Chun-Yan Feng1, Xiu-Rong Huang2, Ming-Xin Qi1, Song-Wen Tang2, Sheng Chen1, Yan-Hong Hu1, Fa-Jie Ke1, Xin Wang3. 1. Department of Ophthalmology, Second Affiliated Peoples Hospital of Fujian University of Traditional Chinese Medicine, Fuzhou 350003, Fujian Province, China. 2. Research Center of Pathophysiology, Fujian University of Traditional Chinese Medicine, Fuzhou 350003, Fujian Province, China. 3. Department of Laboratory, Fujian University of Traditional Chinese Medicine subsidiary Rehabilitation Hospital, Fuzhou 350003, Fujian Province, China.
Abstract
AIM: To investigate the protective effects of the natural medicinal monomer ecdysterone (ECR) with estrogenic activity against oxidative damage in human lens epithelial cells B3 (HLE-B3) caused by hydrogen peroxide 21(H2O2) and to pursue the possible mitochondrial proteomic regularity of the protective effects. METHODS: HLE-B3 cells were treated with H2O2 (300µmol/L), β-estuarial (E2; 10(-8)mol/L) and H2O2, ECR (10(-6)mol/L) and H2O2, or left untreated. Altered expression of all mitochondrial proteins was analyzed by protein array and surface-enhanced 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 expression of two protein spots (with M/Z of 6 532 and 6 809). When E2 mitigated the oxidative damage, the expression of one protein spot (M/Z 6 532) was down-regulated. In contrast, ECR down-regulated both of protein spots (M/Z 6 532 and 6 809). CONCLUSION: ECR could effectively inhibite H2O2 induced oxidative damage in HLE-B3 cells. The protein spot at M/Z of 6 532 might be the target spot of ECR against oxidative damage induced by H2O2.
AIM: To investigate the protective effects of the natural medicinal monomer ecdysterone (ECR) with estrogenic activity against oxidative damage in human lens epithelial cells B3 (HLE-B3) caused by hydrogen peroxide 21(H2O2) and to pursue the possible mitochondrial proteomic regularity of the protective effects. METHODS: HLE-B3 cells were treated with H2O2 (300µmol/L), β-estuarial (E2; 10(-8)mol/L) and H2O2, ECR (10(-6)mol/L) and H2O2, or left untreated. Altered expression of all mitochondrial proteins was analyzed by protein array and surface-enhanced 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 expression of two protein spots (with M/Z of 6 532 and 6 809). When E2 mitigated the oxidative damage, the expression of one protein spot (M/Z 6 532) was down-regulated. In contrast, ECR down-regulated both of protein spots (M/Z 6 532 and 6 809). CONCLUSION: ECR could effectively inhibite H2O2 induced oxidative damage in HLE-B3 cells. The protein spot at M/Z of 6 532 might be the target spot of ECR against oxidative damage induced by H2O2.
Authors: Andrea N Moor; James M Flynn; Srinivas Gottipati; Frank J Giblin; Patrick R Cammarata Journal: Mitochondrion Date: 2005-08 Impact factor: 4.160
Authors: Curtis L Nordgaard; Pabalu P Karunadharma; Xiao Feng; Timothy W Olsen; Deborah A Ferrington Journal: Invest Ophthalmol Vis Sci Date: 2008-03-14 Impact factor: 4.799
Authors: Andrea N Moor; Srinivas Gottipati; Robert T Mallet; Jie Sun; Frank J Giblin; Rouel Roque; Patrick R Cammarata Journal: Exp Eye Res Date: 2004-05 Impact factor: 3.467