Parthenolide-induced cytotoxicity in H9c2 cardiomyoblasts involves oxidative stress

Tien Yao Tsai, Paul Chan, Chi Li Gong, Kar Lok Wong, Tzu Hui Su, Pei Chen Shen, Yuk Man Leung, Zhong Min Liu

研究成果: 雜誌貢獻文章同行評審

9 引文 斯高帕斯(Scopus)

摘要

Background: Cardiac cellular injury as a consequence of ischemia and reperfusion involves nuclear factor-κB (NF-κB), amongst other factors, and NF-κB inhibitors could substantially reducemyocardial infarct size. Parthenolide, a sesquiterpene lactone compound which could inhibit NF-κB, has been shown to amelioratemyocardial reperfusion injury but may also produce toxic effects in cardiomyocytes at high concentrations. The aim of this study was to examine the cytotoxic effects of this drug on H9c2 cardiomyoblasts, which are precursor cells of cardiomyocytes. Method: Cell viability and apoptosis were examined by MTT and TUNEL assay, respectively, and protein expression was analyzed by western blot. Reactive oxygen species (ROS) production was measured using DCFH-DA as dye. Cytosolic Ca2+ concentration and mitochondrial membrane potential were measured microfluorimetrically using, respectively, fura 2 and rhodamine 123 as dyes. Results : Parthenolide caused apoptosis at 30 μM, as judged by TUNEL assay and Bax and cytochrome c translocation. It also caused collapse of mitochondrial membrane potential and endoplasmic reticulum stress. Parthenolide triggered ROS formation, and vitamin C (antioxidant) partially alleviated parthenolide-induced cell death. Conclusions: The results suggested that parthenolide at high concentrations caused cytotoxicity in cardiomyoblasts in part by inducing oxidative stress, and demonstrated the imperative for cautious and appropriate use of this agent in cardioprotection.

原文英語
頁(從 - 到)33-41
頁數9
期刊Acta Cardiologica Sinica
31
發行號1
DOIs
出版狀態已發佈 - 1月 1 2015

ASJC Scopus subject areas

  • 心臟病學與心血管醫學

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