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Copyright (c) 2025 Yongmei Sun, Zongtao Mao, Junzuo Liu, Yanan Geng
This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.
The undersigned hereby assign all rights, included but not limited to copyright, for this manuscript to CMB Association upon its submission for consideration to publication on Cellular and Molecular Biology. The rights assigned include, but are not limited to, the sole and exclusive rights to license, sell, subsequently assign, derive, distribute, display and reproduce this manuscript, in whole or in part, in any format, electronic or otherwise, including those in existence at the time this agreement was signed. The authors hereby warrant that they have not granted or assigned, and shall not grant or assign, the aforementioned rights to any other person, firm, organization, or other entity. All rights are automatically restored to authors if this manuscript is not accepted for publication.Protective effects of matrine on cardiomyocytes infected with coxsackievirus B₃ via modulation of the calpain-2/caspase-12 signaling pathway
Corresponding Author(s) : Yongmei Sun
Cellular and Molecular Biology,
Vol. 71 No. 7: Issue 7
Abstract
Viral myocarditis (VMC) presents a substantial threat, especially for children, often leading to cardiogenic shock and fulminant myocarditis. Our study aimed to evaluate the role of calpain-2 and caspase-12, which were involved in the endoplasmic reticulum apoptosis pathway, and the influence of Matrine on these proteins during Coxsackie virus B₃ (CVB₃)-induced acute VMC mice in vitro and in vivo, shedding light on the potential cardioprotective effects. We first performed primary cultured cardiomyocytes, which were infected with CVB₃in vitro. We observed cell viability, the beating of cardiomyocytes and cytopathic effects. And we utilized Balb/c mice to establish the VMC animal model and determined viral titers, histopathological changes, and myocardial pathological scores. Furthermore, we detected CK-MB levels and myocardial cell apoptosis in vitro and in vivo. In order to further explore the possible mechanisms, the protein expression of calpain-2 (by immunohistochemistry and Western blot) and caspase-12 activity (by fluorescence assay for substrate cleavage) were detected in vitro and in vivo. Our findings indicated that, in comparison to the normal control group, the virus-infected group exhibited increased injured myocardial cells, virus titer, CK-MB levels, and apoptotic cells (P<0.05). Matrine treatment groups significantly reduced CK-MB levels, myocardial cellular damages and apoptosis in vitro and in vivo, with Matrine notably suppressing calpain-2 protein expression and Caspase-12 activity compared to the virus-infected group (P<0.05). In conclusion, our study revealed that calpain-2 and caspase-12 played roles in CVB₃-induced myocardial cell apoptosis. Matrine effectively mitigated myocardial cell injury and reduced apoptosis, thereby providing substantial protection against CVB₃infection in vitro and in vivo, which may be related to the down-regulation of calpain-2/caspase-12 signaling pathway.
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