[Renal protective effects of vitamin E in diabetic rats]

To investigate the renal protective effect of vitamin E on streptozotocin induced diabetic rats, as well as the possible mechanism involved in.

Vitamin E 20 mg x kg(-1) x d(-1) was given to diabetic rats for 8 weeks. Urinary albumin excretion (UAE) was measured by radioimmunoassay. The changes of creatinine clearance rate (Ccr), nitric oxide(NO), nitric oxide synthase (NOS) and endothelin(ET) in the plasma and renal cortical tissue, membrane protein kinase C(PKC) in the renal glomeruli were observed.

At two weeks, diabetic rats had supernormal Ccr[(6.47 +/- 1.51) ml x min(-1) x kg(-1)], UAE[(15.60 +/- 1.64) microg/24h], NO[(37.30 +/- 3.77) micromol/L], NOS[(34.89 +/- 3.83) U/L] and PKC[(86.85 +/- 11.37) pmol x min(-1) x mg protein(-1)] of diabetic rats were increase but ET was decreased. At 8 weeks, PKC[(84.18 +/- 12.14 ) pmol x min(-1) x mg protein(-1)] and ET of diabetic rats was increased significantly, but NO[(22.75 +/- 2.89) micromol/L] and NOS[(21.34 +/- 1.92) U/L] of diabetic rats was lowered. After treated with vitamin E, Ccr[(4.46 +/- 0.49) ml x min(-1) x kg(-1)], UAE[(16.31 +/- 1.12) microg/24h], PKC[(65.19 +/- 8.83) pmol x min(-1) x mg protein(-1)] at 8 weeks were decreased significantly. Both NO[(33.13 +/- 3.77) micromol/L] and NOS[(30.16 +/- 2.89) U/L] in plasma and kidney tissue were lowered as compared with untreated diabetic group in two weeks. Vitamin E also delayed the NO and NOS lowering in 8 weeks.

Vitamin E could ameliorate early diabetic renal hemodynamic abnormality via inhibiting PKC, in which inhibition of NO production might be involved. It is important to reduced the PKC activity so as to prevent or delay the development of diabetic nephropathy.