目的：探讨硫化氢(H₂S)对糖尿病性白内障大鼠氧化应激的作用及其作用机制是否涉及调控沉默信息调节因子1(SIRT1)。

方法：将SD大鼠随机分为正常对照组、糖尿病模型组、低浓度NaHS组、高浓度NaHS组、单用NaHS组。NaHS作为H₂S的供体。糖尿病模型组、低浓度NaHS组、高浓度NaHS组大鼠一次性腹腔注射链脲佐菌素(streptozotocin， STZ，65mg/kg)建立糖尿病大鼠模型。采用BQ900裂隙灯观察各组大鼠晶状体的变化。自实验开始12wk后，采用硫代巴比妥酸法检测MDA的含量，黄嘌呤氧化酶法检测SOD 的含量，二硫代二硝基苯甲酸法检测GSH-Px的含量； Western blotting检测大鼠晶状体SIRT1的表达。

结果：糖尿病组大鼠晶状体出现不同级别的混浊，表明糖尿病性白内障大鼠模型复制成功。分别予低浓度NaHS、高浓度NaHS治疗后糖尿病大鼠晶状体混浊程度得到明显改善。与糖尿病模型组相比，分别给予低浓度NaHS、高浓度NaHS治疗的糖尿病大鼠晶状体MDA的含量明显下降，SOD和GSH-Px的水平显著增加。此外，Western blotting结果显示糖尿病模型组大鼠晶状体SIRT1的表达明显下调，分别予低浓度NaHS、高浓度NaHS治疗能有效逆转该趋势。

结论：H₂S能够抑制糖尿病性白内障大鼠氧化应激水平，其机制可能涉及上调SIRT1的表达。

METHODS:SD rats were randomly divided into control group, diabetic group, low-dosage NaHS-treated group, high-dosage NaHS-treated group, and NaHS treated alone group. NaHS was used as a donor of H₂S. The diabetic model was established by a single intraperitoneally administrating streptozotocin(STZ, 65mg/kg). BQ900 slit lamp was used to recorded the changes of lenses. At the end of experiment, the level of superoxide dismutase(SOD)was measured by xanthine oxidase test, the activity of malondialdehyde(MDA)was detected by thiobarbituric acid test, and glutathione(GSH-Px)were detected by corresponding assay kits. Western blotting was applied to detect the expression of SIRT1.

RESULTS:The lenses of diabetic group showed different levels of turbidity, which demonstrated that diabetic cataract model was successfully established. Low-dosage NaHS and high-dosage NaHS treatment dramatically alleviated turbidity levels of lenses in diabetic rats, respectively. Compared to diabetic group, low-dosage NaHS and high-dosage NaHS treatment obviously decreased the levels of MDA and increased the levels of SOD and GSH-Px. Furthermore, the SIRT1 expression in lens of diabetic rats was downregulated, and low-dosage NaHS as well as high-dosage NaHS treatment significantly reversed this change.

CONCLUSION:H₂S protects against oxidative stress in STZ-induced diabetic rats involving upregulation of SIRT1.