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作 者:孟晶[1] 丁小燕[2] 朱晓波[2] 林少芬[2] 郭梦翔[2] 唐仕波[2]
机构地区:[1]暨南大学第一附属医院眼科,广东广州510630 [2]广州中山大学中山眼科中心,广东广州510060
出 处:《中国病理生理杂志》2009年第11期2192-2196,共5页Chinese Journal of Pathophysiology
基 金:广东省科技计划基金资助项目(No.A050100029);广东省医学科研基金资助项目(No.B2009125)
摘 要:目的:观察银杏内酯B对体外培养的大鼠视网膜神经细胞内钙离子浓度和线粒体功能的影响。方法:采用体外原代培养的大鼠视网膜神经细胞,建立谷氨酸损伤的视网膜神经细胞凋亡模型,与银杏内酯B共同培养,用激光扫描共聚焦显微镜检测对视网膜神经细胞内钙离子浓度和线粒体膜电位的影响。结果:谷氨酸(8mmol/L)作用后,视网膜神经细胞存活率降低,细胞凋亡增加,细胞内钙离子浓度增加,线粒体膜电位下降。GB干预后,钙离子浓度降低,线粒体膜电位显著升高,细胞凋亡明显减少。结论:GB能对抗谷氨酸兴奋性毒性,保护视网膜神经细胞,这一作用可能是通过降低细胞内钙离子浓度和升高线粒体膜电位来实现的。AIM: To observe the effect of ginkgolide B (GB) on the intracellular calcium ion concentration ( [ Ca2 +] i ) and mitochondrial function of cultured rat retinal neurons in vitro. METHODS : in vitro primary culture of rat retinal neurons was used in the experiment. The apoptosis model of glutamate - induced retinal neurons was established and co - cultured with ginkgolide B. The [ Ca2 + ]i and mitochondrial membrane potential of the retinal neurons were detected by laser scanning confocal microscope. RESULTS : Glutamate decreased the survival rate of retinal neurons, increased the apoptosis and the [ Ca2+] i, lowered the mitochondrial membrane potential. The [ Ca2 + ] i was clearly diminished and the mitochondrial membrane potential was significantly increased with the GB intervention, and the apoptosis decreased significantly. CONCLUSION: GB protects retinal neurons from glutamate induced neurotoxicity. The effect of GB on retinal neurons might be due to its ability to decrease the [ Ca2 +] i and increase mitochondrial membrane potential.
关 键 词:银杏内酯B 谷氨酸 细胞内钙离子浓度 线粒体膜电位 视网膜
分 类 号:R339.146[医药卫生—人体生理学]
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