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N-acetylserotonin对H_2O_2诱导大鼠肝BRL细胞氧化损伤的保护作用 被引量:1

Protective effects of N-acetylserotonin on the models of BRL cell oxidative stress induced by H_2O_2
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摘要 目的:探讨N-acetylserotonin(NAS)对H2O2诱导正常大鼠肝BRL细胞氧化损伤的保护作用。方法:选择正常大鼠肝细胞株BRL,采用H2O2诱导法制备BRL细胞氧化应激损伤模型,HE染色和台盼蓝染色观察细胞形态及细胞存活率的变化;比色法检测细胞中超氧化物歧化酶(SOD)活性和丙二醛(MDA)含量的变化。结果:对照组BRL细胞贴壁生长良好,排列紧密,胞膜完整,细胞界限清晰。H2O2诱导后细胞膜皱缩,形态不规则,细胞界限模糊,贴壁能力下降,出现大片细胞缺失;细胞存活率下降;SOD活性降低,而MDA含量升高。NAS可明显改善H2O2引起的细胞形态变化,使细胞存活率升高,增加SOD活性并降低MDA含量。结论:NAS可通过增强抗氧化系统的激活、减轻抗氧化系统受抑制的程度,发挥对H2O2诱导的BRL细胞氧化损伤的保护作用。 Objective To study the protective effect of N-acetylserotonin (NAS) on BRL cell line injury induced by HzO2. Methods The oxidative injury model of BRL cell was induced by H2O2 and divided into the control group, H2O2 group and NAS + H2O2 group. The morphology and activity changes of cell were observed by HE and trypan blue staining, respectively. And the activity of superoxide dismutase (SOD) and the content of malondialdehyde (MDA) were assayed by colorimetric method. Results BRL cells of the control group were adherent good growth, polygonal, tightly arranged. The membranes of cells were integrity and the boundaries were clear. After H2O2-induced, the shape of cells became irregular, accompanied by membrane shrinkage, cell boundaries blurring and cell adherent ability decreasing. Meanwhile, the floating cells increase significantly. Compared with the control group, cell survival rate decreased, the activity of SOD was lowerand the content of MDA was higher. NAS can significantly improve the H2O2-induced changes in cell morphology and cell survival rate, increase the activity of SOD and decreased the content of MDA. Cconclusions NAS could alleviate the HzO2-induced BRL cells injury through deceasing the formation of oxygen free radical and increasing SOD.
出处 《实用医学杂志》 CAS 北大核心 2013年第21期3486-3488,共3页 The Journal of Practical Medicine
基金 山东省"泰山学者"建设工程专项经费自主项目 山东省自然科学基金项目(编号:ZR2010HM006 ZR2010HM065) 山东省教育厅项目(编号:J11LF14)
关键词 氧化性应激 N-ACETYLSEROTONIN BRL细胞 H2O2 细胞凋亡 Oxidative stress N-acetylserotonin BRL cell n202 Apoptosis
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