| Objective: To investigate the role of 17β-estradiol on the expression ofvascular endothelial growth factor (VEGF) and on the releasing rate of lactatedehydrogenase (LDH) in human RPE that was induced by experimental hypoxic injuries.Methods: Establish the model of human RPE induced by hypoxic injuries with CobaltChloride (CoCl2). The experiment was devided into 3 parts. (1) to detect the influenceof hypoxic injuries by CoCl2 on human RPE cells; (2) to research on the effect of17β-estradiol on hypoxia-injuried RPE cells; (3) after the intervention of 17β-estradioland Tamoxifen, go further on studying their influences on RPE cells. The releasing rate ofLDH is detected by chromatometry. The expression of VEGF protein were studied bycellular immunohistochemistry. The VEGF mRNA was detected by RT-PCRtechnique. Result: (1) CoCl2 can elevate the level of VEGF and the releasing rate ofLDH. with the concentration of CoCl2 increasing, both VEGF's expression and thereleasing rate of LDH were increasing, they were concentration-dependent (P＜0.05). (2)with the concentration of 17β-estradiol increasing, the expression of VEGF and thereleasing rate of LDH were degressive (P＜0.05) .(3) when the effect of 17β-estradiolwere obstructed by tamoxifen, the expression of VEGF and the releasing rate of LDHwere not very different with the results of the hypoxia-injuried group, the difference wasnot statistically significant. (P＞0.05) Conclusion: Experimental Cobalt Chloridehypoxic injuries increased the expression of VEGF on human RPE cells, which suggestedVEGF may play an important role in hypoxic injuried mechanism of RPE cells.17β-estradiol can rescue RPE cells from retinal hypoxic injuries through down-regulatingthe expression of VEGF expression and decreasing the releasing rate of LDH. The effectcan be blocked by its antogon-Tamoxifen.
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