AIM:To explore the effects and potential mechanisms of curcumin on retinal Müller cell in early diabetic rats.·METHODS:Diabetic rats were induced by a single intraperitoneal injection of streptozotocin(STZ).Male Sprague-Dawley(SD) rats were randomly assigned into 4groups:control group(nave SD rats administered with a single intraperitoneal injection of citric buffer),diabetic group(STZ-diabetic rats),dimethyl sulfoxide(DMSO)group(diabetic rats intraperitoneally administered with mixture of DMSO and normal saline,once a day) and curcumin group(diabetic rats intraperitoneally administered with curcumin,80mg/kg,once a day).Three months after diabetes onset,malondialdehyde(MDA,indication of oxidative stress level) and reduced glutathione(GSH) in retina were detected with kits,glial fibrillary acidic protein(GFAP) in retina was revealed by immunohistochemistry and Western blot,and retinal glutamine synthetase(GS) were observed by Western blot.·RESULTS:Compared with control group,retinal MDA was increased,and GSH was decreased in diabetic and DMSO groups(P <0.05,respectively).While,retinal MDA and GSH in curcumin group showed no difference compared with control group(P >0.05).Furthermore,upregulation of retinal GFAP and down-regulation of retinal GS were detected in diabetic and DMSO groups,and no alteration could be observed in curcumin group revealed with Western blot.Compared with control group,retinal Müller cells showed significant increase in GFAP immunochemistry staining in diabetic and DMSO groups.Moreover,GFAP-positive staining was decreased in curcumin group compared with diabetic group.·CONCLUSION:Curcumin inhibits diabetic retinal oxidative stress,protects Müller cell,and prevents thedown-regulation of GS in diabetic retina.Therefore,curcumin has a therapeutic potential in the treatment of diabetic retinopathy(DR). AIM: To explore the effects and potential mechanisms of curcumin on retinal Müller cells in early diabetic rats. METHODS: Diabetic rats were induced by a single intraperitoneal injection of streptozotocin (STZ). Male Sprague-Dawley (SD) rats were randomly assigned into 4groups: control group (nave SD rats administered with a single intraperitoneal injection of citric buffer), diabetic group (STZ-diabetic rats), dimethyl sulfoxide (DMSO) group (diabetic rats intraperitoneally administered with mixture of DMSO and normal saline, once a day ) and curcumin group (diabetic rats intraperitoneally administered with curcumin, 80 mg / kg, once a day) .Three months after diabetes onset, malondialdehyde (MDA, indication of oxidative stress level) and reduced glutathione (GSH) in retina were detected with kits, glial fibrillary acidic protein (GFAP) in retina was revealed by immunohistochemistry and Western blot, and retinal glutamine synthetase (GS) were observed by Western blot. RESULTS: Compared with control group, retinal (P <0.05, respectively) .While, retinal MDA and GSH in curcumin group showed no difference compared with control group (P> 0.05) .Furthermore, upregulation of retinal GFAP and down-regulation of retinal GS were detected in diabetic and DMSO groups, and no alteration could be observed in curcumin group revealed with Western blot. Compared with control group, retinal Müller cells showed significant increase in GFAP immunochemistry staining in diabetic and DMSO groups. Moreover , GFAP-positive staining was decreased in curcumin group compared with diabetic group. · CONCLUSION: Curcumin inhibits diabetic retinal oxidative stress, protects Müller cell, and prevents thedown-regulation of GS in diabetic retina. Beforefore, curcumin has a therapeutic potential in the treatment of diabetic retinopathy (DR).