Berberine inhibits cardiac remodeling of heart failure after myocardial infarction by reducing myocardial cell apoptosis in rats

Abstract

The effects of berberine on cardiac function of heart failure after myocardial infarction and its possible mechanism were investigated. The anterior descending branches of 50 female Wistar rats were ligatured to establish the model of heart failure after myocardial infarction. At 4 weeks after successful modeling, the rats were randomly divided into two groups receiving 4-week gavage with saline (Sal group) and berberine (Ber group), while the sham-operation group (Sham group) was set up. After 4 weeks, the hemodynamics and serum BNP in rats were measured. The hearts of rats were taken to detect the degree of myocardial fibrosis. The myocardial cell apoptosis was detected. The expressions and changes in myocardial apoptosis-related proteins, including Bcl-2, Bax and caspase-3, were detected. The expression and changes in GRP78, CHOP and caspase-12 in myocardial tissue were detected. The results showed that Berberine improved the cardiac function of rats after myocardial infarction. After myocardial infarction, myocardial fibrosis and apoptosis were observed around the infarction area, berberine improved the myocardial fibrosis and reduced cell apoptosis. Furthermore, berberine alleviated endoplasmic reticulum stress (ERS) after myocardial infarction. In conclusion, Berberine can inhibit the myocardium cell apoptosis of heart failure after myocardial infarction, and its mechanism may be realized by affecting the ERS in myocardial tissue of heart failure after myocardial infarction and CHOP and caspase-12 apoptotic signaling pathway, upregulating Bcl-2/Bax expression and downregulating caspase-3 expression, thus inhibiting the cardiac remodeling and protecting the cardiac function.

Berberine Promotes Cardiac Function by Upregulating PINK1/Parkin-Mediated Mitophagy in Heart Failure

“…After myocardial infarction, berberine ameliorated the cardiac remodeling and inhibited cardiac dysfunction in HF. Its mechanism may be upregulating Bcl-2/Bax and down-regulating caspase-3 expression ( Liao et al, 2018 ). Notably, in rat model of cardiac hypertrophy berberine could attenuate left ventricular remodeling and cardiomyocyte apoptosis through an autophagy-dependent mechanism via inhibition of mTOR, p38 and ERK1/2 MAPK signaling pathways ( Li et al, 2014 ).…”

The co-treatment of rosuvastatin with dapagliflozin synergistically inhibited apoptosis via activating the PI3K/AKt/mTOR signaling pathway in myocardial ischemia/reperfusion injury rats

“…The myocardial I/R injury models presently showed various hemodynamics parameters such as heart rate, LVSP, LVEDP, +d p /d t max , and −d p /d t max . LVEDP is an index reflecting the left ventricular preload, which depends on the returned blood volume before ventricular systole and cardiac ejection function [ 19 ]. LVEDP and −d p /d t max will be increased, LVSP and +d p /d t max will be decreased when myocardial diastolic and systolic functions are inhibited [ 20 ].…”

Berberine inhibits adipocyte differentiation, proliferation and adiposity through down-regulating galectin-3

“…It is worthwhile to mention that Gal-3 is closely related to the development of fibrosis or remodeling of the heart, lung, liver, and kidney, as demonstrated by animal experiments and a few clinical studies 37–39 . Interestingly, BBR has ameliorative effects on fibrosis or remodeling of these organs, which may be caused by different factors or diseases 40–43 . Whether or not the anti-fibrotic activities of BBR are associated with the down-regulation of Gal-3 needs further investigation.…”