AIM: To explore the effect of hydrogen sulfide(H₂S)on oxidative stress in diabetic cataract rats and its mechanism.

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.