本公眾號(hào)每天分享一篇最新一期Anesthesia & Analgesia等SCI雜志的摘要翻譯,敬請關(guān)注并提出寶貴意見 Oxidative stress regulates cellular bioenergetics in esophageal squamous cell carcinoma cell 背景與目的 本研究目的為觀察CoCl2和H2O2誘導(dǎo)的氧化應(yīng)激對(duì)食道鱗癌細(xì)胞株TE-1能量代謝調(diào)控的影響,并探討其作用機(jī)制,。 方 法 Western blot結(jié)果表明:經(jīng)CoCl2和H2O2的處理,TE-1細(xì)胞線粒體呼吸鏈復(fù)合物亞基的表達(dá)顯著減少,,且細(xì)胞內(nèi)活性氧(ROS)生成增加,。 結(jié) 果 我們進(jìn)一步用CoCl2(一種缺氧模擬試劑)處理TE-1細(xì)胞,發(fā)現(xiàn)處理后的TE-1細(xì)胞氧消耗率(OCR)明顯下降且細(xì)胞外酸化率(ECAR)增加,。但是,,H2O2處理顯著降低了線粒體呼吸和有氧糖酵解水平。此外,,我們發(fā)現(xiàn)H2O2通過激活PARP,、Caspase 3和Caspase 9,從而誘導(dǎo)TE-1細(xì)胞凋亡,。 結(jié) 論 研究結(jié)果表明CoCl2和H2O2可通過上調(diào)ROS以及調(diào)控細(xì)胞能量代謝導(dǎo)致線粒體代謝功能障礙,,從而影響腫瘤細(xì)胞的存活。 原始文獻(xiàn)摘要 Zhang X, Lan L, Niu L, et al. Oxidative stress regulates cellular bioenergetics in esophageal squamous cell carcinoma cell:[J]. Biosci Rep, 2017, 37(6):BSR20171006. The aim of the present study was to explore the effects of oxidative stress induced by CoCl2 and H2O2 on the regulation of bioenergetics of esophageal squamous cell carcinoma (ESCC) cell line TE-1 and analyze its underlying mechanism. Western blot results showed that CoCl2 and H2O2 treatment of TE-1 cells led to significant reduction in mitochondrial respiratory chain complex subunits expression and increasing intracellular reactive oxygen species (ROS) production.We further found that TE-1 cells treated with CoCl2, a hypoxia-mimicking reagent, dramatically reduced the oxygen consumption rate (OCR) and increased the extracellular acidification rate (ECAR). However, H2O2 treatment decreased both the mitochondrial respiration and aerobic glycolysis significantly. Moreover, we found that H2O2 induces apoptosis in TE-1 cells through the activation of PARP, Caspase 3, and Caspase 9. Therefore, our findings indicate that CoCl2 and H2O2 could cause mitochondrial dysfunction by up-regulation of ROS and regulating the cellular bioenergy metabolism, thus affecting the survival of tumor cells. 麻醉學(xué)文獻(xiàn)進(jìn)展分享 聯(lián)系我們 |
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