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作 者:张建波[1] 王晓俏[1] 邱小弟[1] 阮林[1] 黄焕森[1]
机构地区:[1]广州医科大学附属第二医院麻醉科,510260
出 处:《实用医学杂志》2016年第7期1084-1087,共4页The Journal of Practical Medicine
基 金:广州市医药卫生科技项目西医一般引导项目(编号:20151A011076);广州医科大学青年基金项目(编号:2014A04)
摘 要:目的:研究右美托咪定对人肾小管上皮细胞(HK-2)H_2O_2损伤的保护作用。方法:随机将体外培养HK-2细胞分为4组(n=24):正常对照组、右美托咪定组、H_2O_2损伤组、H_2O_2损伤+右美托咪定组。各组采用MTS法测细胞活力,流式细胞仪测凋亡率,Western blot法检测HIF-1α蛋白的表达水平。处理因素:PI3K通路抑制剂LY294002、右美托咪定及H_2O_2刺激损伤,排列组合分成8组处理细胞,分别测定HIF-1α、Bcl-2及Bax蛋白水平及细胞活力。结果 :右美托咪定可上调H_2O_2损伤HK-2细胞的HIF-1α、Bcl-2的蛋白水平,从而改善细胞活力及减少细胞凋亡率,且上述作用可被PI3K抑制剂LY294002逆转。结论:右美托咪定可能兴奋PI3K/Akt/m TOR通路,上调HIF-1α蛋白水平对体外HK-2细胞H_2O_2损伤具有保护作用。Objective To investigate the protection effect of dexmedetomidine against H_2O_2 injury in Human renal tubular epithelial cells(HK-2 cells). Methods HK-2 cells cultured in vitro were randomly divided into four groups(n = 24): control group, dexmedetomidine pretreatment group, H_2O_2 injury group, H_2O_2 injury +dexmedetomidine pretreatment group. Cell viabilities were measured by MTS assay, cell apoptosis were detected using flow cytometry, and expression of HIF-1α protein was quantified by western blot. HK-2 cells were divided into 8 groups by combining with three treatment factors such as PI3 K inhibitor LY294002, dexmedetomidine and H_2O_2 injury. MTS assay was used to detect cell viability and western blot was used to quantify protein expression of HIF-1α,Bcl-2 and Bax after treatment in each group. Results Dexmedetomidine significantly increased the level of HIF-1α 、 Bcl-2 in HK-2 cells after H_2O_2 injury, thus improved viabilities and reduced apotosis of cells. Moreover, effect on H_2O_2 injury cells of Dexmedetomidine was reversed by PI3 K inhibitor LY294002.Conclusion Dexmedetomidine could protect against H_2O_2 injury by up-regulating HIF-1α expression through activating PI3 K / Akt / m TOR signaling pathway in HK-2 cells.
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