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Silymarin ameliorates diabetic cardiomyopathy via inhibiting TGF‐β1/Smad signaling
Author(s) -
Meng Songyan,
Yang Fan,
Wang Yueqiu,
Qin Ying,
Xian Huimin,
Che Hui,
Wang Lihong
Publication year - 2019
Publication title -
cell biology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.932
H-Index - 77
eISSN - 1095-8355
pISSN - 1065-6995
DOI - 10.1002/cbin.11079
Subject(s) - diabetic cardiomyopathy , smad , medicine , fibrosis , endocrinology , myocardial fibrosis , transforming growth factor , cardiac fibrosis , western blot , streptozotocin , masson's trichrome stain , diabetes mellitus , signal transduction , h&e stain , cardiomyopathy , chemistry , immunohistochemistry , heart failure , biochemistry , gene
Diabetic cardiomyopathy (DCM) is the leading cause of morbidity and mortality in diabetes mellitus (DM) patients. Previous studies have shown that the transforming growth factor‐beta 1 (TGF‐β1)/Smad signaling pathway plays a key role in the development of myocardial fibrosis in DCM. Silymarin (SMN) is used clinically to treat liver disorders and acts by influencing TGF‐β1. However, the possible effects of silymarin on DCM remain to be elucidated. In our study, the DM animal model was induced by streptozotocin (STZ) injection. Fasting blood glucose level was measured, and the structure and function of the heart were measured by hematoxylin and eosin (H&E) and Masson staining, echocardiography, and transmission electron microscopy (TEM). Western blot was used to detect the expression of TGF‐β1, Smad2/3, phosphorylation Smad2/3(p‐Smad2/3), and Smad7. Our results showed that silymarin downregulated blood glucose level and significantly improved cardiac fibrosis and collagen deposition in DM rats detected by H&E, Masson staining, and TEM assays. The echocardiography results showed that silymarin administration attenuated cardiac dysfunction in DM rats. Additionally, compared with untreated DM rats, levels of TGF‐β1 and p‐Smad2/3 were decreased, whereas Smad7 was increased following silymarin administration. These data demonstrate that silymarin ameliorates DCM through the inhibition of TGF‐β1/Smad signaling, suggesting that silymarin may be a potential target for DCM treatment.