首页|神经调节蛋白4对2型糖尿病小鼠主动脉内皮细胞凋亡的影响

神经调节蛋白4对2型糖尿病小鼠主动脉内皮细胞凋亡的影响

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目的 探讨神经调节蛋白 4(Nrg4)对 2 型糖尿病小鼠主动脉内皮细胞凋亡的影响.方法 将C57 小鼠分为对照(Vehicle)组、糖尿病(DM)组和Nrg4 干预糖尿病小鼠(Nrg4)组.Nrg4 组腹腔注射Nrg4 重组蛋白(100 μg/kg,3 次/周),Ve-hicle组与DM组小鼠注射等量生理盐水,干预周期均为 8 周.实验结束后,TUNEL荧光染色检测主动脉内皮细胞凋亡,West-ern blot检测主动脉内皮组织凋亡相关蛋白Bax、Bcl-2及Cleaved-caspase 3 的表达.结果 与Vehicle组相比,DM组主动脉内皮细胞凋亡率明显升高[(33.0±5.4)%vs.(20.5±3.0)%;P<0.05],促凋亡蛋白Bax与凋亡执行蛋白Cleaved-caspase 3 表达明显增多,抗凋亡蛋白Bcl-2表达显著减少(P<0.05);而Nrg4 干预明显抑制糖尿病小鼠主动脉内皮细胞凋亡[(19.2±3.8)%vs.(33.0±5.4)%;P<0.05],降低Bax与Cleaved-caspase 3 的表达并促进Bcl-2 表达(P<0.05).结论 Nrg4 干预能缓解 2 型糖尿病小鼠主动脉内皮细胞凋亡.
Effects of neuregulin 4 on apoptosis of aortic endothelial cells in type 2 diabetic mice
Objective To investigate the effects of neuregulin 4(Nrg4)on the apoptosis of endothelial cells in type 2 diabetic mice.Methods C57 mice were randomly divided into Vehicle group,diabetes mellites(DM)group and Nrg4 administration group(NRG4).Nrg4 group was intraperitoneally(i.p.)injected with Nrg4 recombinant protein(100 μg/kg,3 times/week)and the same volume of saline was i.p.injected in the other two groups for 8 weeks.After the experiment,TUNEL staining was used to evaluate ap-optotic rate of endothelial cells,and Western blot was used to investigate the protein levels of apoptosis-associated proteins.Results Compared with Vehicle group,DM significantly promoted cell apoptosis[(33.0±5.4)%vs.(20.5±3.0)%;P<0.05],in-creased Bax and cleaved-caspase 3 expression,and decreased Bcl-2 expression(P<0.05),while Nrg4 administration obviously de-creased endothelial apoptosis[(19.2±3.8)%vs.(33.0±5.4)%;P<0.05],decreased Bax and cleaved-caspase 3 expression,and increased Bcl-2 expression(P<0.05).Conclusions Nrg4 administration can alleviate the apoptosis of aortic endothelial cells in type 2 diabetic mice.

neuregulin 4diabetes mellitusendothelial cellcell apoptosis

刘星宇、王莹、焦婷、方文灿、于汉英、张海松

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100120 北京,解放军总医院京中医疗区综合内科

100853 北京,解放军医学院

071000 保定,河北大学附属医院肿瘤科/河北省肿瘤放化疗机制与规程研究重点实验室

神经调节蛋白4 糖尿病 内皮细胞 细胞凋亡

军队某课题

2024

武警医学
中国人民武装警察部队后勤部卫生部

武警医学

CSTPCD
影响因子:0.747
ISSN:1004-3594
年,卷(期):2024.35(7)
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