| The effect of HIF-1αin SD rats' retinal ischemia-reperfusion injuryObjective To investigate the potential role and protective effects of hypoxia inducible factor-1α(HIF-1α) in SD rats' retinal ischemia-reperfusion injury model.Methods SD rats were divided at random.Rats' optic nerve sheaths were clamped by mini-vessel forceps for 30 seconds and then unclamped immediately to make the retinal ischemia-reperfusion injury model.2h,4h,8h,12h,24h,48h after ischemia-reperfusion injury,the expression of HIF-1αand its downstream target gene products HO-1,P53 and VEGF in retina were confirmed by real-time PCR,Western immunoblot analysis and immunohistochemistry.SOD-1 and anti-apoptosis gene Bcl-2 were also detected.The expression of GFAP was detected by fluorescence immunohistochemistry to confirm the activation of M(U|¨)ller cells.Results The number of apoptotic retinal neurons is increased obviously after ischemia-reperfusion injury and peak on 24h.The expression of HIF-1 a protein,HO-1 mRNA,P53 mRNA and VEGF mRNA all present parabola tendency.And they peak on 12h,8h,24h and 12h respectively.The expression of SOD-1 and Bcl-2 decrease sharply at the beginning and then increase stably.The tendency of SOD-1 and Bcl-2 are same with HO-1 while the tendency of Bcl-2 is contracted to P53.The expression of HIF-1αincrease after ischemia-reperfusion injury by immunohistochemistry and its distribution mainly on the nerve fiber layer,retinal ganglion cell layer and inner nuclear layer.Conclusions ischemia-reperfusion injury start oxidative stress and apoptosis,and then injure retinal neurons and neuroglial cells.HIF-1αis significant in the whole reaction.The activation of HIF-1αstart the expression of tarhet gene HO-1,P53 and VEGF.And HO-1 has the effect of anti- oxidative stress and anti-apoptosis.M(U|¨)ller cells participate in.
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