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目的观察二苯乙烯苷对谷氨酸 (Glu)致原代培养大鼠海马神经元损伤的保护作用。方法原代培养大鼠海马神经元细胞与不同浓度的二苯乙烯苷 (5— 10 0 μmol/L)共同孵育 2 4h ,加入工具药Glu(终浓度为 5 0 0 μmol/L)孵育。四甲基偶氮唑盐(MTT)法测定细胞存活率 ;乳酸脱氢酶 (LDH )漏出率法测定细胞膜损伤 ;使用荧光指示试剂Fluo 3 /AM负载后 ,在激光共聚焦显微镜下观察不同细胞内Ca2 + 的荧光强度。结果不同浓度的二苯乙烯苷与细胞孵育 2 4h后可明显拮抗Glu介导的神经毒性作用 ,细胞存活率明显增加 ,LDH漏出减少 ,细胞死亡率降低 ,并呈明显剂量依赖关系 ;细胞内的Ca2 + 荧光强度降低。结论二苯乙烯苷拮抗Glu诱导的神经毒作用的机制可能为选择性抑制大剂量Glu引起的Ca2 + 浓度异常升高。
Objective To observe the protective effects of stilbene glucoside on hippocampal neurons injury induced by glutamate (Glu) in primary cultures. Methods Primary cultured rat hippocampal neurons were incubated with different concentrations of stilbene glucoside (5–10 μmol/L) for 24 hours and incubated with the vehicle drug Glu (final concentration of 500 μmol/L). MTT assay was used to determine cell viability; lactate dehydrogenase (LDH) leakage rate method was used to measure cell membrane damage; after loading with fluorescent indicator Fluo 3 /AM, different cells were observed under laser confocal microscope The fluorescence intensity of Ca2+. RESULTS: Different concentrations of stilbene glycosides incubated with cells for 24 hours significantly antagonized Glu-mediated neurotoxicity, cell survival was significantly increased, LDH leakage was decreased, cell death was decreased, and the dose was significantly dependent; intracellular Ca2+ fluorescence intensity decreases. Conclusion The mechanism of antagonism of stilbene glucoside on Glu-induced neurotoxicity may be the selective inhibition of abnormally elevated Ca 2+ concentration induced by large doses of Glu.