Aim To investigate the effects of Ginkgo biloba extract （GbE） on renal fibrosis in STZ induced diabetic rats and high glucose （HG） cultured proximal tubular epithelial cells （NRK-52E）. Methods In vivo, rats were randomized into six groups termed normal control, diabetes mellitus , low dose of GbE （50 mg · kg^-1 · d^-1） , in- termediate dose of GbE （100 mg · kg^-1·d^-1）, high dose of GbE （200 mg · kg^-1 · d^-1） and rapamycin （1 mg·kg^-1·d^-l）. After 12 weeks, the rats were sacrificed and then fasting blood glucose, creatinine （Cr） , blood u- rea nitrogen （BUN） , urine protein, kidney index, glycogen and collagen accumulation, and collagen IV and lami- NRK-52E cells were divided into six groups： normal nin expression were measured by different methods. In vitro, glucose （5.56 mmol · L^-1）, high glucose （60 mmol · L^-1）, low dose of GbE （10 mg · L^-1）, intermediate dose of GbE （20 mg· L^-1）, high dose of GbE （40 mg· L^-1） and rapamycin （20 nmol · L^-l）. The morphological changes of cells were observed by microscopy after culturing for 48 h. Akt, roTOR and p70S6K, were examined by western blotting both in the renal cortex of rats and NRK-52E cells. Results Compared with diabetic rats, the lev- els of Cr, BUN, urine protein, kidney index, accumulation of glycogen and collagen, and expression of collagen IV and laminin in the renal cortex were all decreased in GbE treated rats. Furthermore, GbE ameliorated the morpho- logical changes of NRK-52E cells caused by HG. In addition, GbE reduced the expression of E-cadherin, oL-SMA, snail and phosphorylation of Akt, roTOR and p70S6K in diabetic renal cortexes and NRK-52E cells exposed to HG. Conclusion GbE was a satisfactory agent to prevent renal fibrosis in diabetic nephropathy, and this effect might be associated with the inhibition of the Akt/mTOR signaling pathway.
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