OBJECTIVE  To establish a mouse model of myocardial hypertrophy by intrabitoneal injection of isoproterenol (ISO), observe the pharmacological effect of emodin on improving myocardial hypertrophy, and preliminarily explore the mechanism of emodin.

METHODS  The 40 SPF mice were randomly divided into 4 groups with 10 mice in each group, which were blank group, emodin toxicity validation group, model group and emodin administration group. Mice in the model group and emodin administration group were intraperitoneally injected with ISO daily for 4 weeks at a dose of 5 mg·kg⁻¹. Emodin toxicity validation group and emodin administration group was given 50 mg·kg⁻¹ emodin intragastric daily for 14 d. After administration, the heart to weight ratio and cardiac morphology of mice in each group were observed, the pathological changes of heart tissue were observed by HE staining, and the serum GSH and MDA contents were detected by kit. Western blotting was used to analysis emodin's antifibrotic, anti-inflammatory and antioxidant effects.

RESULTS  Compared with the blank group, the heart to weight ratio, serum MDA content, ANP, BNP, β-MHC, Collagen I, TGF-β, TNF-α and IL-6 protein expression levels of the model group were significantly increased, while the serum GSH content, SOD and CAT protein expression levels were significantly decreased. After emodin administration, the heart to weight ratio of mice was significantly decreased, the above inflammatory and oxidative stress related indexes were improved.

CONCLUSION  Emodin can effectively inhibit the expression of ISO-induced myocardial inflammatory factors in mice, regulate the level of oxidative stress, and improve myocardial hypertrophy.