Mechanism of emodin improving cardiac hypertrophy in mice based on p38/ERK pathway
10.12360/CPB202410042
- VernacularTitle:基于p38/ERK信号通路探讨大黄素改善小鼠心肌肥厚的机制
- Author:
Jia SHI
1
;
Sai-Ge SUN
;
Yi-Lin HE
;
Li XU
;
Long-Xing LIU
;
Zi-Jie GE
;
Xiao-Yi ZOU
;
Yu MA
;
Yao-Cheng DING
;
Kai QIAN
Author Information
1. 宜春学院化学与生物工程学院
- Publication Type:Journal Article
- Keywords:
emodin;
cardiac hypertrophy;
anti-inflam-mation;
anti-oxidation;
p38;
ERK
- From:
Chinese Pharmacological Bulletin
2025;41(7):1245-1252
- CountryChina
- Language:Chinese
-
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.
