本文選題：高壓氧 + 減壓病　； 參考：《軍事醫(yī)學(xué)》2017年03期

【摘要】：目的探討線粒體呼吸鏈在高壓氧(hyperbaric oxygen,HBO)誘導(dǎo)細(xì)胞活性氧產(chǎn)生中的作用。方法采用特異性熒光探針DHE和Mito-SOX分別標(biāo)記全細(xì)胞和線粒體內(nèi)超氧陰離子(O_2·~-),以熒光顯微技術(shù)檢測HBO暴露后人臍靜脈內(nèi)皮細(xì)胞(human umbilical vein endothelium cells,HUVEC)內(nèi)O_2·~-的生成。結(jié)果 HBO暴露后全細(xì)胞O_2·~-升高(31±8)%(P0.01),線粒體內(nèi)O_2·~-升高(137±19)%(P0.01);給予呼吸鏈復(fù)合體Ⅱ抑制劑TTFA后,兩者O_2·~-的增長分別被抑制(55±11)%(P0.05)和(61±8)%(P0.01)。結(jié)論 HBO主要通過線粒體呼吸鏈增加HUVEC活性氧生成。
[Abstract]:Aim to investigate the role of mitochondrial respiratory chain in the production of reactive oxygen species (Ros) induced by hyperbaric oxygenated HBO (HBO). Methods specific fluorescent probes DHE and Mito-SOX were used to label O _ 2C in whole cells and mitochondria, respectively. The generation of O _ 2 ~ (2 +) in human umbilical vein endothelial cells (HBO) exposed to HBO was detected by fluorescence microscopy. Results after exposure to HBO, the whole cell O 2 + increased by 31 鹵8 + P 0.01, and the mitochondrial O 2 + increased by 137 鹵19% P0.01.The increase of O 2 + was inhibited by 55 鹵11% P 0.05 and 61 鹵8% P 0.01 after TTFA was given to the respiratory chain complex 鈪，

本文編號：1805001