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作 者:徐志伟[1] 孙琪[2] 敖海清[1] 王文竹[1] 富文俊[1]
机构地区:[1]广州中医药大学基础医学院,广东广州510006 [2]宁夏医科大学中医学院,宁夏银川750004
出 处:《广州中医药大学学报》2011年第1期36-42,108,共8页Journal of Guangzhou University of Traditional Chinese Medicine
基 金:国家自然科学基金项目(编号:30801525);广东省中医药强省基金项目(编号:2007054);广州中医药大学创新基金项目(编号:K0070010)
摘 要:【目的】观察逍遥散含药血清对慢性应激状态下大鼠海马神经细胞天冬氨酸受体(NR)各亚基mRNA表达的影响。【方法】采用Taqman荧光探针定量PCR法测定、2-△△Ct相对定量法计算NR各亚基表达量相对值。【结果】模型血清与谷氨酸模拟的慢性应激微环境可致海马神经细胞NR各亚基mRNA表达出现不同程度的上调;在拟慢性应激作用前对细胞进行地佐环平(MK-801)预处理,即阻滞NR后,NR2A mRNA、NR2B mRNA表达水平明显降低,但未达到正常水平;逍遥散含药血清使NR2AmRNA表达水平明显上调,NR2B mRNA表达水平较慢性应激组显著降低,NR1 mRNA表达水平则无明显下降;MK-801与逍遥散含药血清共同作用后,NR2A mRNA、NR2B mRNA表达水平接近正常。【结论】逍遥散含药血清能够纠正NR各亚基mRNA表达失衡的状态,促进机体恢复或保持NR2A与NR2B的正常比例,对维持海马神经细胞的稳定起到一定作用,从而发挥保护神经元、对抗慢性应激损伤的作用。Objective To observe the effect of serum containing Xiaoyao Powder (XP) on the mRNA expression of subunits of N-methyl-D-aspartic acid receptors (NR) NR1, NR2A and NR2B in the cultured hippocampal neurons of stressed rats. Methods The methods of Taqman fluorescence probe real-time quantitative PCR and relative quantification were used to determine the mRNA expression of NMDA receptor subunits. Results NR1 , NR2A and NR2B mRNA expression in the cultured hippocampal neurons was up-regulated to various degrees in the micro environment simulated by chronic stress rat serum and glutamate. After pretreated with MK-801 (for blocking NR) , NR2A and NR2B mRNA expression was decreased obviously in the micro-environment sinmlated by chronic stress rat serum and glutamate, but did not arrive to the normal level. Serum containing XP could up-regulate NR2A mRNA expression and down-regulate NR2B mRNA expression, but had no effect on NR1 mRNA expression in the micro-environment simulated by glutamate. The combination of MK-801 and serum containing XP regulated NR2A and NR2B mRNA expression in the micro-environment simulated by glutamate. Conclusion Serum containing XP can maintain the stability of hippocampal neurons, and protect the hippocampal neurons against injury induced by chronic stress through correcting the imbalance of NR subunits and promoting the recovery of NR2A/NR2B ratio in rats under chronic stress.
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