| Objective: To study the protective effect of resveratrol on glomerular mesangial cells(HBZY-1)under oxidative stress induced by palmitic acid,so as to provide scientific basis for the prevention and treatment of diabetic nephropathy.Methods:(1)In the whole experiment,wild type C57/LB6 mice and C57/LB6 spontaneous diabetic mice were used.Under the condition that C57/LB6 spontaneous diabetic mice produce serious diabetes,the expression difference of inflammatory and fibrogenic factors in the glomeruli of C57/LB6 mice was detected by immunoconfocal method.(2)In vitro experiments,the cultured HBZY-1 cells were divided into three groups.There are normal control group(blank control group,NC group),model control group(Palmitic Acid group,PA group),model experimental group(Palmitic Acid + Resveratrol group,PA + RES group).Western blot was used to detect the expression of NF-кBp65,BTG2,Fox O1 A,FN,α-SMA and Bax in HBZY-1 cells.Results:(1)The expression of NF-кBp65 and α-SMA in the glomeruli of spontaneous diabetic mice increased significantly with the aggravation of the incidence of diabetes(P ﹤ 0.01).(2)Compared with NC group,NF-кBp65,FN and α-SMA in PA group increased significantly in expression groups(P﹤0.01).In the mean time,the expression of apoptosis factors Fox O1 A and Bax also increased(P﹤0.01),while the expression of anti proliferation factor BTG2 protein decreased(P﹤0.01),and the degree of decrease was dose-response relationship with the content of palmitic acid.(3)After the intervention of resveratrol on the mesangial cells cultured in oxidative stress,it was found that the expression of NF-кBp65,FN,α-SMA,Fox O1 A and Bax decreased in PA + RES group,but the expression of BTG2 increased significantly compared with PA group(P﹤0.01).Conclusions:Resveratrol has the role of reduced the expression of those factor of NF-кBp65,FN,α-SMA,Fox O1 A and Bax in HBZY-1 which stimulated by palmitic acid,and up regulated the factor expression of BTG2.This study illustrates that resveratrol can reduce or inhibit the glomerular inflammatory response and fibrosis formation process through the expression change of these factors. |