and subsequently suppressing downstream proinflammatory cytokines expression and secretion.
