β-淀粉样肽诱发的细胞内钙离子、内质网钙通道蛋白表达变化及二苯乙烯苷干预效果  

Calcium homeostasis and expression changes of RyR3 in pyramidal neurons of the rat hippocampus induced by β-amyloid and effects of sfilbene glucoside on them

作　　者：罗红波[1] 杨金升[1] 石向群[1] 杨期东[2] 张志强[1] 王为民[1] 周琳[2] 

机构地区：[1]兰州军区兰州总医院神经内科,兰州730050 [2]中南大学湘雅医院神经内科,长沙410008

出　　处：《中华神经医学杂志》2011年第7期654-657,共4页Chinese Journal of Neuromedicine

摘　　要：目的探讨β-淀粉样肽（Aβ）诱发的细胞内钙失衡机制中位于内质网上的鱼尼丁受体（RyRs）的作用及二苯乙烯苷（TSG）的干预效果。方法Wistar大鼠80只采用完全随机数字表法分为对照组、假手术组、模型组及TSG组，每组20只。后3组在立体定向仪下注射Aβ。至大鼠海马部位，建立AD模型；对照组不做任何处理。激光扫描共聚焦显微镜观察细胞内钙离子浓度。RT—PCR法检测RyR3mRNA的表达。结果各组大鼠海马细胞内钙离子浓度差异有统计学意义，其中模型组明显高于对照组及假手术组，TSG组明显低于模型组，差异有统计学意义（P〈0．05）。RT—PCR半定量分析结果显示，模型组RyR3／β-actin值明显降低，与对照组及假手术组比较差异有统计学意义（P〈0．05）；TSG组RyR3／β-actin值略微升高，与对照组及假手术组比较差异没有统计学意义（P〉0．051。结论Aβ神经毒性作用引起的细胞内钙稳态失衡并非通过IWR3介导的钙释放途径，而是通过细胞膜通透性改变所致。TSG可通过纠正细胞内钙超载来抵抗Aβ神经毒性损伤。Objective To study the effects of stilbene glucoside （TSG） on calcium homeostasis and expression of RyR3 in pyramidal neurons of the rat hippocampus induced by β-amyloid （Aβ）. Methods Eighty Wistar rats were equally randomized into 4 groups （n=20）： control group, sham-operated group, model group and TSG inducement group. AD models in the later 3 groups were induced by stereotactic injection of Aβ1-42 to the rat hippocampus; and rats of the control group did not give any treatment. The mRNA expression of RyR3 was detected by real time PCR （RT-PCR） and monitored under laser scanning confocal microscope. Results The concentration of intracellular calcium between each 2 groups was significantly different （P〈0.05）; that in the model group was obviously higher than that in the control and sham-operated groups, and that in the TSG inducement group was obviously lower than that in the model group （P〈0.05）. Semi-quantitative RT-PCR indicated that the value of RyR3/β-actin in the model group was obviously decreased as compared with that in the control and sham-operated groups （P〈0.05）; the value of RyR3/β-actin in the TSG inducement group was slightly increased, but no significant difference was noted as compared with that in the control and sham-operated groups （P〉0.05）. Conclusion Aβ neurotoxicity causes disorder ofintracellular calcium homeostasis, which is not through the pathway of Caa＋-induced Ca2＋ release induced by RyR3, but through the changes of permeability of cytomembrane. TSG plays a protection role from Aβ neurotoxicity by calcium homeostasis.

关 键 词：淀粉样蛋白 钙失衡 Ryanodine受体-3 二苯乙烯苷 

分 类 号：R749.16[医药卫生—神经病学与精神病学]