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目的探讨沉默转化生长因子β1(TGF-β1)表达与抑制肾小管上皮(HK-2)细胞Notch信号通路的相关性。方法检测TGF-β1在DN的表达;TGF-β1小干扰RNA(TGF-β1-siRNA)和阴性对照(siRNA-NC)转染HK-2,空脂质体转染细胞为对照,检测各组TGF-β1;将HK-2分为低糖、高糖、siRNA-NC+高糖和TGF-β1-siRNA组+高糖组,检测细胞存活,凋亡及Cleaved caspase 3、Notch1和Hes1表达。结果 TGF-β1在DN表达高于正常肾组织(P<0.05);TGF-β1-siRNA组TGF-β1表达低于对照组(P<0.05);高糖组细胞存活低于低糖组,凋亡率、Cleaved caspase 3、Notch1和Hes1高于低糖组(P<0.05),siRNA-NC+高糖组细胞存活、凋亡及Cleaved caspase 3、Notch1和Hes1表达与高糖组相当(P>0.05);TGF-β1-siRNA+高糖组细胞存活高于高糖组,凋亡及Cleaved caspase 3、Notch1和Hes1低于高糖组(P<0.05)。加入GSI细胞存活、凋亡及Cleaved caspase 3、Notch1和Hes1表达与沉默TGF-β1一致。结论 TGF-β1在DN高表达,高糖能抑制HK-2的存活,促进凋亡,沉默TGF-β1能减弱这种效果,可能与Notch信号通路调控有关。
Objective To investigate the relationship between the expression of silencing transforming growth factor-β1 (TGF-β1) and the Notch signaling pathway in renal tubular epithelial cells (HK-2). Methods The expression of TGF-β1 in DN was detected by MTT assay. The transfected cells were transfected with TGF-β1 siRNA and NC-siRNA into HK-2 cells. TGF-β1. HK-2 cells were divided into low glucose, high glucose, siRNA-NC + high glucose and TGF-β1-siRNA group and high glucose group. Cell viability, apoptosis and expression of Cleaved caspase 3, Notch1 and Hes1 were detected. Results The expression of TGF-β1 in DN was higher than that in normal kidney (P <0.05). The expression of TGF-β1 in TGF-β1-siRNA group was lower than that in control group Cleaved caspase 3, Notch1 and Hes1 were higher than those in low glucose group (P <0.05). The survival, apoptosis and the expressions of Cleaved caspase 3, Notch1 and Hes1 in siRNA-NC + high glucose group were similar to those in high glucose group (P> 0.05). The survival rate of TGF-β1-siRNA + high glucose group was higher than that of high glucose group, and the apoptosis and Cleaved caspase 3, Notch1 and Hes1 were lower than those of high glucose group (P <0.05). Add GSI cell survival, apoptosis and Cleaved caspase 3, Notch1 and Hes1 expression consistent with the silence of TGF-β1. Conclusion TGF-β1 is highly expressed in DN. High glucose can inhibit the survival of HK-2 and promote apoptosis. Silencing TGF-β1 can attenuate this effect, which may be related to the regulation of Notch signaling pathway.