Key result
Guanxin V improves post-AMI cardiac function in hamsters by reducing chymase levels and mast cells.
Why the study?
Acute myocardial infarction carries high disability and mortality, and previous studies demonstrated that Guanxin V improved cardiac function and hemodynamics in AMI rats.
Does Guanxin V improve cardiac function and attenuate ventricular remodeling in a Syrian hamster model of acute myocardial infarction?
Does Guanxin V improve cardiac function and attenuate ventricular remodeling in a Syrian hamster model of acute myocardial infarction?
In a hamster model of acute myocardial infarction, Guanxin V improved cardiac function and attenuated ventricular remodeling by inactivating the renin-angiotensin-aldosterone system and reducing mast cell accumulation.
Hypothesis-generating for Guanxin V post-AMI remodeling in hamsters; human trials needed before any clinical consideration.
BACKGROUND: Acute myocardial infarction (AMI) is the most serious and lethal manifestation of coronary heart disease worldwide, presenting extremely high disability and mortality. Our previous studies have shown that Guanxin V (GXV) could significantly improve the cardiac function and the blood flow dynamics, and reduce serum levels of inflammatory factors in AMI rats, thus triggering ventricular remodeling (VR) at post-AMI. METHODS: An in vivo AMI model was established in Syrian hamsters by performing the ligation of the left anterior descending coronary artery. Syrian hamsters were randomly divided into four groups, namely Sham operation group (n = 12), AMI group (n = 12), GXV group (GXV 6 g/Kg/d, n = 12), and Tranilast group (Tra 105 mg/Kg/d, n = 12). Drug intervention was conducted for consecutive 8 weeks. Relative biological indicators were measured in the 4th and 8th week, respectively. RESULTS: Cardiac functions were improved, and the infarcted size and heart weight index were limited in Syrian hamsters of GXV and Tra groups compared with those in AMI group. Furthermore, GXV was able to decrease the number of mast cells and chymase level in Syrian hamsters with AMI. Administration of GXV remarkably inactivated the renin-angiotension-aldosterone system, and alleviated myocardial fibrosis and cardiomyocyte apoptosis, thus slowing down VR at post-AMI. CONCLUSION: GXV slows down the process of VR at post-AMI by reducing chymase level and mast cells number, as well as inactivating the reninangiotension-aldosterone system..
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Zhang et al. (2021) studied Acute myocardial infarction (n=48). Guanxin V (GXV) vs. Sham operation, AMI control, and Tranilast (105 mg/Kg/d) was evaluated on Cardiac function, infarcted size, and heart weight index. Guanxin V improved cardiac function, limited infarct size, and slowed ventricular remodeling post-AMI in Syrian hamsters by reducing chymase levels and mast cell numbers.
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