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Probucol recovers pathological damage in viral Myocarditis through improvement of myocardium-related proteins.
Microbial Pathogenesis ( IF 3.3 ) Pub Date : 2020-05-25 , DOI: 10.1016/j.micpath.2020.104257
Wei Zhang 1 , Kai Ma 1 , Naihua Han 2
Affiliation  

This study explored the effects of probucol on myocardial injury, oxidative stress, and Cav-3 and Smad3 expression in myocardial tissues by establishing VMC rat models, in order to provide a basis for exploring the mechanism of probucol in treatment of VMC. Sixty rats were randomly divided into control group, model group, probucollowdose group, andprobucol highdose group, with 15 in each group. Except for the control group, rats in each group were intraperitoneally injected coxsackievirus B3 diluent (0.2 ml) to replicate VMC models every 4 days. The results showed that Caspase-3 and Caspase-9, myocardial enzymes, cTn I, and MDA levels in the model group significantly increased (P < 0.05), while the SOD level significantly decreased (P < 0.05); and after probucol treatment, Caspase-3 and Caspase-9, myocardial enzymes, cTn I and MDA levels significantly decreased (P < 0.05), and the SOD level significantly increased (P < 0.05). Compared with the control group, there was an increase in myocardial fibers with significant lesions in the model group, and the pathological scores and the mRNA and protein expression levels of Cav-3 and Smad3 in myocardial cells significantly increased (P < 0.05). Compared with the control group, the myocardial tissue lesions were improved in the probucol low dose group and highdose group, and the pathological scores and the mRNA and protein expression levels of Cav-3 and Smad3 in myocardial cells were significantly reduced (P < 0.05). In conclusion, probucol can significantly improve the pathological damage of myocardial tissue in VMC rats, and its mechanism may be related to improving the expression of myocardium-related proteins Caspase-3 and Caspase-9, inhibiting oxidative stress response, and down-regulating Cav-3 and Smad3 gene expression in myocardial tissue of VMC rats.



中文翻译:

普罗布考通过改善心肌相关蛋白来恢复病毒性心肌炎的病理损伤。

本研究通过建立VMC大鼠模型探索了普罗布考对心肌损伤,氧化应激以及心肌组织中Cav-3和Smad3表达的影响,从而为探索普罗布考治疗VMC的机制提供了依据。60只大鼠随机分为对照组,模型组,普罗布考低剂量组和普罗布考高剂量组,每组15只。除对照组外,每组大鼠腹腔注射柯萨奇病毒B3稀释剂(0.2 ml),每4天复制一次VMC模型。结果表明,模型组Caspase-3和Caspase-9,心肌酶,cTn I和MDA水平显着升高(P <0.05),而SOD水平显着降低(P <0.05);普罗布考治疗后,心肌酶Caspase-3和Caspase-9 cTn I和MDA水平显着降低(P <0.05),SOD水平显着升高(P <0.05)。与对照组相比,模型组心肌纤维增多,病变明显,心肌细胞Cav-3和Smad3的病理评分及mRNA和蛋白表达水平显着升高(P <0.05)。普罗布考低剂量组和高剂量组与对照组相比,心肌组织损伤得到改善,心肌细胞中Cav-3和Smad3的病理学评分以及mRNA和蛋白表达水平明显降低(P <0.05)。 。总之,普罗布考可以显着改善VMC大鼠心肌组织的病理损伤,

更新日期:2020-05-25
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