| Diabetes mellitus is the most common serious metabolic disorder disease. The complications would cause a series of functional and structural damage in the peripheral nervous system and central nervous system. In addition, diabetic nephropathy is one of the most common vascular complications of diabetes mellitus. Apoptosis of cells closely involved in the occurrence of diabetic nephropathy. In recent years, It was found that the extracts of Ginkgo biloba leaves (EGb) could inhibit the apoptosis of renal tubular epithelial cells. The main active ingredients of EGb are flavonoid glycoside and Ginkgo lactone. Flavonoid glycoside has been confirmed with scavenging free radicals and anti lipid peroxidation. It has reported that EGb can capture free radicals and inhibition cell apoptosis induced by the free radicals.Aim Male Wistar rats were used as the subjects. The protective effect of of extracts of ginkgo biloba leaves (EGb) on renal cortex and its mechanism in diabetic rats were explored through the detection of biochemistry, histology and molecular biology.Methods The diabetic rats model was produced by injecting streptozotocin (STZ,50 mg.kg-1). After 3 months, detection mRNA expression of Bax and Bcl-2 by RT-PCR, and the Bcl-2 and Bax protein expression in renal cortex of diab-etic rats were respectively detected by immunohistochemistry and westernblot technique.Results After treatment, blood glucose test showed that Ins group was lower than that in M, GL (50mg.kg-1EGb), GH (100mg.kg-1EGb) group (P<0.05). RT-PCR results showed that EGb significantly increased the expression of Bax in kidneys of mRNA level (compared with M group GL group GH group P<0.05, P<0.01), and the expression of Bcl-2 mRNA levels (compared with M group, GL group P<0.05 and GH group P<0.01). The results of immunohistochemistry showed that, compared with the normal group, the protein expression of Bcl-2 in renal cortex of diabetic rats group decreased significantly (P<0.01), and the expression of Bax increased markedly (P<0.01).Compared with the model group, the expression of Bcl-2 in renal cortical significantly increased respectively(P<0.05, P<0.01) in EGb (50,100 mg.kg-1)-treated groups. There was no obviously diference in the expression of Bax between EGb (50mg.kg-1) treated group and the model group (P>0.05), while the expression of Bax in EGb (100mg.kg-1) treatment group decreased significantly (P<0.05).Conclusion EGb can significantly increase Bcl-2 protein expression and inhibit Bax protein expression in renal cortex of diabetic rats, which may account for the protective effects. |
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