[Mechanism of combined treatment with Shenkangling Decoction and prednisone in rats with adriamycin-induced nephropathy].

OBJECTIVE

To study the mechanism of Shenkangling (SKL), a compound traditional Chinese herbal medicine, combined with prednisone in treating adriamycin-induced nephropathy in rats.

METHODS

Sixty-six SD male rats were randomly divided into normal control group, untreated group, prednisone group, SKL group and SKL plus prednisone group. Except the normal control group, rats were injected once via caudal vein with adriamycin (5.5 mg/kg) to induce nephropathy. Then, the rats were administered with prednisone, SKL, prednisone plus SKL or distilled water for 3 weeks, respectively. After harvest, 24-hour urine protein excretion, tumor necrosis factor-alpha (TNF-alpha) and nitric oxide (NO) contents in serum, and content of nuclear transcription factor-kappa B (NF-kappaB) p65 in mononuclear cells were determined, and correlation analysis among these parameters was performed. The content of NF-kappaB p65 was assayed with the patented method of Active Motif; TNF-alpha was assayed with enzyme-linked immunosorbent assay, and the content of NO was assessed by the method of nitrate reductase. The change of foot process in renal glomerulus was observed under an electron microscope.

RESULTS

When the rats were administered with prednisone, SKL correspondingly, the contents of NF-kappaB p65, TNF-alpha and NO as well as 24-hour urine protein excretion were lower than those in the untreated group (P<0.01), and the fusion of foot process only recovered partially. Compared with other treated groups, the contents of NF-kappaB p65 and NO as well as 24-hour urine protein excretion were significantly decreased in SKL plus prednisone group (P<0.01, P<0.05), and the fusion of foot process recovered mostly also. There was no interaction between SKL and prednisone in decreasing the content of TNF-alpha.

CONCLUSION

Renal injury can be postponed and improved when treated with SKL plus prednisone; it may contribute to the depression of abnormal activation of NF-kappaB, and the inhibition of production of TNF-alpha and NO.