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作 者:王馨[1] 严磊[2] 苗加伟[3] 封玉玲[3] 李晶[3]
机构地区:[1]重钢总医院药剂科,重庆400080 [2]重庆医科大学动物实验中心,重庆400016 [3]重庆三峡医药高等专科学校基础医学部,重庆404120
出 处:《中国医院药学杂志》2015年第10期917-920,共4页Chinese Journal of Hospital Pharmacy
基 金:重庆市卫生局医学科研计划重点项目(编号:20121096);重庆市高等教育教学改革研究项目(编号:132128;133309)
摘 要:目的:观察表没食子儿茶素没食子酸酯[(–)-Epigallocatechin-3-gallate,EGCG]对细菌脂多糖(LPS)所致原代神经胶质细胞炎性反应的保护作用。方法:取新生乳鼠原代神经胶质细胞培养,利用LPS引起其炎症反应。用酶联免疫吸附试验(ELISA)测定炎性因子肿瘤坏死因子(TNF-α)、白介素-1β(IL-1β)、白介素-1β(IL-8)表达情况和蛋白免疫印记法(Western blot)检测炎症因子(诱导型一氧化氮合酶)i NOS蛋白含量变化。结果:LPS激活神经胶质细胞后诱导炎症因子过度表达,大幅上调TNF-α、IL-1β、IL-8炎性因子(P<0.05),i NOS蛋白质水平显著升高(P<0.05),不同浓度EGCG干预组均可明显抑制炎症因子的过度产生,一定程度上减轻LPS诱导神经胶质细胞的炎性反应。结论:一定浓度范围内,EGCG能减弱LPS引起的体外培养神经胶质细胞的炎症反应。OBJECTIVE To determine effects of EGCG on lipopolysaccharide (LPS)-induced neuroinflammation and further investigate the role of EGCG mediated neuroprotectiorL METHODS Primary rat gliacyte cultures were used as an in vitro mod- el to examine effects of EGCG on LPS-induced neuronal damage. Protein levels of inducible nitric oxide synthase (iNOS), tumor necrosis factor-alpha (TNF-α), interleukin-1β (IL-1β) and interleukin-8 (IL-8) were determined by ELISA and western blot. RESULTS Compared with blank control group, LPS apparently induced production of intracellular inflammatory re- sponse, and increased releases of TNFα, IL-1β and IL-8 in supernatant of culture (P〈0. 05). Compared with LPS group, ECK;G groups significantly reduced release of TNFα, IL-1β and IL-8 (P%0. 05) and level of iNOS protein (P〈0. 05). CON-CLUSION ECA2G is effective in protecting against LPS-induced neuroinflammation by anti-inflammatory effects.
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