Effect of Atorvastatin on the JAK/STAT Signaling Pathway and SOCS-1 in Renal Tissue of the Diabetic Nephropathy Rats

Objective:To investigate the effects of atorvastatin on the JAK-STAT-SOCS regulating mechanism in the diabetic nephropathy rats.Methods:Totally 60 Wistar rats were divided randomly into three groups: normal control (control group),DN control (model group),atorvastatin treated group,20 rats in each group.The rat models were induced by right nephrectomy (50 mg/kg) and peritoneal injection of low-dosage streptozotocin.Atorvastatin (8 mg·kg-1·d-1) was administrated by gavage for 12 weeks.Body weight,the microalbuminuria (MALB-U),the urinary protein quantity in 24h (24 h Upr),serum creatinine(Scr) and urea nitrogen(BUN) were measured.PAS、HE staining was used to observe morphological changes of renal tissue under light microscope.Expression levels of p-STAT3,p-JAK2,SOCS-1 in renal tissue of rats detected by immunohistochemistry.Results:In 12w,MALB-U,24 h Upr,Scr and BUN of model group rats were higher distinctly than those of control group (respectively,P0.05).After treatment of atorvastatin,those were reduced distinctly (respectively,P0.05).Immunohistochemistry staining showed that in model group,the expressions of p-STAT3,p-JAK2,SOCS-1 in 12-week were higher significantly than those in control group (respectively,P0.05).After treatment of atorvastatin,the expression of SOCS-1 of renal tissue in treatment group was higher significantly compared with model group in the same period (respectively,P0.05),the expressions of p-STAT3 and p-JAK2 of renal tissue in treatment group were lower compared with those of model group in the same period (respectively,P0.05).Conclusion:Atorvastatin could reduce glomerular damage in DN,which mechanism may be involved in the in the inhibition of JAK-STAT-SOCS regulating mechanism.