Objective To explore the protective effect and molecular mechanism of electroacupuncture(EA) preconditioning on renal injury induced by streptozotocin(STZ) in hyperglycemic mice. Methods Eighty male C57 BL/6 mice were randomly divided into 4 groups: control

model

EA and sham EA groups

n=20 in each group. The hyperglycemic model was established by intraperitoneal injection of 0.1% STZ solution(50 mg/kg) for 5 days. EA preconditioning or sham EA was applied at "Zusanli"(ST36) and "Shenshu"(BL23)

once daily for 7 successive days in the EA or sham EA group. Three days after mode-ling

the blood glucose was measured after fasting for 6 hours. The degree of renal injury was observed by HE staining and PAS staining; the expressions of transient receptor potential cation channel 6(TRPC6) and Nephrin protein in glomerulus were observed by immunohistochemistry; the expressions of TRPC6 and Nephrin protein in renal cortex were detected by Western blot. Results Compared with the control group

the blood glucose level was significantly increased(P<0.01)

the glomerular cross-sectional area was apparently increased(P<0.000 1)

the glomerular capillaries dilated

the matrix proliferated

the brush edge of renal tubules disappeared

the proportion of abnormal renal tubules increased(P<0.000 1)

and the expressions of TRPC6 and Nephrin in glomeruli and renal tissue were significantly increased(P<0.01) in the model group. Following EA treatment and compared with the model and sham EA groups

the blood glucose was significantly down-regulated(P<0.01)

the renal tissue injury was apparently alleviate

the cross-sectional area of glomerulus was reduced(P<0.05)

the brush edge of renal tubules changes were obviously improved

the proportion of abnormal renal tubules decreased(P<0.000 1)

and the expressions of TRPC6 and Nephrin in glomerulus and renal tissue decreased(P<0.05) in the EA group. Conclusion EA preconditioning can alleviate renal injury in hyperglycemic mice

which is closely related to its effects in reducing renal TRPC6 and Nephrin expressions and inhibiting podocyte activation.