过表达BI-1对妊娠糖尿病中内质网介导滋养细胞增殖和凋亡的影响

Effect of overexpression of BI-1 on endoplasmic reticulum-mediated trophoblast proliferation and apoptosis in gestational diabetes

目的探讨过表达BI-1对妊娠糖尿病中内质网介导滋养细胞增殖和凋亡的影响及机制。方法免疫组织化学法和Westernblot检测BI-1在妊娠糖尿病患者与阴性对照者中的表达;qRT-PCR和Westernblot检测BI-1在HTR-8/SVneo细胞中的表达;CCK-8检测HTR-8/SVneo细胞的活力;EDU检测HTR-8/SVneo细胞的增殖情况;Western blot检测内质网相关蛋白的表达;细胞流式术检测HTR-8/SVneo细胞的凋亡情况。结果 BI-1在妊娠糖尿病患者中低表达,也在高糖(HG)诱导HTR-8/SVneo细胞中低表达;过表达BI-1在HG诱导的HTR-8/SVneo细胞中高表达(P<0.01);过表达BI-1使HG诱导的HTR-8/SVneo细胞活力增加(P<0.05),细胞中EDU阳性细胞数目比例增加(P<0.05);且过表达BI-1使HG诱导的HTR-8/SVneo中CRP78、CHOP、ATF6蛋白表达水平下调(均P<0.05),细胞凋亡率明显下降(P<0.01)。结论 BI-1在妊娠糖尿病患者和HG诱导的HTR-8/SVneo中低表达,且过表达BI-1使HG诱导的HTR-8/SVneo细胞增殖能力提高,凋亡率下降。

Objective To explore the effect and mechanism of overexpressing BI-1 on endoplasmic reticulum-mediated trophoblast proliferation and apoptosis in gestational diabetes.Methods Immunohistochemistry and Western blot was uesd to detecte the BI-1 expression in gestational diabetes patients and negative controls;qRT-PCR and Western blot was used to detect the expression of BI-1 in HTR-8/SVneo cells;CCK-8 was used to measure the viability of HTR-8/SVneo cells;EDU was uesd to detect the proliferation of HTR-8/SVneo cells;Western blot was uesd to detect the ER-related protein expression;Cell flow cytometry was used to detect the apoptosis of HTR-8/SVneo cells.Results BI-1 was under-expressed in patients with gestational diabetes and was also under-expressed in high glucose(HG)-induced HTR-8/SVneo cells;Overexpression of BI-1 was highly expressed in HTR-8/SVneo cells induced by HG(P<0.01);Overexpression of BI-1 increased the viability of HTR-8/SVneo cells induced by HG(P<0.05),and the proportion of EDU positive cells in the cells increased(P<0.05);Overexpression of BI-1 down-regulated the expression levels of CRP78,CHOP and ATF6(all P<0.05),and significantly decreased the apoptosis rate in HTR-induced HTR-8/SVneo(P<0.01).Conclusion BI-1 was under-expressed in gestational diabetes patients and HG-induced HTR-8/SVneo,and overexpression of BI-1 increased the proliferation ability of HG-induced HTR-8/SVneo cells and decreased the apoptosis rate.