目的：探讨气体信号分子硫化氢(H₂S)对大鼠视网膜缺血再灌注损伤（retinal ischemia-reperfusion injury,RIRI）过程中细胞凋亡及Bcl-2和Bax蛋白表达的影响。 方法：以硫氢化钠（NaHS）作为H₂S的供体。将54只SD大鼠随机分成正常组、视网膜缺血再灌注损伤组（RIRI组）及硫氢化钠（NaHS）干预组，后两组进一步分为再灌注后6，24，48，72h组。采用前房灌注加压的方法建立RIRI模型，TUNEL法检测视网膜神经细胞凋亡，免疫组织化学法检测视网膜组织中Bcl-2和Bax蛋白的表达。 结果：细胞凋亡出现于缺血灌注后6h，并逐渐递增, 24h达到高峰, 48h开始下降。与RIRI组比，NaHS组Bcl-2蛋白表达增多，Bax蛋白表达减少（均P<0.05）。 结论：H₂S预处理可通过上调Bcl-2蛋白表达、下调Bax蛋白表达、升高Bcl-2/Bax比值从而调控细胞凋亡，对大鼠RIRI进行保护作用。

To explore the effect of hydrogen sulfide(H₂S) on cell apoptosis and expression of Bcl-2/Bax in rat retinal ischemia-reperfusioninjury(RIRI). METHODS:A total of 54 SD rats were randomly divided into normal control group,ischemia-reperfusion model group and sodium hydrosulfide(NaHS) treatment group,the last two groups were subdivided into group 6, 24, 48, 72 hours after reperfusion. The models of RIRI were made by elevating intraocular pressure.Apoptosis was assessed by the terminal deoxynucleoitidyl transferase mediated dUTP nick end labeling method,and the expression of Bcl-2/Bax was studied by immunohistochemistry. RESULTS:There was a significant number of TUNEL positive cells 6 hours after transient ischemia peaked at the 24 hours, followed by a decrease at the 48 hours. Compared with RIRI group, Bcl-2 protein expression was increased, Bax protein level were decreased in NaHS group (all P<0.05). CONCLUSION: H₂S can enhance the expression of Bcl-2,decrease the expression of Bax, increase the Bcl-2 /Bax ratio and decrease the apoptosis of ganglion cells. H₂S shows a significant protection for retinal ganglion cells with RIRI.