[Electroacupuncture preconditioning alleviates kidney injury in hyperglycemic mice].

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 C57BL/6 mice were randomly divided into 4 groups: control, model, EA and sham EA groups, =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 (<0.01), the glomerular cross-sectional area was apparently increased (<0.000 1), the glomerular capillaries dilated, the matrix proliferated, the brush edge of renal tubules disappeared, the proportion of abnormal renal tubules increased (<0.000 1), and the expressions of TRPC6 and Nephrin in glomeruli and renal tissue were significantly increased (<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 (<0.01), the renal tissue injury was apparently alleviate, the cross-sectional area of glomerulus was reduced (<0.05), the brush edge of renal tubules changes were obviously improved, the proportion of abnormal renal tubules decreased (<0.000 1), and the expressions of TRPC6 and Nephrin in glomerulus and renal tissue decreased (<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.