高压氧通过调控PI3K/Akt/mTOR途径缓解氧化型低密度脂蛋白诱导的血管平滑肌细胞损伤的机制  

Mechanism of hyperbaric oxygen alleviating ox-LDL induced vascular smooth muscle cell damage via regulating the PI3K/Akt/mTOR pathway

作　　者：张国宁 李伟 代兴利 Zhang Guoning;Li Wei;Dai Xingli(Department of Cardiology,The First People’s Hospital of Qingzhen,Qingzhen 551400,China;The Afflicated Hospital of Guizhou Medical University,Guiyang 550004,China)

机构地区：[1]清镇市第一人民医院心内科,清镇551400 [2]贵州医科大学附属医院,贵阳550004

出　　处：《中华航海医学与高气压医学杂志》2023年第1期43-46,52,共5页Chinese Journal of Nautical Medicine and Hyperbaric Medicine

摘　　要：目的基于氧化型低密度脂蛋白(ox-LDL)诱导的血管平滑肌细胞(VSMCs)氧化应激损伤模型,探讨高压氧(HBO)缓解动脉粥样硬化(AS)的分子机制。方法利用ox-LDL处理VSMCs以构建VSMCs氧化应激损伤模型。采用CCK-8法检测VSMCs的增殖能力,Annexin V-FITC细胞染色联合流式细胞术检测VSMCs的凋亡水平,Western blotting实验检测VSMCs中凋亡相关蛋白以及PI3K/Akt/mTOR相关蛋白的表达水平。结果ox-LDL可显著抑制VSMCs的增殖能力并促进其凋亡(P<0.05),而HBO处理可逆转ox-LDL对VSMCs的损伤(P<0.05)。此外,HBO处理可显著激活PI3K/Akt/mTOR信号通路(P<0.05),同时下调细胞程序性凋亡相关蛋白C-caspase-3和Bax的表达水平,上调抗凋亡蛋白Bcl-2的表达水平(P<0.05)。结论HBO可通过激活PI3K/Akt/mTOR通路保护氧化应激损伤的VSMCs,从而达到缓解AS的目的。Objective To investigate the molecular mechanism of hyperbaric oxygen(HBO)alleviating atherosclerosis(AS)in the model of vascular smooth muscle cell(VSMC)oxidative stress damage induced by oxidative low density lipoprotein(ox-LDL).Methods VSMCs were treated with ox-LDL to establish a VSMC oxidative stress injury model.Cell Counting Kit-8(CCK-8)assay was used to detect the proliferative ability of VSMCs.Annexin V-FITC cell staining combined with flow cytometry was used to detect the apoptosis of VSMCs.Western blot was used to detect the expression of apoptosis-related proteins and PI3K/Akt/mTOR-related proteins in the cells.Results Ox-LDL could significantly inhibit the proliferative ability of VSMCs and promote the apoptosis of VSMCs(P<0.05).HBO could reverse the damages of VSMCs caused by ox-LDL(P<0.05).HBO could significantly activate the PI3K/Akt/mTOR signaling pathway(P<0.05),down-regulate the expressions of the proteins associated with programmed apoptosis,such as c-caspase3 and bax,and up-regulate the expression of the anti-apoptotic protein bcl-2(P<0.05).Conclusion HBO can alleviate AS by activating PI3K/Akt/mTOR pathway to protect VSMCs damaged by oxidative stress.

关 键 词：高压氧 动脉粥样硬化 氧化型低密度脂蛋白 血管平滑肌细胞 PI3K/AKT/MTOR 

分 类 号：R54[医药卫生—心血管疾病]