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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
引用本文:罗红波,杨金升,石向群,杨期东,张志强,王为民,周琳.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[J].中华神经医学杂志,2011,10(7).
作者姓名:罗红波  杨金升  石向群  杨期东  张志强  王为民  周琳
作者单位: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
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Aβ1-42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RyR3 mRNA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>0.05).结论 Aβ神经毒性作用引起的细胞内钙稳态失衡并非通过RyR3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.
Abstract:
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 of intracellular calcium homeostasis,which is not through the pathway of Ca2+-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

Calcium homeostasis and expression changes of RyR3 in pyramidal neurons of the rat hippocampus induced by β-amyloid and effects of stilbene glucoside on them
LUO Hong-bo,YANG Jin-sheng,SHI Xiang-qun,YANG Qi-dong,ZHANG Zhi-qiang,WANG Wei-min,ZHOU Lin.Calcium homeostasis and expression changes of RyR3 in pyramidal neurons of the rat hippocampus induced by β-amyloid and effects of stilbene glucoside on them[J].Chinese Journal of Neuromedicine,2011,10(7).
Authors:LUO Hong-bo  YANG Jin-sheng  SHI Xiang-qun  YANG Qi-dong  ZHANG Zhi-qiang  WANG Wei-min  ZHOU Lin
Abstract: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 of intracellular calcium homeostasis,which is not through the pathway of Ca2+-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.
Keywords:Amyloid  Imbalance of calcium homeostasis  Ryanodine receptor-3  Stilbene glucoside
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