Effects of Jianpi Qinghua Chinese herbal compound on TLR4-MyD88-dependent pathway protein expression and TNF-αin animal model of chronic atrophic gastritis(CAG) in rats / 中国药理学通报

ABSTRACT

Aim To investigate Jianpi Qinghua Chinese herbal compound( JQCC) on the expressions of the rel-evant proteins of TLR4 and its downstream MyD88-de-pendent pathways, and on the inflammatory factor TNF-α in the animal model of chronic atrophic gastritis ( CAG) in rats, so as to discuss the molecular mecha-nism of JQCC in the treatment of CAG. Methods 53 Wistar rats were randomly divided into the blank con-trol group(n=8) and the CAG model group(n=45), and the animal model of CAG in rats was replicated by the “ammonia + sodium deoxycholic acid + ethanol”method. After the successful modeling was confirmed, the rest of the 40 CAG rats in the CAG model group were divided into the model group, the vitacoenzyme-tablet group, the low dose of JQCC group, the medium dose of JQCC group, the high dose of JQCC group ( each group n =8 ) . The experimental animals of all the groups were given intragastric administration of medication continuously for 30 days. Then the patho-logical histological changes were observed by HE stai-ning. The protein expressions of TLR4, MyD88, NF-КB and COX-2 were tested by Western-blot assay. And the serum TNF-α level was measured by ELISA. Results The protein expressions of TLR4 , MyD88 , NF-КB and COX-2 and the serum TNF-α level in the rats in the model group were increased evidently ( P<0. 01). Compared with the model group, the gastric mucosa lesions were improved in the low dose of JQCC group, the medium dose of JQCC group, the high dose of JQCC group, together with significant decreases of the protein expressions of TLR4 , MyD88 , NF-κB and COX-2 and the serum TNF-α level ( P <0. 05 or P <0. 01 ) . Conclusion JQCC could effectively improve the pathological and histological changes in the gastric mucosa in CAG rats, and the therapeutic mechanism might be related to the expressions of the relevant pro-teins of TLR4-MyD88-dependent pathways and the ex-pressions of anti-inflammatory cytokines.