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作 者:吴云[1] 王晓坤[1] 梁庆成[2] 张苏明[2] 丛林[1]
机构地区:[1]哈尔滨医科大学附属二院神经内科,黑龙江哈尔滨150086 [2]华中科技大学同济医学院,湖北武汉430030
出 处:《中风与神经疾病杂志》2010年第10期898-901,共4页Journal of Apoplexy and Nervous Diseases
基 金:2008年黑龙江省卫生厅科研课题资助(2007-333);哈医大二院2007年院博士科研基金项目资助(BS2007-11)
摘 要:目的探讨磷酸二酯酶(PDE)3抑制剂西洛他唑对大鼠脑微血管内皮细胞糖氧剥离损伤的影响及作用机制。方法原代培养大鼠皮层微血管内皮细胞,建立糖氧剥离细胞模型模拟"缺血"过程,分5组:正常对照组、西洛他唑组、依达拉奉组、溶剂对照组、模型组。糖氧剥离6h后,测定细胞上清中内皮型一氧化氮合酶(eNOS)和诱导型一氧化氮合酶(iNOS)水平、细胞内环磷腺苷酸(cAMP)浓度,及采用四唑盐(MTT)比色实验测定细胞活力。结果西洛他唑及依达拉奉均可明显提高缺血细胞模型上清中eNOS水平,同时降低iNOS水平,提高细胞内cAMP水平及细胞存活率(均P<0.05),且西洛他唑作用更为显著。结论西洛他唑对培养大鼠皮层微血管内皮细胞在缺血损伤中具有保护作用,其作用机制可能是通过选择性抑制PDE3从而增加cAMP水平,间接增加eNOS水平、降低iNOS水平来实现的。Objective To study the effects and possible mechanism of cilostazol on cultured brain microvascular endothelial cells deprived of oxygen and glucose in rats in vitro.Methods Brain microvascular endothelial cells of the Wistar rats were cultured in vitro,and then cell model of ischemia was established by oxygen-glucose deprivation (OGD) mimicking cerebral ischemia.All the cells were divided randomly into the normal group,cilostazol group,edaravone group,solvent group and OGD group.Concentrations of endothelial nitric oxide synthase (eNOS) and inducible nitric oxide synthase (iNOS) in supernatants,concentrations of cyclic adenosine monophosphate (cAMP) in cells,and cells viability were measured after 6h of OGD cell culture.Results Compared with the OGD group,concentrations of iNOS were significantly decreased,levels of eNOS and intracellular cAMP were obviously increased,and cells viability were markedly increased in the cilostazol group and edaravone group (all P0.05),especially in the cilostazol group.Conclusions Our results showed that cilostazol had protective effects on cultured rat brain microvascular endothelial cells in ischemic injury model.And the mechanisms may involve increased levels of cAMP by inhibiting PDE3,which can induce levels of eNOS increased and levels of iNOS reduced.
分 类 号:R743[医药卫生—神经病学与精神病学]
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