Mitochondrial proteomic analysis of ecdysterone protection against oxidative damage in human lens epithelial cells

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(H2 O2) 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; 10-8mol/L) and H2 O2,ECR(10-6mol/L) and H2 O2,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 downregulated 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 H2 O2.

Mitochondrial Proteomic Analysis of Isopsoralen Protection against Oxidative Damage in Human Lens Epithelial Cells

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.

Quantitative mitochondrial proteome of pancreatic INS-1β cells stimulated with prolonged high glucose using SILAC

Most type 2 diabetics are accompanied with deficiency of insulin secretion and hyperglycemia. It has reported that glucose-stimulated insulin secretion of β cell (GSIS)

Mitochondrial Proteomics

Mitochondria are one of the most important organelles in a cell, playing essential roles in cell physiological processes including energy production, metabolism, ion homeostasis, aging