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机构地区:[1]长沙市第一医院神经内科,湖南长沙410005
出 处:《中国医药导报》2016年第7期20-23,共4页China Medical Herald
摘 要:目的观察谷氨酸所致脑缺血再灌注的钙超载损伤,探究谷氨酸参与调控钙超载的分子机制。方法建立大鼠脑缺血再灌注模型以及体外培养小鼠的小脑颗粒神经元,随机分组:对照组(5只)、二甲基亚砜溶剂组(3只)、谷氨酸组(5只)、硝苯地平组(4只)、谷氨酸+硝苯地平组(4只)、TRPC1中和性抗体组(5只)、谷氨酸+TRPC1中和性抗体组(5只)。采用干湿重法测定大鼠脑水肿程度,采用激光共聚焦显微镜fura-2探针检测神经元细胞内Ca^(2+)水平。结果在大鼠MCAO模型中,谷氨酸明显增加脑水肿(P<0.05),硝苯地平显著抑制由谷氨酸引起的脑水肿(P>0.05),而TRPC1中和性抗体无此效应(P<0.05)。在体外神经元培养中,谷氨酸显著增加细胞内Ca2+水平,而硝苯地平能降低由谷氨酸引起的神经元内Ca2+升高,差异有统计学意义(P<0.05);TRPC1中和性抗体只能部分降低谷氨酸引起的神经元内Ca2+升高,差异无统计学意义(P>0.05)。结论谷氨酸在脑缺血再灌注中所致钙超载,主要通过L-型钙通道钙内流后激活钙库释放,最终导致脑水肿。钙库调控的TRPC1通道不参与谷氨酸所致的钙超载。Objective To observe calcium overload in cerebral ischemia reperfusion injury caused by glutamic acid and investigate glutamic acid molecular mechanism involved in the regulation of calcium overload. Methods Middle cerebral artery occlusion(MCAO) rats model and in vitro cultivation of cerebellar granule neurons in mice were built, random allocation: control without any treatment(n = 5), DMSO solvent(n = 3), Glu treated with 30 mmol/L glutamate(n =5), L-calcium channel inhibitor nifedipine(n = 4), 30 mmol/L glutamate plus nifedipine(n = 4), TRPC1 inhibitor(n =5), 30 mmol/L gulatmate plus TRPC1 inhibitor(n = 5). Brain hemisphere edema was detected with dry and wet weight method, and intracellular calcium concentration [Ca2+] was investigated with probe fura-2 by fluorescence confocal fluorescence microscopy. Results In MCAO model, glutamate significantly increased brain edema(P 〈 0.05), and L-calcium channel inhibitor nifedipine significantly decreased brain edema by gulatmate(P 〈 0.05), however, TRPC neutralizing antibody had no effect(P 〈 0.05). In cultured neuron cell in vitro, enhance of([Ca2+]) induced by glutamate was inhibited by nifedipine, however, L-calium cnannel in hibitor nifedipine significantly decreased the rise of intracellular(Ca2+) caused by glutamic acid, the difference was statistically significant(P 〈 0.05), however, TRPC neutralizing antibody could only partly decrease the rise of intracellular([Ca2+]) caused by glutamic acid, the difference was not statistically significant(P 〉 0.05). Conclusion Calcium overload induced by glutamate toxicity in middle cerebral artery occlusion mainly activate calcium by L- calcium in calcium channel flow after the release and eventually lead to brain edema, but calcium library regulation of TRPC1 channel doesn’t participate in calcium overload in cerebral ischemia reperfusion injury caused by glutamic acid.
关 键 词:大脑中动脉栓塞 谷氨酸 细胞内CA2+ L-型钙通道
分 类 号:R743.31[医药卫生—神经病学与精神病学]
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