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作 者:王昆[1] 刘超[1] 袁庆欣[1] 刘翠萍[1] 徐宽风 茅晓东[1]
机构地区:[1]南京医科大学第一附属医院内分泌科,江苏南京210029
出 处:《南京医科大学学报(自然科学版)》2006年第8期636-639,648,共5页Journal of Nanjing Medical University(Natural Sciences)
摘 要:目的:探讨肝细胞生长因子(HGF)对高糖及结缔组织生长因子(CTGF)诱导肾小管上皮细胞(HKC)纤维化的影响。方法:体外培养HKC,分别在高糖及CTGF环境下加入不同浓度人重组肝细胞生长因子(rhHGF),以RT-PCR检测转化生长因子β1(TGF-β1)、CTGF、以及纤维化指标Ⅳ型胶原(COL4A1)、纤连蛋白(FN)、α平滑肌肌动蛋白(α-SMA)等的基因表达。结果:高糖及CTGF刺激下,细胞因子和纤维化指标表达均不同程度增加,其中,CTGF作用下,COL4A1表达明显低于高糖组(P<0.01)。高糖及CTGF环境下加入rhHGF后,纤维化指标显著降低(P<0.01),其中高糖+rhHGF组,CTGF表达减少,TGF-β1表达无明显改变(P>0.05)。结论:HGF可通过抑制TGF-β下游因子CTGF的表达,发挥抗肾小管上皮细胞纤维化作用,但CTGF并不是其惟一的阻断途径。Objective: To investigate the protective effect of hepatocyte growth factor (HGF) on human renal tubular epithelial cells induced by high glucose and connective tissue growth factor(CTGF). Methods.. Different concentrations of rhHGF were added into the cullure media containing glucose and CTGF respectively. The expression of TGF-β1, CTGF,and collagen Ⅳ A1 (COIAA 1 ),fibronectin (FN) ,α-smooth muscwlar actin(α-SMA) mRNA were measured by RT-PCR. Results: The cytokines and fibrosis indexes were elevated at different levels after the HKC were incubated with high glucose and CTGF, and expression of COL4A1 was significantly higher in high glucose group compared with CTGF group. The fibrosis indexes were decreased significantly in rhHGF-treated group. The expression of CTGF was down-regulated and that of TGF-β1 remained unchanged in high glucose and rhHGF group. Conclusion: HGF can inhibit the fibrosis of human renal tubular epithelial cells via suppressing the synthesis of CTGF, but other independent pathway still exists.
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