Effect of Huangqin Tang on the function of regulatory TLR4/MyD88 signal pathway in rats with ulcerative colitis
10.16438/j.0513-4870.2016-0480
- VernacularTitle:黄芩汤对溃疡性结肠炎大鼠TLR4/MyD88通路调控作用研究
- Author:
Dun-fang WANG
1
;
Yan-li WANG
1
;
Yi-wei WANG
1
;
Shan-shan GUO
1
;
Shuai-xing ZHUANG
1
;
Hang-yu XU
1
;
Tao LI
2
;
Wei-peng YANG
1
Author Information
1. Institute of Chinese Materia Medica, China Academy of Chinese Medical Sciences, Beijing 100700, China
2. The Experimental Research Center, China Academy of Chinese Medical Sciences, Beijing 100700, China
- Publication Type:ORIGINAL ARTICLES
- Keywords:
Huangqin Tang;
ulcerative colitis;
TLR4;
MyD88;
cytokine
- From:
Acta Pharmaceutica Sinica
2016;51(10):1558-
- CountryChina
- Language:Chinese
-
Abstract:
This study was designed to investigate the effect of Huangqin Tang (HQT) on TLR4/Myd88 pathway and the downstream cytokines in rats with ulcerative colitis (UC) to explore its underlying mechanisms of action. The model of UC rats with cell immunoreactivity was made using a compound method (trinitrobenzene sulfonic acid plus ethanol). Rats were randomly divided into the control group, the model group, the salazosulfapyridine (SASP) group, high, medium and low dose (20, 10, 5 g·kg-1) of HQT groups. After a three-day treatment, production of NO in serum was detected by Griess assay, the levels of interleukin (IL)-4, IL-10, IL-17 and prostaglandin E2 (PGE2) in serum were detected by ELISA. After a five-day treatment, the positive protein expressions of COX-2 and iNOS in the colon tissue were determined by ICH method, the protein expressions of TLR4 and MyD88 in colon tissue were determined by Western blot. Compared with the control group, the levels of NO, IL-17, PGE2, the protein expressions of TLR4, MyD88 and the protein positive expressions of COX-2, iNOS were apparently higher in the model group. Compared with model group, the above indexes were significantly improved in the SASP and high-dose HQT groups (P<0.05). These results show that HQT has a definite effect on UC in rats. Its mechanisms of action may be achieved by inhibiting the activity of TLR4/MyD88/NF-κB signal pathway and down-regulation of NO, IL-17 and PGE 2 production.
