Abstract
Cardiovascular disease has become the main cause of death among complications of diabetes. Myocardial fibrosis is a crucial pathological change of cardiovascular disease. Tangshen Formula (TSF) shows a good clinical effect in the treatment of diabetic kidney disease (DKD). However, whether TSF alleviates diabetes-associated myocardial fibrosis is still unknown. In the present research, we studied the effect and mechanism of TSF in the treatment of myocardial fibrosis in vivo and in vitro. We found that TSF treatment significantly downregulates myocardial fibrosis-related markers, including collagens I and III, and α-SMA. TSF also protects primary mouse cardiac fibroblast (CF) from transforming growth factor-β1- (TGF-β1-) induced damage. Moreover, TSF decreased the expression levels of TGF-β/Smad-related genes (α-SMA, collagens I and III, TGF-β1, and pSmad2/3), and increased Smad7 gene expression. Finally, TSF decreased the expressions of wnt1, active-β-catenin, FN, and MMP7 to regulate the Wnt/β-catenin pathway. Taken together, TSF seems to attenuate myocardial fibrosis in KKAy mice by inhibiting TGF-β/Smad2/3 and Wnt/β-catenin signaling pathways.
Highlights
Diabetes mellitus (DM) is a global epidemic
After 16 weeks of treatment, blood glucose levels in KKAy+Tangshen Formula (TSF) and KKAy+irbesartan groups were lower than the levels in the KKAy group, but without a significant difference (Figure 1B)
We validated that TSF could relieve fibrosis in the KKAy mice model and in cardiac fibroblast (CF) induced by TGF-β1
Summary
Diabetes mellitus (DM) is a global epidemic. Half a billion people worldwide have diabetes, and this number is expected to increase by 25% in 2030 and by 51% in 2045 [1]. Among the complications of diabetes, diabetic cardiomyopathy is a common cause of death [2]. Myocardial fibrosis is a typical pathology in cardiovascular diseases and is marked by profuse deposition and disruption of extracellular matrix (ECM) and the over-proliferation of activated cardiac fibroblasts (CFs) [3]. Despite strict blood glucose control, the incidence of diabetic cardiomyopathy remains high. It is crucial to search for new drugs to treat myocardial fibrosis
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