Protective Effect of Ethanolic Extract of Hemsleya chinensis on HCl/Ethanol-induced Acute Gastric Ulcer in Rats Based on p38 MAPK/NF-κB Signaling Pathway
10.13422/j.cnki.syfjx.20221249
- VernacularTitle:基于p38 MAPK/NF-κB信号通路探讨中华雪胆醇提物对盐酸/乙醇诱导的大鼠急性胃溃疡的保护作用
- Author:
Yang ZHANG
1
;
Hui GUO
1
;
Feihe LIAN
1
;
Xi XIANG
1
;
Qingxia LI
1
;
Xiaoqian LIU
2
;
Zhimin WANG
1
;
Liping DAI
1
;
Erping XU
1
Author Information
1. Henan University of Chinese Medicine，Zhengzhou 450046，China
2. Institute of Chinese Materia Medica，China Academy of Chinese Medical Sciences，Beijing 100700，China
- Publication Type:Journal Article
- Keywords:
ethanol extract of Hemsleya chinensis;
acute gastric ulcer;
inflammatory mediators;
p38 mitogen activated protein kinase;
nuclear transcription factor-κB;
interleukin;
staining
- From:
Chinese Journal of Experimental Traditional Medical Formulae
2023;29(2):37-44
- CountryChina
- Language:Chinese
-
Abstract:
ObjectiveTo investigate the mechanism of protective effect of ethanol extracts of Hemsleya chinensis （HC-EE） on hydrochloric acid/ethanol （HCl/EtOH）-induced acute gastric ulcer in rats. MethodLipopolysaccharide （LPS）-induced RAW264.7 cells were used to evaluate inhibitory effect of HC-EE on the production of inflammatory mediators in vitro. A rat acute gastric ulcer model induced by HCl/EtOH （60% ethanol in 150 mmol·L-1 HCl） was used to evaluate protective effect of HC-EE on acute gastric ulcer. Rats were divided into five groups， including normal group， model group， HC-EE low dose （HC-EE 30， 30 mg·kg-1） group， HC-EE high dose （HC-EE 60， 60 mg·kg-1） group and ranitidine （35 mg·kg-1） group. For model and drug-treated groups， vehicle solvent or drugs were orally administered twice daily for 7 consecutive days before the rats were subjected to HCl/EtOH to induce acute gastric ulcer. After being anesthetized， ulcer surface of each rat was obtained and recorded using electronic imaging technology， and the ulcer inhibition rate was calculated by ImageJ 1.8.0. Hematoxylin-eosin （HE） and periodic acid-Schiff （PAS） staining were used to observe the pathological histological changes in rats. Content of nitric oxide （NO） in cell culture medium was measured by the Griess method. The levels of interleukin-1β （IL-1β）， tumor necrosis factor-α （TNF-α）， IL-6， vascular cell adhesion molecule-1 （VCAM-1） and prostaglandin E2 （PGE2） in rat serum （or cell culture medium） were determined by enzyme linked immunosorbent assay （ELISA）. The protein expressions of phosphorylation （p）-p38 mitogen activated protein kinase （MAPK）/p38 MAPK and p-nuclear transcription factor-κB （NF-κB） p65/NF-κB p65 in rat gastric tissue were detected by Western blot. ResultIn vitro assay showed HC-EE could significantly down-regulate the expressions of NO， TNF-α， IL-1β， IL-6 and VCAM-1 in LPS-induced cells （P<0.05， P<0.01）. In vivo experimental results showed that， compared with the normal group， gastric tissue of the model group was severely damaged， and the area of gastric ulcer was significantly enlarged， levels of TNF-α， IL-6 were significantly increased （P<0.01）， and the level of PGE2 was significantly decreased （P<0.01）， the phosphorylation levels of of p38 MAPK， NF-κB p65 in gastric tissue were significantly increased （P<0.01）. Compared with the model group， HC-EE dose-dependently improved HCl/EtOH-induced gastric tissue injury and inflammatory cell infiltration， and it could increase ulcer inhibition rate， significantly decreased the release of TNF-α and IL-6 （P<0.01）， HC-EE 60 group could increase the content of PGE2 （P<0.05）， and significantly inhibit the phosphorylation levels of p38 MAPK and NF-κB p65 （P<0.05， P<0.01）. ConclusionHC-EE can exert protective effect on HCl/EtOH-induced acute gastric ulcer in rats， and its mechanism may be related to the inhibition of expression of inflammatory mediators mediated by p38 MAPK/NF-κB signaling pathway.
