[Effect of Kangxianling Decoction on expression of hepatocyte growth factor mRNA and phosphorylations of extracellular signal-regulated protein kinase 1/2 and p38 in renal tissue of rats with unilateral ureteral obstruction].

OBJECTIVE: To study the effect of Kangxianling Decoction (KXLD), a compound traditional Chinese herbal medicine, on expression of hepatocyte growth factor (HGF) mRNA and phosphorylations of extracellular signal-regulated protein kinase 1/2 (ERK 1/2) and p38 in renal tissue of rats with unilateral ureteral obstruction (UUO).

METHODS: Eighteen male SD rats were randomly divided into 3 groups: sham-operated group, untreated group and KXLD-treated group. A rat model of renal interstitial fibrosis was established by UUO. Rats with UUO were sacrificed after intragastric administration of KXLD for 14 days, and the parameters such as serum creatinine (SCr), blood urea nitrogen (BUN) and hydroxyproline in the kidney of rats in 3 groups were analyzed. The expression of HGF mRNA in kidney tissue was determined by reverse transcription polymerase chain reaction. The expressions of c-Met protein, ERK1/2 protein, p38 protein and the phosphorylations of ERK1/2 and p38 were determined by Western blotting method.

RESULTS: The levels of SCr, BUN and hydroxyproline in the untreated group were significantly increased as compared with those in the sham-operated group (P<0.05). The expression of HGF mRNA in the untreated group was significantly down-regulated. The expression of c-Met protein and the phosphorylations of ERK1/2 and p38 in the kidney tissue of rats with UUO in the untreated group were significantly up-regulated. After intervention with KXLD, the phosphorylations of ERK1/2 and p38 were all significantly inhibited except for c-Met expression. The HGF mRNA was increased in KXLD-treated group.

CONCLUSION: KXLD can decrease the level of collagen in the obstructed kidney of rats with UUO and alleviate the renal interstitial fibrosis in rats with UUO through enhancing the HGF mRNA expression and inhibiting the phosphorylations of ERK1/2 and p38.