作 者: (隋淼); (杨晓辉); (于扬); (张弢); (许静宜);
机构地区: 大连大学附属中山医院内分泌一科,116001
出 处: 《中国糖尿病杂志》 2017年第8期697-702,共6页
摘 要: 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 explore the relationship between silencing TGF-β1 expression and Notch signaling pathway in human renal tubular epithelial cells (HK-2). Methods TGF-β1 small interfering RNA (TGF-β1-siRNA) and negative control (siRNA-NC) were transfected into HK-2 cells. According to the expression of TGF-131 in diabetic nephropathy, HK-2 cells were divided into low glucose group, high glucose group, siRNA-NC + high glucose group,TGF-βl-siRNA group q- high glucose group. The TGF- β1 expression cell survival,apoptosis and Cleaved caspase 3, Notchl and Hesl expressions were detected. Results The expression of TGF-β1 in TGF-β1-siRNA group was lower than in control group (P〈0.05). The survival rate in high glucose group was lower than in low glucose group (P〈0.01). The cell survival rate,apoptosis rate and Cleaved caspase 3, Notchl and Hesl expression between siRNA-NC q- high glucose group and high glucose group had no differences(P〈0. 05). The cell survival rate was higher, the apoptosis rate and Cleaved caspase 3, Notchl and Hesl expression in TGF-β1-siRNA q- high glucose group were lower compared with high glucose group (P〈0.05). Silencing of TGF-β1 expression was consistent with the addition of Notch signaling inhibitor GSI. Conclusion TGF-β1 is highly expressed in DN. High glucose can inhibit the survival of HK-2 and promote apoptosis. Silencing TGF-β1 can weaken this effect,which may be related to Notch signaling pathway.