Vitamin B17 alleviates Sorafenib-induced cardiotoxicity in Ehrlich Ascites Carcinoma mice via modulation of inflammatory and fibrotic pathways

维生素B17通过调节炎症和纤维化通路减轻索拉非尼诱导的艾氏腹水癌小鼠心脏毒性

阅读:2

Abstract

Chemotherapy-induced cardiotoxicity remains a major clinical concern, with Sorafenib (Sor) being among the agents associated with adverse cardiac effects. Vitamin B17 (VB17), known for its antioxidant and anti-inflammatory properties, has shown promise in mitigating cardiovascular damage. This study investigated the cardioprotective potential of VB17, alone or in combination with Sor, in a mouse model of Ehrlich Ascites Carcinoma (EAC)-induced cardiomyopathy. Seventy-two male Swiss albino mice were divided into 12 groups and treated with VB17, Sor, or their combination via intraperitoneal or oral routes. Assessments included tumor volume, viable EAC cell count, cardiac enzyme levels (cardiac troponin (cTn), CK-MB, LDH), oxidative stress markers (malondialdehyde (MDA), glutathione (GSH), superoxide dismutase (SOD)), gene expression (IL-1β, NF-κB, TGF-β, MMP-9, P53), histological analysis, and molecular docking. Combination therapy significantly reduced tumor burden and EAC cell viability while improving cardiac function. VB17 co-treatment lowered elevated troponin I levels and normalized creatine kinase-MB (CK-MB) and lactate dehydrogenase (LDH). Oxidative stress was reduced, evidenced by a 50% decrease in MDA and increases in GSH and SOD activities. Gene analysis showed reduced expression of pro-inflammatory and fibrotic markers (IL-1β, NF-κB, TGF-β, MMP-9) and enhanced P53 expression. Histopathological findings confirmed reduced myocardial damage in the combination group compared to Sor alone. These findings suggest that VB17 enhances the cardioprotective effects of Sor by modulating key inflammatory and apoptotic pathways. The combination therapy shows promise as a potential strategy to counteract chemotherapy-induced cardiomyopathy. Further research is needed to validate these results and explore clinical applications.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。