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作 者:王宇恒[1] 焦晶华[1] 李明选[1] 孙晓峰[1]
机构地区:[1]沈阳医学院附属中心医院麻醉科,辽宁沈阳110024
出 处:《解剖科学进展》2017年第6期630-633,共4页Progress of Anatomical Sciences
基 金:辽宁省教育厅基金(L2015540);沈阳医学院临床研究发展基金(20156049)
摘 要:目的观察并探讨α2肾上腺素能受体激动剂右美托咪定(dexmedetomidine,DEX)对化学性低氧模拟剂氯化钴(cobalt chloride,CoCl_2)诱发人支气管上皮细胞(BEAS-2B)氧化应激损伤的影响。方法以人支气管上皮细胞株BEAS-2B为研究对象,将其随机分为4个实验组:正常对照组、CoCl_2组、0.01μmol/LDEX+Co Cl2组、0.1μmol/LDEX+CoCl_2组。MTT比色法检测细胞的存活率;DCFH-DA染色流式细胞仪检测细胞内活性氧自由基水平(reactive oxygen species,ROS);试剂盒测定细胞上清液中丙二醛(malonaldehyde,MDA)释放量;Western Blot检测细胞内血红素加氧酶-1(HO-1)和超氧化物歧化酶(SOD)的蛋白表达。结果与正常对照组相比,BEAS-2B细胞经低氧处理后,细胞存活率降低,ROS含量升高,MDA释放增多。经DEX+CoCl_2联合处理后,能明显抑制低氧导致的BEAS-2B细胞氧化损伤,呈现剂量依赖性;并且细胞内HO-1和SOD的蛋白表达水平明显高于CoCl_2组。结论右美托咪定能保护BEAS-2B细胞对抗化学性低氧诱发的氧化应激损伤,可能与上调细胞内HO-1和SOD等氧化酶的表达,抑制ROS水平相关。Objective To evaluate the effects of dexmedetomidine, an α 2-adrenergic receptor agonist, on oxidative stress injury induced by chemical hypoxia-mimetic agent cobalt ehloride(CoCl2) in human bronchial epithelial cells(BEAS-2B). Methods BEAS-2B cells were divided into: control group, CoCl2 group, 0.01 μmol/LDEX+CoCl2 group, 0.1 μmol/LDEX+CoCl2 group. The cell survival rate was measured by MTT assay. The content of reactive oxygen speeies(ROS) in cells was detected by DCFH-DA probe. The level of malonaldehyde(MDA) in the culture medium was assessed by kits. The expressions of HO-1 and SOD proteins were detected by Western blot. Results Compared with control group, hypoxia could decrease the cell survival rate, increase ROS level and MDA concentration in BEAS-2B cells. Dexmedetomidine could inhibit the hypoxia-induced oxidative stress damages of BEAS-2B cells in a dose-dependent manner. Compared with CoC1z group, dexmedetomidine could remarkably increase the levels of HO-1 and SOD proteins. Conclusion The protective effect of Dexmedetomidine on BEAS-2B cells against oxidative stress induced by CoCl2 might be related to upregulating the expression of HO-1 and SOD.
关 键 词:右美托咪定 低氧 人支气管上皮BEAS-2B细胞 氧化应激
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