Protective Effect of 2,4′,5′-Trihydroxyl-5,2′-dibromo diphenylmethanone, a New Halophenol, against Hydrogen Peroxide-Induced EA.hy926 Cells InjuryReportar como inadecuado




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1

School of Pharmaceutical Science, Shanxi Medical University, 56 Xinjian South Road, Taiyuan 030001, China

2

School of Public Health Science, Shanxi Medical University, Taiyuan 030001, China

3

Shanxi Key Laboratory of Drug Toxicology and Drug for Radiation Injury, China Institute for Radiation Protection, Taiyuan 030006, China





*

Author to whom correspondence should be addressed.



Academic Editor: Derek J. McPhee

Abstract Vascular endothelial cells produce reactive oxygen species ROS during the process of energy metabolism in aerobic respiration. A growing body of evidence indicates that excessive ROS is implicated in the pathogenesis of cardiovascular diseases including atherosclerosis. The newly synthesized halophenol, 2,4′,5′-trihydroxyl-5,2′-dibromo diphenylmethanone TDD, exhibits antioxidative and cytoprotective activities in vitro. In this study, the protective effect of TDD against hydrogen peroxide H2O2-induced oxidative injury of EA.hy926 cells was investigated. Cell viability was measured by 3-4,5-dimethylthiazol-2-yl-2,5-dephenyltetrazolium bromide MTT assay, while the effect of TDD on the transcription profile of EA.hy926 cells subjected to H2O2-induced oxidative injury was evaluated by microarray analysis. Several signaling pathways, including apoptosis, were significantly associated with TDD. Flow cytometric analysis was used to evaluate anti-apoptotic effect of TDD. Subsequently, RT-PCR and Western blot were used to detect the expressions of the apoptosis-associated protein, Bcl-2 and Bax. Meanwhile the expression of cleaved caspase-3, an executioner of apoptosis, was also detected by Western blot. The results showed that pretreatment of EA.hy926 cells with TDD prevented the decrease of cell viability induced by H2O2, and attenuated H2O2-induced elevation of Bax and cleaved caspase-3 while increased Bcl-2 expressions. In summary, TDD inhibited H2O2-induced oxidative injury of EA.hy926 cells through negative regulation of apoptosis. These findings suggest that TDD is a potential candidate for therapeutic intervention in oxidative stress-associated cardiovascular diseases. View Full-Text

Keywords: 2,4′,5′-trihydroxyl-5,2′-dibromo diphenylmethanone; EA.hy926 cells; H2O2; apoptosis; microarray analysis 2,4′,5′-trihydroxyl-5,2′-dibromo diphenylmethanone; EA.hy926 cells; H2O2; apoptosis; microarray analysis





Autor: Jianguo Li 1,2,3, Xiue Feng 1, Rui Ge 1, Jiankuan Li 1 and Qingshan Li 1,2,*

Fuente: http://mdpi.com/



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