中国药理学通报2025，Vol.41Issue(7)：1245-1252,8.DOI:10.12360/CPB202410042
基于p38/ERK信号通路探讨大黄素改善小鼠心肌肥厚的机制
Mechanism of emodin improving cardiac hypertrophy in mice based on p38/ERK pathway
摘要
Abstract
Aim Mouse model of myocardial hypertro-phy was established via intraperitoneal injection of iso-proterenol(ISO)in mice.This approach allows for an in-depth investigation into the pharmacological effects and mechanisms of action of emodin,offering novel in-sights and directions for the improvement of myocardial hypertrophy.Methods The mice were randomly di-vided into the following groups:control group(CON),emodin group(EMO),MAPK activator control group(EMO+Ani),model group(ISO),treatment group(ISO+EMO),and activator intervention group(ISO+EMO+Ani).After treatment with emodin and inter-vention with MAPK activator,the heart weight ratio and cardiac size of each group were observed.Hematoxy-lin-eosin(HE)staining was used to observe the patho-logical changes in cardiac tissue,and kits were utilized to measure the levels of GSH,LDH,and MDA in the serum.Western blot was employed to detect the protein expression levels of inflammatory and oxidative factors,as well as p-p38,p-ERK,p38,and ERK in cardiac tis-sue.Results Emodin can significantly inhibit the production of myocardial inflammatory and oxidative factors induced by ISO,thereby effectively alleviating the degree of myocardial hypertrophy and fibrosis.Af-ter the p38/ERK signaling pathway was specifically ac-tivated by farnesol,the improvement effect of emodin on myocardial hypertrophy was weakened.Further comparison revealed that,compared with the myocardi-al hypertrophy pathological model group,the pathologi-cal protein expression levels in the farnesol-treated group showed no significant difference,and were even higher in some indicators.Conclusion Emodin can effectively inhibit the release of inflammatory factors and improve the state of oxidative stress by modulating the p38/ERK signaling pathway,thereby exerting an ameliorative effect on myocardial hypertrophy.关键词
大黄素/心肌肥厚/抗炎/抗氧化/p38/ERKKey words
emodin/cardiac hypertrophy/anti-inflam-mation/anti-oxidation/p38/ERK分类
医药卫生引用本文复制引用
石佳,钱凯,孙赛格,何艺林,徐力,刘龙兴,葛子杰,邹小已,马毓,丁耀成..基于p38/ERK信号通路探讨大黄素改善小鼠心肌肥厚的机制[J].中国药理学通报,2025,41(7):1245-1252,8.基金项目
江西省教育厅科技项目(No GJJ2401615) （No GJJ2401615）
江西省教育厅数改项目(MJXJG-24-15-15) （MJXJG-24-15-15）
