Effects of ecdysterone on the expression of NF-kappaB p65 in H2O2 induced oxidative damage of human lens epithelial cells / 中国中西医结合杂志

<p><b>OBJECTIVE</b>To study the effects of ecdysterone (ECR) on the expression of nuclear factor (NF)-kappaB in H2O2 induced oxidative damage of human lens epithelial cells (HLECs).</p><p><b>METHODS</b>The cultured HLECs were divided into 5 groups, i.e., the control group, the H2O2 group, the beta-estradiol (E2) group, the ECR group, and the pyrrolidine dithiocarbamate group (PDTC) group. The expression rate of NF-kappaB p65 in the HLECs were detected by flow cytometer (FCM).</p><p><b>RESULTS</b>The expression of NF-kappaB p65 occurred in normal HLECs (9. 53%). The expression rate of NF-kappaB p65 in the H2O2 group obviously increased (39.87%, P < 0.01). The expression rate of NF-kappaB p65 in the PDTC group obviously decreased (5.90%, P < 0.01). The expression rates of NF-kappaB p65 in the ECR group (13.99%) and the E2 group (25.18%) ranged between the control group and the H2O2 group, but still lower than that of the H2O2 group (P < 0.01).</p><p><b>CONCLUSIONS</b>The activation of NF-kappaB in the HLECs could be induced by H2O2 ECR with the estrogenic activity could effectively inhibit the activation of NF-kappaB.</p>

Mitochondrial proteomic analysis of isopsoralen protection against oxidative damage in human lens epithelial cells / 中国结合医学杂志

<p><b>OBJECTIVE</b>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 (H(2)O(2)) and to pursue the possible mitochondrial proteomic regularity of the protective effects.</p><p><b>METHODS</b>HLE-B3 cells were treated with H(2)O(2) (300 μ mol/L), β-estradiol (E(2): 10(-8) mol/L) and H(2)O(2), ISR (10(-5) mol/L) and H(2)O(2), 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.</p><p><b>RESULTS</b>H(2)O(2) up-regulated the expressions of two protein spots (with m/z of 6532 and 6809). E(2) 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).</p><p><b>CONCLUSIONS</b>ISR could effectively inhibit H(2)O(2)-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 H(2)O(2).</p>

Effect of Rhizoma Curcumae and arsenite trioxide on proliferation and signal transduction molecule of lens epithelial cell / 中国中药杂志

<p><b>OBJECTIVE</b>To investigate the effect of Rhizoma Curcumae (RC), arsenite trioxide (As2O3) on proliferation ana signal transduction molecule in lens epithelial cell (LEC), in order to provide experiment evidence for prevention and treatment of after cataract.</p><p><b>METHOD</b>Proliferation of cultured bovine LEC were induced by induced by recombinant human basic fibroblast growth factor (rhbFGF); Inhibitory rates of LEC proliferation induced by RC, As2O3 were detected by methyl thiazolyl tetrazolium (MTT); Inhibitory effects of expression of proliferating cell nuclear antigen (PCNA) induced by RC, As2O3 in LEC were assayed via flow cytometer (FCM); Concentrations of LEC calcium ([Ca2+]i) were determined by spectrofluoremeter, intracellular concentrations of cyclic adenosine monophosphate (cAMP) and cyclic guanosine monophosphate (cGMP) of LEC were measured by radioimmunoassay.</p><p><b>RESULT</b>Inhibitory rates of RC, As2O3 on LEC proliferation induced by rhbFGF increased significantly, showing dose-dependent (P < 0.01). PCNA expression of LEC proliferation induced by rhbFGF were down regulated obviously by RC, As2O3, showing dose-dependent (P < 0.01). Concentrations of [Ca2+]and cAMP increased and cGMP decreased significantly in LEC of proliferation inhibited by RC, As2O3 (P < 0.01).</p><p><b>CONCLUSION</b>RC, As2O3 can inhibit LEC proliferation obviously. Signal transductions of [Ca2+]i, cAMP, cGMP may be the important molecular mechanism. There are broad prospect for RC, As2O3 on prevention and treatment of after cataract.</p>