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Mitochondrial proteomic analysis of isopsoralen protection against oxidative damage in human lens epithelial cells
  
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Author NameAffiliationE-mail
Chun-yan Feng Fujian University of Traditional Chinese Medicine, Fuzhou, 350003, China

Research Center of Pathophysiology, Fujian University of Traditional Chinese Medicine, Fuzhou, 350003, China 
 
Xiu-rong Huang Department of Ophthalmology, Second Affiliated Peoples Hospital of Fujian University of Traditional Chinese Medicine, Fuzhou, 350003, China qihuang@netease.com 
Ming-xin Qi Research Center of Pathophysiology, Fujian University of Traditional Chinese Medicine, Fuzhou, 350003, China  
Song-wen Tang Department of Ophthalmology, Second Affiliated Peoples Hospital of Fujian University of Traditional Chinese Medicine, Fuzhou, 350003, China  
Yan-hong Hu Research Center of Pathophysiology, Fujian University of Traditional Chinese Medicine, Fuzhou, 350003, China  
Sheng Chen Research Center of Pathophysiology, Fujian University of Traditional Chinese Medicine, Fuzhou, 350003, China  
Fa-jie Ke Research Center of Pathophysiology, Fujian University of Traditional Chinese Medicine, Fuzhou, 350003, China  
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Abstract:
      

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 μ mol/L), β-estradiol (E2: 10?8 mol/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 surfaceenhanced laser desorption 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.
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