AIM: To investigate the influence of propylene glycol mannite sulfate(PGMS)on the expression of tumor necrosis factor -α(TNF-α)and interleukin-1β(IL-1β), in diabetic retinopathy by a rat model, to study the mechanism of PGMS against diabetic retinopathy, and provide a reliable theoretical and experimental evidence for the PGMS to be applied to clinical prevention and treatment of diabetic retinopathy.

METHODS: Male Wistar rats were randomized into 4 groups, normal control group, diabetic control group and PGMS in group, the PGMS in groups included the doses of 50mg/kg and 100mg/kg. 1% streptozotocin(STZ)of 60 mg/kg was intraperitoneally injected in rats to establish the diabetic models. The PGMS with the doses of 50mg/kg and 100mg/kg were used to gavage in different groups of models for 12wk. Twelve weeks later, the animals were sacrificed and retinas were isolated. The aqueous humors and serums were taken, expressions of TNF-α and IL-1β protein in retinas, aqueous humors and serums were detected by enzyme-linked immunosorbent assay(ELISA), respectively. The location and the expression of TNF-α and IL-1β protein in retina tissue was detected by immunohistochemistry.

RESULTS: Twelve weeks after the use of PGMS, the level of blood glucose was not changed. ELISA showed that the expression of TNF-α and IL-1β protein in serum and retina was significantly increased in diabetic control group than in normal control group(P<0.05), but in the groups which PGMS was given reduced, lower than those in diabetes mellitus(DM)group, especially as the concentration of PGMS increased(P<0.05). But the levels of aqueous humor's TNF-α and IL-1β proteins in PGMS group were not reduced. Immunohistochemistry showed that the TNF-α protein was almost not expressed in normal control group. But the TNF-α protein was highly expressed in diabetic control group. The expression mainly located in the ganglion cell layer, the inner plexiform layer, outer plexiform layer and pigment epithelium. The TNF-α protein was weakly expressed at the group of 50mg/kg PGMS, the TNF-α protein was almost not expressed at the group of 100mg/kg PGMS. When the normal control group was detected, the IL-1β protein was weakly expressed in the outer plexiform layer. But the IL-1β protein was also highly expressed in diabetic control group.The expression mainly located in the inner plexiform layer, outer plexiform layer and pigment epithelium. The IL-1β protein was weakly expressed at the group of 50mg/kg and 100mg/kg PGMS.

CONCLUSION: PGMS can treat the diabetic retinopathy by downregulating the expressions of TNF-α and IL-1β in early diabetic retinopathy. PGMS maybe have a good control effect on early diabetic retinopathy.