Aim ,To study the mechanism relative to therapeutic effects of matrine on adenine-induced renal interstitial fibrosis in rats. Methods Sixty male Wistar rats were selected and randomly divided into 3 groups： normal c...Aim ,To study the mechanism relative to therapeutic effects of matrine on adenine-induced renal interstitial fibrosis in rats. Methods Sixty male Wistar rats were selected and randomly divided into 3 groups： normal control group （NCG） consisted of 8 rats, adenine treated group （ATG） 28 rats, and matrine treated group （MTG） 24 rats. Each rat in ATG and MTG was gavaged with adenine （250 mg·kg^-1·d^-1 ） for 21 d. After gavage with adenine for one week, each rat in MTG was administered intraperitoneally matrine（20 mg·kg^-1·d^-1 ） in vehicle （ 1 mL of 0.9% sodium chloride） daily. On days 14, 21, and 28, the serum levels of urea nitrogen, creatinine, and IL-6 were determined and the rat kidneys of ATG, MTG and NCGwere examined pathologically. Radioimmunoassay for serum IL- 6 immunohistochemical staining for TGF-β1 expression in the kidney and semiquantitative analysis were performed. HE staining for semiquantitative analysis of tubulointerstitial injury. Results The serum levels of urea nitrogen and creatinine in MTG were lower as compare to ATG （ P 〈 0.05 ） whereas serum IL- 6 and renal TGF-β1 expression levels were significantly lower than those in ATG （P 〈0.05 ）, but all these indexes were higher than those in NCG （P 〈 0.01 ）. In MTG, the index of tubulointerstitial lesion was lower than that in ATG （P 〈 0.05 ）. Conclusion Matrine inhibits the renal tubulointerstial fibrosis in the adenine-induced rat model by suppressing serum level of IL-6 and expression of TGF-β1 in the tubulointerstitium.展开更多
文摘Aim ,To study the mechanism relative to therapeutic effects of matrine on adenine-induced renal interstitial fibrosis in rats. Methods Sixty male Wistar rats were selected and randomly divided into 3 groups： normal control group （NCG） consisted of 8 rats, adenine treated group （ATG） 28 rats, and matrine treated group （MTG） 24 rats. Each rat in ATG and MTG was gavaged with adenine （250 mg·kg^-1·d^-1 ） for 21 d. After gavage with adenine for one week, each rat in MTG was administered intraperitoneally matrine（20 mg·kg^-1·d^-1 ） in vehicle （ 1 mL of 0.9% sodium chloride） daily. On days 14, 21, and 28, the serum levels of urea nitrogen, creatinine, and IL-6 were determined and the rat kidneys of ATG, MTG and NCGwere examined pathologically. Radioimmunoassay for serum IL- 6 immunohistochemical staining for TGF-β1 expression in the kidney and semiquantitative analysis were performed. HE staining for semiquantitative analysis of tubulointerstitial injury. Results The serum levels of urea nitrogen and creatinine in MTG were lower as compare to ATG （ P 〈 0.05 ） whereas serum IL- 6 and renal TGF-β1 expression levels were significantly lower than those in ATG （P 〈0.05 ）, but all these indexes were higher than those in NCG （P 〈 0.01 ）. In MTG, the index of tubulointerstitial lesion was lower than that in ATG （P 〈 0.05 ）. Conclusion Matrine inhibits the renal tubulointerstial fibrosis in the adenine-induced rat model by suppressing serum level of IL-6 and expression of TGF-β1 in the tubulointerstitium.
