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5-羟甲基糠醛对皮质酮损伤型海马神经元P-synapsinⅠ蛋白表达的影响 被引量:9
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作者 张丽娜 张天良 +2 位作者 金国琴 戴薇薇 林梅 《中国老年学杂志》 CAS CSCD 北大核心 2015年第9期2305-2307,共3页
目的观察熟地有效成分5-羟甲基糠醛对高浓度皮质酮致海马神经元损伤及学习记忆相关蛋白P-synapsin I蛋白表达的影响。方法用24 h新生大鼠制备原代海马神经细胞。培养第8天用皮质酮、RU38486、5-HMF处理细胞,将细胞分为正常组、模型组(1&... 目的观察熟地有效成分5-羟甲基糠醛对高浓度皮质酮致海马神经元损伤及学习记忆相关蛋白P-synapsin I蛋白表达的影响。方法用24 h新生大鼠制备原代海马神经细胞。培养第8天用皮质酮、RU38486、5-HMF处理细胞,将细胞分为正常组、模型组(1×10-4mol/L皮质酮)、拮抗剂组(10-4mol/L皮质酮+3 nmol/L RU38486)、5-羟甲基糠醛组(10-4mol/L皮质酮+0.5 mg/L 5-HMF)。24 h后,通过SYTO13-PI双荧光染色法观察各组细胞的形态及存活情况,MTT法测定细胞活性,生化方法检测衰老特异性指标β-半乳糖苷酶活性,Western印迹检测学习记忆相关分子P-synapsinⅠ的蛋白表达。结果与正常组相比,模型组细胞死亡较多,细胞活力下降,β-半乳糖苷酶活性升高,P-synapsinⅠ蛋白表达显著性降低;如上改变均被皮质酮受体拮抗剂RU38486逆转;一定浓度的5-羟甲基糠醛明显减少死细胞数量,提高细胞活力,降低β-半乳糖苷酶活性,提高模型细胞PsynapsinⅠ蛋白表达。结论 0.5 mg/L 5-羟甲基糠醛可以保护大鼠海马神经细胞免遭高浓度皮质酮的损伤,通过调节学习记忆信号转导途径中的重要蛋白P-synapsinⅠ的蛋白表达,可能在延缓学习记忆功能退化中发挥作用。 展开更多
关键词 5-羟甲基糠醛 海马神经元 皮质酮 p-synapsin 熟地
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Acrylamide-induced Subacute Neurotoxic Effects on the Cerebral Cortex and Cerebellum at the Synapse Level in Rats 被引量:2
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作者 ZHANG Bin SHAO Hua +7 位作者 WANG Xiu Hui CHEN Xiao LI Zhong Sheng CAO Peng ZHU Dan YANG Yi Guang XIAO Jing Wei LI Bin 《Biomedical and Environmental Sciences》 SCIE CAS CSCD 2017年第6期432-443,共12页
Objective To investigate acrylamide (ACR)-induced subacute neurotoxic effects on the central nervous system (CNS) at the synapse level in rats. Methods Thirty-six Sprague Dawley (SD) rats were randomized into th... Objective To investigate acrylamide (ACR)-induced subacute neurotoxic effects on the central nervous system (CNS) at the synapse level in rats. Methods Thirty-six Sprague Dawley (SD) rats were randomized into three groups, (1) a 30 mg/kg ACR-treated group, (2) a 50 mg/kg ACR-treated group, and (3) a normal saline (NS)-treated control group. Body weight and neurological changes were recorded each day. At the end of the test, cerebral cortex and cerebellum tissues were harvested and viewed using light and electron microscopy. Additionally, the expression of Synapsin I and P-Synapsin I in the cerebral cortex and cerebellum were investigated. Results The 50 mg/kg ACR-treated rats showed a significant reduction in body weight compared with untreated individuals (P 〈 0.05). Rats exposed to ACR showed a significant increase in gait scores compared with the NS control group (P 〈 0.05). Histological examination indicated neuronal structural damage in the 50 mg/kg ACR treatment group. The active zone distance (AZD) and the nearest neighbor distance (NND) of synaptic vesicles in the cerebral cortex and cerebellum were increased in both the 30 mg/kg and 50 mg/kg ACR treatment groups. The ratio of the distribution of synaptic vesicles in the readily releasable pool (RRP) was decreased. Furthermore, the expression levels of Synapsin I and P-Synapsin I in the cerebral cortex and cerebellum were decreased in both the 30 mg/kg and 50 mg/kg ACR treatment groups. Conclusion Subacute ACR exposure contributes to neuropathy in the rat CNS. Functional damage of synaptic proteins and vesicles may be a mechanism of ACR neurotoxicity. 展开更多
关键词 Acrylamide (ACR) Synapsin I p-synapsin I Synaptic vesicles NEUROTOXICITY
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