Effect of TanshinoneⅡA on Renal Tumor Growth Factor-beta 1 and Nuclear Factor-kappa B in Diabetic Nephropathy Rats / 广州中医药大学学报

ABSTRACT

Objective To observe the effect of tanshinone ⅡA on renal transforming growth factor beta 1 (TGF-β1) and nuclear factor-kappa B (NF-κB) p65 mRNA and protein expression in diabetic nephropathy (DN) rats, thus to evaluate the therapeutic effect and mechanism of tanshinone ⅡA. Methods SD rats were used as the experimental animal. DN rat model was induced with 40 mg/kg of streptozocin ( STZ) . The rats were randomized into normal group, model group, and tanshinone ⅡA ( 10 mg·kg -1·d -1, im) group. On the experimental day 30, we examined the body weight, water in-take volume, 24-hour urine protein, fasting glucose ( Glu) , serum creatinine ( Cr) , blood urea nitrogen ( BUN) , total protein ( TP) and albumin ( Alb). Renal slices after periodic acid Schiff staining ( PAS) were used for the observation of renal pathology. Semi-quantitative reverse transcription polymerase chain reaction ( RT-PCR) was used for the detection of renal TGF-β1 and NF-κB p65 mRNA expression, and Western blotting method was used for the measurement of TGF-β1 and NF-κB p65 protein expression in rats of different groups. Results Compared with the normal group, body weight was decreased, water in-take volume and 24-hour urine protein were increased, serum Glu, Cr, and BUN levels were elevated, TP and Alb levels were decreased, renal pathological damage occurred, and renal TGF-β1 and NF-κB p65 mRNA and protein expressin were promoted in the model group (P<0.05 or P<0.01). Tanshinone ⅡA group had an effect on decreasing water in-take volume, 24-hour urine protein, serum levels of Glu, Cr and Bun, increasing TP and Alb levels, relieving renal pathological damage, and reducing the protein and mRNA expression of renal TGF-β1 and NF-κB p65 ( P<0.05 or P<0.01 compared with the model group). Conclusion Tanshinone ⅡA has protective effect on kidney probably through inhibiting renal TGF-β1 and NF-κB p65 expression in DN rats.