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[Effects of huangkui capsule on renal inflammatory injury by intervening p38MAPK signaling pathway in rats with adriamycin-induced nephropathy].

OBJECTIVE
To explore the potential mechanisms of huangkui capsule (HKC), an extract from Abelmoschus manihot (AM), for ameliorating renal inflammatory injury by regulating p38 mitogen-activated protein kinase (MAPK) signaling pathway in rats with adriamycin-induced nephropathy (ADRN).


METHOD
Nineteen Sprague-Dawley (SD) rats were randomly divided into three groups, the sham-operation group, the untreated model group,and the HKC-treated group. Rats in the untreated model group and the HKC-treated group were made into ADRN model by right nephrectomy and twice intravenous injections of adriamycin( ADR, 0.4 mL and 0.2 mL respectively within 4 weeks). After the model successfully established, rats in the HKC-treated group were orally given HKC (2 mg x kg(-1) per day), while rats in the untreated model group and the sham-operation group were intervened with distilled water respectively. The intervention for all rats was 4 weeks. Rats' body weight were weighted and 24 h urinary protein excretion (Upro) was detected at the end of the 1st, 2nd, 3rd, and 4th week after the intervention of HKC or distilled water. All rats were sacrificed at the end of the 8th week after nephrectomy, and then, to withdraw blood and kidney to examine the blood biochemical parameters, the glomerular morphological changes, alpha-smooth muscle actin (alpha-SMA) and collagen type I expressions,and the glomerular macrophages infiltration. Besides, the protein expression of transforming growth factor (TGF)-beta1, p38MAPK, as well as phosphorylated p38MAPK (p-p38MAPK) in renal tissues were detected by Western blotting.


RESULT
As compared with rats in the untreated model group, in the HKC-treated group,the HKC treatment significantly improved Upro, serum albumin, mesangial cell proliferation, extracellular matrix (ECM) and collagen deposition,and decreased the expression of alpha-SMA and collagen type I and the infiltration of ED1+ and ED3+ cells in glomeruli. In addition, it significantly down-regulated the protein expression of TGF-beta1 and p-p38MAPK in renal tissues.


CONCLUSION
HKC had the effects on ameliorating renal inflammatory injury in vivo. It could reduce the expression of TGF-beta1 and improve the infiltration and activation of inflammatory cells in glomeruli by way of intervening p38MAPK signaling pathway in kidney through down-regulating the protein expression of p-p38MAPK, as the key signal molecule.