| 张 佳,王小丽,于东升,胡巧云,唐传峰,刘培玉,盛 亮.高糖诱导血管内皮细胞凋亡机制的研究[J].,2018,(11):2012-2018 |
| 高糖诱导血管内皮细胞凋亡机制的研究 |
| Study on the Mechanism of High Glucose-induced Endothelial Cell Apoptosis |
| 投稿时间：2017-12-05 修订日期：2018-01-03 |
| DOI：10.13241/j.cnki.pmb.2018.11.003 |
| 中文关键词: 高糖血症 己糖激酶Ⅱ 血管内皮细胞 电压依赖性阴离子通道1 线粒体 |
| 英文关键词: Hyperglycemia HexokinaseⅡ Vascular endothelial cells Voltage-Dependent Anion Channel 1 Mitochondria |
| 基金项目:国家自然科学基金项目（81400613，81770862）；江苏省自然科学基金项目（BK20140901） |
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| 中文摘要: |
| 摘要 目的：探讨高糖诱导血管内皮细胞凋亡的分子机制。方法：在高浓度葡萄糖的培养基中培养人脐静脉内皮细胞（human umbilical vein endothelium cells，HUVECs），模拟高糖血症条件下内皮细胞的病理状态。通过MTT检测HUVEC细胞生存情况；JC-1检测HUVEC细胞线粒体膜电位；逆转录-聚合酶链反应和荧光素酶报告基因检测己糖激酶Ⅱ（hexokinaseⅡ，HKⅡ）的转录；免疫印迹和免疫共沉淀检测VDAC1、HKⅡ、Bcl-2、Bax线粒体上蛋白表达水平和它们之间的相互作用。结果：25 mM和100 mM葡萄糖诱导HUVEC细胞生存率分别下降了19.21 %±4.13 %和25.29 %±5.78 %；线粒体膜电位分别降低了34.19 %±5.13 %和58.63 %±4.78 %；HKⅡ蛋白表达水平分别降低了13.97 %±6.32 %和35.13 %±5.18 %；使得HKⅡ同VDAC1互作减弱，代偿性增强了VDAC1同Bax互作。结论：高糖下调HUVEC细胞HKⅡ表达水平，增强线粒体膜通透性，最终诱导了细胞凋亡。 |
| 英文摘要: |
| ABSTRACT Objective: To investigate the molecular mechanism of hyperglycemia-induced apoptosis of vascular endothelial cells. Methods: HUVEC cells were used to mimic the pathological status of endothelial cells in the condition of hyperglycemia. The cell viability was detected by MTT assay, the mitochondrial membrane potential was detected with JC-1 staining and flow cytometry assay, the transcription levels of hexokinaseⅡ (HKⅡ) were detected using reverse transcription-polymerase PCR and luciferase assay. Western blot and immune co-precipitation were used to analyse the expression of VDAC1, HKⅡ, Bcl-2 and Bax on the mitochondrial outer membrane and their interactions. Results: The viability of HUVEC cells incubated in medium containing 25 or 100 mM glucose was reduced by 19.21 %±4.13 % and 25.29 %±5.78 % respectively; mitochondrial membrane potential was reduced by 34.19 %±5.13 % and 58.63 %±4.78 % respectively; HKⅡ protein expression levels were reduced by 13.97 %±6.32 % and 35.13 %±5.18 % respectively; the interactions between HKⅡ and VDAC1 were both reduced in the two groups, while the Bax and VDAC1 interactions were compensatorily enhanced. Conclusion: High glucose reduced the HKⅡexpression, increased mitochondrial permeability and eventually induced the apoptosis of HUVEC cells. |
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