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Mitochondrial Proteomic Analysis of Isopsoralen Protection against Oxidative Damage in Human Lens Epithelial Cells 被引量:3

Mitochondrial Proteomic Analysis of Isopsoralen Protection against Oxidative Damage in Human Lens Epithelial Cells
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摘要 目的将在上皮的房间 B3 (HLE-B3 ) 由氢过氧化物(H2O2 ) 引起了的人的透镜对氧化损坏与雌激素的活动调查自然药用的单体 isopsoralen (ISR ) 的保护的效果并且追求保护的效果的可能的 mitochondrial proteomic 整齐。 Objective: To investigate the protective effects of the natural medicinal monomer isopsoralen (ISR) with estrogenic activity against oxidative damage in human lens epithelial cells B3 (HLE-B3) caused by hydrogen peroxide (H2O2) and to pursue the possible mitochondrial proteomic regularity of the protective effects. Methods: HLE-B3 cells were treated with H2O2 (300 μMol/L), β-estradiol (E2:10^-8mol/L) and H2O2, ISR (10^-5 mol/L) and H2O2, or left untreated. Altered expressions of all mitochondrial proteins were analyzed by protein array and surface- enhanced laser desorpUon ionization time of flight mass spectrometry (SELDI-TOF-MS). The mass/charge (m/z) ratios of each peak were tested by the Kruskal-Wallis rank sum test, and the protein peak value of the m/z ratio for each treatment by pair comparison was analyzed with the Nemenyi test. Results: H2O2 up-regulated the expressions of two protein spots (with m/z of 6532 and 6809). E2 mitigated the oxidative damage, and the expression of one protein spot (m/z 6532) was down-regulated. In contrast, ISR down-regulated both of protein spots (m/z 6532 and 6809). Conclusions: ISR could effectively inhibit H2O2-induced oxidative damage in HLE-B3 cells. The protein spot at m/z of 6532 might be the target spot of ISR against oxidative damage induced by H2O2.
出处 《Chinese Journal of Integrative Medicine》 SCIE CAS 2012年第7期529-533,共5页 中国结合医学杂志(英文版)
基金 Supported by the Foundation of Fujian Province Health Department Fund(No.2009-1-30) Fujian Provincie Department of Education Issues(No.JA10176)
关键词 晶状体上皮细胞 线粒体蛋白质 氧化损伤 异补骨脂素 蛋白质组 保护作用 过氧化氢 学分 isopsoralen, mitochondrial proteomics, lens epithelial cell, senile cataract
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