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目的:研究镰形棘豆总黄酮防治肾间质纤维化作用及其机制。方法:大鼠按300 mg.kg-1ig镰形棘豆总黄酮,连续给药3 d后制备含药血清,空白组大鼠ig同体积生理盐水制备空白血清。将人肾小管上皮细胞(HK-2)用含10%胎牛血清的DMEM/F12(1∶1)培养基培养,分为4组:空白对照组、单纯转化生长因子-β1(TGF-β110μg.L-1)诱导组、空白血清对照组(TGF-β110μg.L-1+10%空白血清)、干预组(TGF-β110μg.L-1+10%镰形棘豆总黄酮含药血清)。药物干预24 h后,荧光定量PCR检测结缔组织生长因子(CTGF)、纤溶酶原激活物抑制物-1(PAI-1)、基质金属蛋白酶-9(MMP-9)mRNA的表达。结果:HK-2细胞经TGF-β1诱导后,CTGF,PAI-1 mRNA的表达显著上升,而MMP-9 mRNA的表达减弱,与空白对照组相比有统计学意义(P<0.05),经镰形棘豆总黄酮药物血清干预后,CTGF、PAI-1 mRNA的表达逐步下降,而MMP-9 mRNA的表达逐步上升,与单纯TGF-β1诱导组相比有统计学意义(P<0.05)。结论:镰形棘豆总黄酮在一定程度上能够抑制TGF-β1诱导的人肾小管上皮细胞纤维化,其机制可能与调节纤维化细胞因子CTGF,PAI-1和MMP-9的mRNA表达有关。
Objective: To study the effect and mechanism of total flavonoids of Oxytropis falcate on prevention and treatment of renal interstitial fibrosis. Methods: The rats were treated with 300 mg.kg-1ig total flavonoids of Oxytropis ochrocephala. Serum was prepared after continuous administration for 3 days. Blank serum was prepared by the same volume of normal saline in the blank group. Human renal tubular epithelial cells (HK-2) were cultured in DMEM / F12 (1: 1) medium containing 10% fetal bovine serum and divided into 4 groups: blank control group, transforming growth factor- (TGF-β110μg.L-1 + 10% blank serum), and the intervention group (TGF-β110μg.L-1 + 10% . The expression of connective tissue growth factor (CTGF), plasminogen activator inhibitor-1 (PAI-1) and matrix metalloproteinase-9 (MMP-9) mRNA were detected by real- Results: After induced by TGF-β1, the expression of CTGF and PAI-1 mRNA in HK-2 cells was significantly increased, while the expression of MMP-9 mRNA was down-regulated in HK-2 cells compared with the blank control group The expression of CTGF and PAI-1 mRNA decreased gradually and the expression of MMP-9 mRNA gradually increased after the serum of Oxytropis ochrocephala total flavonoids was intervened, which was statistically significant compared with TGF-β1 induction group (P <0.05) . CONCLUSION: The total flavonoids of Oxytropis ochrocephala can inhibit the TGF-β1-induced fibrosis of human renal tubular epithelial cells in a certain extent. The mechanism may be related to the regulation of mRNA expression of fibroblast cytokines CTGF, PAI-1 and MMP-9.