Abstract
Objectives We investigated the role of cardiomyocyte autophagy and its regulatory mechanisms by WenxinKeli (WXKL) in cells subjected to hypertrophy. Methods H9C2 cardiomyocytes were divided into 8 groups. Cytoskeletal proteins as well as endogenously expressed autophagy marker proteins were studied by confocal imaging. Western blotting was used to assess the levels of light chain-3 (LC3) and mechanistic target of rapamycin (mTOR). The cell viability assay was used to detect the content of ATP. Flow cytometry was used to detect apoptotic cardiomyocytes. Results (1) Compared with the control group, the length and width of cells in the Angiotensin II (AngII) group were significantly increased, while those in the 3-methyladenine (3-MA) and the WXKL groups were decreased. (2) Compared with AngII group, the expression of LC3 II/I protein in the 3-MA and WXKL groups was downregulated, while the expression of mTOR protein was upregulated. (3) Compared with the AngII group, the cardiomyocytes in the WXKL group showed increased ATP and decreased apoptosis rate and number of autophagosome. Conclusions We propose a novel role of WXKL as a likely inhibitor of cardiac hypertrophy by regulation of pathological autophagy.
Highlights
Epidemiological data show that heart failure is a leading cause of morbidity and mortality worldwide [1]
The results showed that the expression of light chain-3 (LC3) II protein was significantly upregulated in the starvation and induced by rapamycin, which was consistent with the effect of 10−7 mol/L Angiotensin II (AngII) on LC3 II protein in cardiomyocytes (P < 0 05, n = 3)
The results showed that compared with the control group, the fluorescence intensity of LC3 protein in cardiomyocytes was significantly increased after AngII treatment, which is consistent with the increase of the fluorescence intensity of LC3 protein after starvation and rapamycin treatment
Summary
Epidemiological data show that heart failure is a leading cause of morbidity and mortality worldwide [1]. Cardiac remodeling is a chronic adaptation process, its characteristics include progressive ventricular expansion, myocardial hypertrophy, fibrosis, and cardiac performance deterioration. It is amended by the adaptability of cardiomyocytes, as well as the adaptability of the negative aspects, such as the interaction between myocardial cell death and fibrosis [5]. Cardiac function is continuously reduced and hypertrophy gradually transitions to heart failure, which is progressive and accompanied by a growing enlargement of the ventricular cavity with fibrosis and disarray. Investigation of the mechanism of cardiac hypertrophy could help us to discover targets for the prevention and cure of heart failure
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