Effects of huangqi jianzhong decoction on duodenal ulcer and tlr-2 mediated intestinal mucosal immune barrier in rats
10.3969/j.issn.1001-1978.2019.08.026
- Author:
Hou-Pan SONG
1
Author Information
1. Institute of Tradition Chinese Medicine Diagnostics
- Publication Type:Journal Article
- Keywords:
Cytokines;
Duodenal ulcer;
Huangqi jianzhong decoction;
Immune barrier;
Myd88;
Tlr
- From:
Chinese Pharmacological Bulletin
2019;35(8):1172-1178
- CountryChina
- Language:Chinese
-
Abstract:
Aim To study the therapeutic effect of Huangqi Jianzhong decoction ( HQJZ) on duodenal ul-cer(DU) in rats and its effect on intestinal mucosal immune barrier function mediated by TLR-2. Methods SD rats were divided into normal group, model group, positive drug group and HQJZ group. DU model was established by methods of multiple factors. The body weight, food intake, and rectal temperature were measured. The ulcer index (UI) was calculated. The pathological changes of duodenal mucosa were observed by HE staining. The contents of cytokines were detec-ted by EL1SA. The expression of mRNx^ and protein were detected by qRT-PCR and immunohistochemistry, respectively. Results Compared with normal group, the body weight, food intake, and rectal temperature of model group decreased significantly. The UI significantly increased. The contents of serum IL-4 and IL-10 markedly decreased, and TNF-a content evidently in creased. The expressions of TLR-2 and MyD88 mRNA and protein significantly increased. Compared with model group, after treatment with HQJZ, the body weight, food intake, and rectal temperature were significantly up-regulated, while the UI was significantly down-regulated. The morphology of duodenal mucosa returned to normal status, and the villus height and crypt depth increased significantly. The levels of serum IL-4 and IL-10 were significantly elevated, while TNF- A significantly declined. The expressions of TLR-2 and MyD88 mRNA and protein were apparently down-regu-lated. Conclusions HQJZ can promote the healing of DU, and the mechanism may be related to the intervention of TLR-2 mediated intestinal mucosal immune barrier function.
