当前位置:主页 > 医学论文 > 临床医学论文 >

PUMA-α蛋白在高糖诱导的人腹膜间皮细胞凋亡及纤维化中的作用

发布时间:2018-04-11 13:10

  本文选题:细胞凋亡 + PUMA-α蛋白 ; 参考:《解放军医学杂志》2017年09期


【摘要】:目的探讨p53上调凋亡调节因子(PUMA)-α蛋白在高糖刺激诱导的人腹膜间皮细胞(HPMC)凋亡及纤维化中的作用。方法以50mmol/L D型葡萄糖和甘露醇分别刺激HPMC 72h后,采用流式细胞仪检测细胞凋亡率,Western blotting检测凋亡及纤维化相关蛋白的表达。分别以Lenti-PUMA-α和sh RNA-PUMA-α转染正常的HPMC和高糖刺激72h后的HPMC,采用流式细胞仪检测凋亡细胞数目,Western blotting检测凋亡及纤维化相关蛋白的表达。结果高糖刺激HPMC 72h后,流式细胞仪检测结果显示细胞凋亡率增加;Western blotting检测结果显示,促进凋亡及纤维化的蛋白表达增加,而抑制凋亡及纤维化的蛋白表达减少。上调PUMA-α的表达可促进HPMC的凋亡及纤维化;下调PUMA-α的表达可抑制HPMC的凋亡及纤维化(P0.05)。结论高糖刺激通过上调PUMA-α的表达,促进了HPMC的凋亡及纤维化。
[Abstract]:Objective to investigate the role of p53 up-regulation of apoptosis regulatory factor (PUMA- 伪) protein in hyperglycemic induced apoptosis and fibrosis of human peritoneal mesothelial cells (HPMCs).Methods after stimulation of HPMC with 50mmol/L D glucose and mannitol for 72 hours, apoptosis rate was detected by flow cytometry and the expression of fibrosis related protein was detected by Western blotting.Lenti-PUMA- 伪 and sh RNA-PUMA- 伪 were transfected into normal HPMC and HPMC stimulated by high glucose for 72 h, respectively. The number of apoptotic cells and the expression of fibrosis-related protein were detected by flow cytometry and Western blotting.Results after stimulation of HPMC with high glucose for 72 hours, the results of flow cytometry showed that the rate of apoptosis was increased. Western blotting analysis showed that the expression of protein that promoted apoptosis and fibrosis increased, but the protein expression of inhibiting apoptosis and fibrosis decreased.Upregulating the expression of PUMA- 伪 could promote the apoptosis and fibrosis of HPMC, and down-regulating the expression of PUMA- 伪 could inhibit the apoptosis and fibrosis of HPMC.Conclusion High glucose stimulates apoptosis and fibrosis of HPMC by upregulating the expression of PUMA- 伪.
【作者单位】: 解放军273医院内三科;解放军69008部队卫生队;解放军273医院内一科;陕西省友谊医院消化内科;第四军医大学西京医院肾脏内科;
【分类号】:R459.5


本文编号:1736144

资料下载
论文发表

本文链接:https://www.wllwen.com/linchuangyixuelunwen/1736144.html


Copyright(c)文论论文网All Rights Reserved | 网站地图 |

版权申明:资料由用户33eb7***提供,本站仅收录摘要或目录,作者需要删除请E-mail邮箱bigeng88@qq.com