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机构地区:[1]广州医科大学药学院药理教研室,广州广东510082 [2]暨南大学药学院药理教研室,广州广东510630
出 处:《中国病理生理杂志》2014年第4期706-710,共5页Chinese Journal of Pathophysiology
基 金:广东省自然科学基金资助项目(No.S2011040003942);广州市教育局基金资助项目(No.10A178)
摘 要:目的:探讨α7烟碱型乙酰胆碱受体(α7nAChR)在生理浓度糖皮质激素(GCs)抗炎过程中的作用。方法:MTT法检测不同浓度氢化可的松对小胶质细胞BV-2活性的影响;在建立LPS刺激的BV-2细胞炎症模型基础上,实验分组如下:(1)空白对照组;(2)LPS组;(3)GCs+LPS组;(4)α7nAChR阻断剂甲基牛扁亭碱(MLA)+GCs+LPS组,ELISA法测定细胞上清中TNF-α和IL-1β的含量。结果:2 000和1 000 nmol/L氢化可的松可分别使细胞存活率降低至(76.9±5.5)%和(90.8±7.3)%,表现出超生理剂量GCs的细胞损伤作用。LPS明显刺激BV-2细胞释放TNF-α和IL-1β,并呈现时间和剂量依赖性。生理浓度(500和250 nmol/L)的氢化可的松均可减少LPS诱导BV-2细胞释放TNF-α和IL-1β,10 nmol/L MLA预处理BV-2细胞能拮抗GCs抑制炎症因子释放的作用。结论:α7nAChR参与了生理浓度GCs的抗炎作用。AIM: To explore the role of or7 nicotinic acetylcholine receptor (ct7nAChR) in anti-inflammation of glucocorticoids (GCs) at physiological concentrations. METHODS: MTY assay was used to measure the viability of BV-2 ceils, which were processed by hydrocortisone at different concentrations. On the basis of inflammatory model induced by LPS in BV-2 cells, experimental groups were divided as follows : ( 1 ) control; (2) LPS; (3) GCs + LPS; (4) methyl- lycaconitine (MLA) + GCs + LPS. The levels of TNF-a and IL-1B in the cell supernatants were detected by ELISA. RE- SULTS : Hydrocortisone at concentrations of 2 000 and 1 000 nmol/L decreased the cell viability to (76.9 ± 5.5 ) % and (90.8 ± 7.3 ) %, respectively, indicating the cellular injury by GCs at over-physiological doses. LPS significantly induced the releases of TNF-a and IL-113 in a time- and dose-dependent manner in BV-2 cells. Hydrocortisone at physiological con- centrations (500 and 250 nmol/L) reduced the releases of TNF-a and IL-1B in BV-2 cells stimulated by LPS, and MLA at concentration of 10 nmol/L antagonized the anti-inflammatory effect of GCs. CONCLUSION: ct7nAChR is involved in the anti-inflammatory effect of the physiological concentrations of GCs.
关 键 词:糖皮质激素 a7碱型乙酰胆碱受体 小神经胶质细胞 脂多糖类
分 类 号:R338.2[医药卫生—人体生理学]
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