Interventional effects of fosinopril on TGF-β1/Smad signaling pathway in glomerular mesangial cells / 临床儿科杂志

ABSTRACT

Objective To observe the effects of fosinopril(FOS)on secretion of ColⅠ,expression of Smad2、Smad7 mRNA in TGF-β1-induced glomerulomesangial cells(GMC)in rat model. Methods Rat glomerular mesangial cells were cultured in vitro,passages 3 - 10 cells were used in the study after identification,and the cells were divided into 3 groupscontrol group(Ctrl group),TGF-β1 group,and fosinopril group. Expression of Col Ⅰ in cell culture supernatant was detected by the enzyme-linked immunosorbent assay(ELISA)at 6 h,24 h and 48 h. Changes of Smad2,Smad7 mRNA expression were evaluated by fluorescent quantitation PCR. Results Glomerular mesangial cells had Col Ⅰ protein expression. Secretion of Col Ⅰ was significantly higher in TGF-β1 group than those in Ctrl group at each time point(P ＜ 0.01),however the Col Ⅰ was significantly lower in fosinopril group at all time points than that in TGF-β1 groups(P ＜ 0.05). Glomerular mesangial cells also had Smad2,Smad7 mRNA expressions. The expressions of Smad2,Smad7 mRNA were significantly higher in TGF-β1 group than those in Ctrl group at each time point. Expression of Smad2 mRNA was significantly lower in fosinopril group than that in TGF-β1 group at all time points,while the difference in Smad7 mRNA expression between TGF-β1 group and fosinopril group showed no statistical significance(P ＞ 0.05). Conclusions Fosinopril could inhibit the secretion of Col Ⅰ and expression of Smad2 mRNA in glomerular mesangial cells induced by TGF-β1,suggesting that fosinopril might delay glomerular sclerosis through inhibiting the expression of Smad2 in TGF-β1/Smad signaling pathway.