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Shenmai Injection Improves Hypertensive Heart Failure by Inhibiting Myocardial Fibrosis via TGF-β 1/Smad Pathway
Si-Yuan Hu1,2, Yao Zhou3, Sen-Jie Zhong4
1School of Sports Art, Hunan University of Chinese Medicine, Changsha, 410208, China.
Shenmai Injection effectively treats hypertensive heart failure by inhibiting myocardial fibrosis. This treatment improves heart function and reduces fibrosis through the TGF-β1/Smad signaling pathway.
Area of Science:
- Cardiovascular Medicine
- Pharmacology
- Integrative Medicine
Background:
- Hypertensive heart failure is characterized by significant myocardial fibrosis, a key pathological manifestation.
- Existing treatments may not fully address the underlying fibrotic processes contributing to heart failure progression.
Purpose of the Study:
- To investigate the therapeutic effects of Shenmai Injection (SMI) on hypertensive heart failure in a rat model.
- To elucidate the mechanism by which SMI inhibits myocardial fibrosis, focusing on the TGF-β1/Smad signaling pathway.
Main Methods:
- Salt-sensitive rats were induced with hypertension and heart failure via a high-salt diet.
- Model rats were treated with Shenmai Injection (SMI) or pirfenidone (PFD) and compared to a heart failure (HF) group.
- Cardiac function, blood pressure, myocardial fibrosis, and molecular markers (Col I, TGF-β1, Smad2/3) were assessed using echocardiography, ELISA, histology, and qPCR.
Main Results:
- High-salt diet significantly increased blood pressure, reduced cardiac function (LVEF, LVFS), and induced myocardial fibrosis and inflammation.
- Shenmai Injection treatment significantly improved cardiac function (LVEF, LVFS) and reduced myocardial fibrosis compared to the HF group.
- SMI downregulated the expression of collagen type I (Col I), transforming growth factor β 1 (TGF-β1), Smad2, and Smad3 at both mRNA and protein levels.
Conclusions:
- Myocardial fibrosis is a critical factor in hypertensive heart failure.
- Shenmai Injection demonstrates significant efficacy in improving heart function and inhibiting myocardial fibrosis in this model.
- The therapeutic effect of SMI is mediated by the regulation of the TGF-β1/Smad signaling pathway.
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