Why the study?
Chronic heart failure remains a major public health concern, and the effect of Wenyang Zhenshuai Granules on cardiomyocyte apoptosis via exosomal microRNA-155 and p38 MAPK signaling required investigation.
Does Wenyang Zhenshuai Granules-containing serum reduce cardiomyocyte apoptosis and improve cell viability by regulating the p38 MAPK signaling pathway via exosomal miR-155 in a doxorubicin-induced H9c2 cardiomyocyte injury model?
Does Wenyang Zhenshuai Granules-containing serum reduce cardiomyocyte apoptosis and improve cell viability by regulating the p38 MAPK signaling pathway via exosomal miR-155 in a doxorubicin-induced H9c2 cardiomyocyte injury model?
In a preclinical doxorubicin-induced cardiomyocyte injury model of chronic heart failure, Wenyang Zhenshuai Granules exerted anti-apoptotic and cytoprotective effects by promoting exosomal miR-155 secretion and inhibiting p38 MAPK pathway activation.
Does not support clinical use of WZG; hypothesis-generating for miR-155 effects in doxorubicin cardiomyopathy.
Background: Chronic heart failure (CHF) represents a significant global public health concern, warranting further investigation and intervention. Wenyang Zhenshuai Granules (WZG) is an in-hospital preparation of the First Affiliated Hospital of Hunan University of Chinese Medicine, which has been approved by the Hunan Provincial Drug Administration (Approval No.: Z20190105000) for the treatment of CHF. The objective of this study was to examine the impact of WZG on cardiomyocyte apoptosis in CHF through the regulation of the p38 mitogen-activated protein kinase (MAPK) signaling pathway by exosomal microRNA-155. Methods: Doxorubicin (DOX) was employed to construct a model of cardiomyocyte injury associated with CHF. The H9c2 cells were divided into four groups: the normal control group (NC), the DOX group (DOX), the DOX + drug-containing serum group (DOX+WZG), and the DOX + enalapril (ENP) group (DOX+ENP). The morphology of the cardiomyocytes was observed at 15, 30, and 45 h into the experiment using an inverted microscope. The viability of cells and the number of apoptotic cells were determined through the use of a CCK-8 assay and flow cytometry, respectively. Subsequently, exosomes were extracted and subjected to morphological characterization and identification. The expression of exosomal miR-155, the p38 MAPK signaling pathway, and apoptotic proteins were examined. Results: The results demonstrated that WZG could enhance the morphology of H9c2 cells, diminish the apoptosis rate of cells, and augment the viability of cells. Western blot and RT-qPCR assays provided further confirmation that WZG could promote the secretion of exosomes from cardiomyocytes, increase the content of miR-155 in exosomes, and inhibit the activation of the p38 MAPK signaling pathway. Conclusion: WZG inhibits p38 MAPK protein phosphorylation via exosomal miR-155, thereby exerting anti-apoptotic effects on cardiomyocytes in CHF.
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Peng et al. (2025) studied this question.
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