溶酶体组织蛋白酶B增加自噬保护缺氧诱导的心脏微血管内皮细胞损伤

被引：10

作者：

高路

姚瑞

李亚彭

梁翠

肖莉丽

张彦周

机构：

[1] 郑州大学第一附属医院心血管内科

来源：

中国药理学通报 | 2022年 / 38卷 / 01期

关键词：

心脏缺氧损伤; 内皮细胞损伤; 溶酶体组织蛋白酶B; 自噬; 凋亡; 炎症;

D O I：

暂无

中图分类号：

R54 [心脏、血管（循环系）疾病];

学科分类号：

100201 [内科学];

摘要：

目的探讨CTSB是否参与缺氧诱导的心脏微血管内皮细胞损伤。方法采用缺氧诱导内皮细胞损伤模型;分离CTSB基因敲除小鼠心脏微血管内皮细胞,采用腺病毒过表达CTSB,采用巴弗洛霉素阻断细胞自噬;采用ELISA法检测炎症因子的释放水平;采用TUNEL染色法检测细胞凋亡数量;采用caspase-3试剂盒检测细胞caspase-3的活性;细胞感染LC3-GFP-mCherry双标病毒,检测细胞自噬流的水平。结果CTSB基因敲除可明显加重缺氧诱导的内皮细胞炎症、凋亡,增加细胞自噬。CTSB过表达可减轻缺氧诱导的内皮细胞炎症、凋亡,增加细胞自噬。但是巴弗洛霉素处理可明显抵消CTSB过表达对细胞炎症、凋亡的抑制作用和对细胞自噬的保护作用。结论 CTSB基因敲除加重缺氧诱导的内皮细胞炎症和凋亡,而CTSB基因过表达减轻缺氧诱导的内皮细胞损伤。CTSB通过维持内皮细胞正常的自噬降解发挥作用。

引用

页码：53 / 60

页数：8

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