| Objective To investigate the role of 17β-estradiol on the expression of hypoxia inducible factor-1 alpha(HIF-1α) in human RPE that was induced by experimental hypoxic injuries.Methods Cultured human RPE cells were subcultured and divided into normal control group(simple culture group),hypoxic injury group,17β-estradiol treatment group and 17β-estradiol+Tamoxifen group.The cultured cells were treated with CoCl2 of different concentration(50μmol/L,100μmol/L,200μmol/L和400μmol/L) for 4 hours to establish the hypoxic injury model in hypoxic injury group.The 17β-estradiol was administrated for 24 hours before 200μmol/L CoCl2 injury and subdivided into three subgroups according to different concentration of 17β-estradiol(10-4mol/L,10-5mol/L,10-6mol/L) in 17β-estradiol treatment group.The 17β-estradiol and Tamoxifen were administrated simultaneously for 24 hours before 200μmol/L CoCl2 injury.The expression of HIF-1αprotein was evaluated by immunocytochemical technique after injury.The expression of HIF-1αmRNA was detected by RT-PCR.Result(1) CoCl2 can elevate the level of HIF-1α..With the increasing concentration of CoCl2,the expression of HIF-1αwas increasing,and it was concentration-dependent(P＜0.05).(2) With the increasing concentration of 17β-estradiol,the expression of HIF-1αwas degressive(P＜0.05).(3) When the effect of 17β-estradiol was obstructed by tamoxifen,the expression of HIF-1αwas not very different with the results of the hypoxia-injuried group,the difference was not statistically significant.(P＞0.05) Conclusion Experimental Cobalt Chloride hypoxic injuries increased the expression of HIF-1αin human RPE cells,which suggested HIF-1αmay play an important role in hypoxic injuried mechanism of RPE cells.17β-estradiol can rescue RPE cells from retinal hypoxic injuries through down-regulating the expression of HIF-1αexpression.The effect can be blocked by its antagon Tamoxifen.
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