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氢气通过抑制活性氧减少血管内皮细胞凋亡

已有 4214 次阅读 2013-4-11 13:36 |个人分类:氢气细胞学研究|系统分类:论文交流| 氢气, 影响, 活性氧


Int J Mol Med Early Online ijmm.2013.1334.pdf

氢气通过抑制活性氧影响细胞凋亡

第三军医大学附属医院整形外科的最新研究发现,氢气可以对抗糖基化终产物诱导的内皮细胞凋亡,这一研究目前在线发表在 Int J Mol Med. 2013 Apr 5. doi: 10.3892/ijmm.2013.1334.文章题目为Hydrogen-rich medium suppresses the generation of reactive oxygen species, elevates the Bcl-2/Bax ratio and inhibits advanced glycation end product-induced apoptosis.


本研究目的是确定含氢气培养基对AGEs糖基化终产物advanced glycation end products)诱导的内皮细胞凋亡的保护作用。分离成年SD大鼠主动脉内皮细胞进行培养,加入AGEs和氢气培养基共培养(对照组不加氢气)24小时,Annexin V/7-AAD TUNEL染色鉴定细胞凋亡,萤光探针结合流式细胞仪监测细胞内活性氧水平。抗氧化酶SOD和谷胱氨肽过氧化物酶mRNA水平用定量PCR进行监测,酶活性采用化学发光法监测。凋亡相关蛋白Bcl-2Bax采用western blot监测并计算相对水平。结果发现AGEs可以剂量依赖性诱导大血管内皮细胞凋亡增加细胞内活性氧水,氢气加入细胞培养基可以提高细胞抗氧化能力,减少细胞内活性氧水平,减少细胞凋亡。

The purpose of the present studywas to determine whether using hydrogen-rich medium (HRM) to increase hydrogenlevels in endothelial cells (ECs) protects ECs  from apoptosis induced by advancedglycation end products (AGEs). The thoracic aorta was removed from 2-3-year-oldSprague-Dawley rats, and ECs were isolated and cultured. After culturing ECsin the presence of AGEs and/or with HRM for 24 h, Annexin V/7-AAD andTUNEL staining were carried out to detect apoptosis. Intracellular ROS were detected byfluorescent probe and quantified by flow cytometry. The expression ofantioxidative enzymes (superoxide dismutase, glutathione peroxidase) wasdetermined by real-time PCR analysis and enzymatic assay. The relative expressionlevels of Bcl-2 and Bax were analyzed by western blotting. The addition of AGEsincreased the apoptosis of ECs in a concentration-dependent manner andHRM reduced the AGE (400 μg/ml)-induced apoptosis from 21.61±2.52 to11.32±1.75%. HRM also significantly attenuated the AGE-induced intracellular ROSinduction and decrease in the expression of antioxidative enzymes. Inconclusion, hydrogen exhibits significant protective effects against AGE-induced ECinjury possibly through reducing ROS generation,intracellular antioxidant enzymesystem protection and elevation of the Bcl-2/Baxratio.

PMID: 23563626  [PubMed - assupplied by publisher]




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