{"title":"苦参碱通过调节calpain-2/caspase-12信号通路对感染柯萨奇病毒B₃的心肌细胞的保护作用","authors":"Yongmei Sun, Zongtao Mao, Junzuo Liu, Yanan Geng","doi":"10.14715/cmb/2025.71.7.4","DOIUrl":null,"url":null,"abstract":"<p><p>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.</p>","PeriodicalId":520584,"journal":{"name":"Cellular and molecular biology (Noisy-le-Grand, France)","volume":"71 7","pages":"21-30"},"PeriodicalIF":0.0000,"publicationDate":"2025-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Protective effects of matrine on cardiomyocytes infected with coxsackievirus B₃ via modulation of the calpain-2/caspase-12 signaling pathway.\",\"authors\":\"Yongmei Sun, Zongtao Mao, Junzuo Liu, Yanan Geng\",\"doi\":\"10.14715/cmb/2025.71.7.4\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>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.</p>\",\"PeriodicalId\":520584,\"journal\":{\"name\":\"Cellular and molecular biology (Noisy-le-Grand, France)\",\"volume\":\"71 7\",\"pages\":\"21-30\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2025-07-30\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Cellular and molecular biology (Noisy-le-Grand, France)\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.14715/cmb/2025.71.7.4\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Cellular and molecular biology (Noisy-le-Grand, France)","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.14715/cmb/2025.71.7.4","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Protective effects of matrine on cardiomyocytes infected with coxsackievirus B₃ via modulation of the calpain-2/caspase-12 signaling pathway.
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.