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芍药苷对丙烯醛诱导的 H9c2 心肌细胞凋亡的保护作用。

Protective effects of paeoniflorin on acrolein-induced apoptosis in H9c2 cardiomyocytes.

机构信息

Department of Pharmacy, Ruikang Hospital, Guangxi University of Chinese Medicine, Nanning, Guangxi, PR China.

出版信息

Pak J Pharm Sci. 2020 Jul;33(4):1585-1592.

Abstract

Acrolein is a highly toxic unsaturated aldehyde which is abundant in many circumstances. People exposed to acrolein may have significant clinical relevance in human cardiotoxicity situations. Paeoniflorin (PEF) is a bioactive glucoside isolated from the roots of Paeonia lactiflora Pall. It is reported that PEF performs a beneficial role in cardiovascular system. The aim of the current research was to evaluate the potential protective effect of PEF against acrolein-induced apoptotic damage in H9c2 cardiomyocytes. This study revealed that PEF exerted a protective effect on acrolein-induced cardiomyocyte apoptosis. Furthermore, treatment with acrolein could markedly increase the levels of reactive oxygen species (ROS) and expression of cleavage of caspase-9 and caspase-3 in H9c2 cardiomyocytes, which were significantly reversed by co-treatment with PEF (100uM). These results demonstrated that PEF protects H9c2 cardiomyocytes against acrolein-induced cardiomyocyte injury via decreasing ROS production and down regulating caspases cascade reaction, indicating that PEF is a potential therapeutic agent for cardiac toxic environmental pollutant injury.

摘要

丙烯醛是一种在许多情况下含量丰富的高毒性不饱和醛。接触丙烯醛的人可能在人类心肌毒性情况下具有重要的临床相关性。芍药苷(PEF)是从芍药根中分离得到的一种生物活性糖苷。有报道称,PEF 在心血管系统中发挥有益作用。本研究旨在评估 PEF 对丙烯醛诱导的 H9c2 心肌细胞凋亡损伤的潜在保护作用。这项研究表明,PEF 对丙烯醛诱导的心肌细胞凋亡具有保护作用。此外,用丙烯醛处理可显著增加 H9c2 心肌细胞中活性氧(ROS)的水平和半胱天冬酶-9 和半胱天冬酶-3 的裂解表达,用 PEF(100μM)共同处理可显著逆转这一现象。这些结果表明,PEF 通过减少 ROS 产生和下调半胱天冬酶级联反应来保护 H9c2 心肌细胞免受丙烯醛诱导的心肌细胞损伤,表明 PEF 是治疗心脏毒性环境污染物损伤的潜在治疗剂。

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