| 王梅 戚大石 胡晓彤 刘亚萍 张芳.NMDA受体介导脑缺血/再灌注诱导GluR6 巯基亚硝基化的研究[J].现代生物医学进展英文版,2016,16(32):6235-6238. |
| NMDA受体介导脑缺血/再灌注诱导GluR6 巯基亚硝基化的研究 |
| NMDA Receptor Involved in Cerebral Ischemia-Reperfusion Induced GluR6S-nitrosylation |
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| DOI： |
| 中文关键词: 脑缺血再灌注 NMDA 受体 S-亚硝基化 谷氨酸受体6 |
| 英文关键词: Cerebral ischemia reperfusion NMDA recepter S-nitrosylation GluR6 |
| 基金项目:国家自然科学基金青年基金项目（81500977）；江苏省高校自然科学研究面上项目（14KJB180022）；江苏省脑病生物信息重点实
验室开放研究课题（1505）；江苏省普通高校自然科学研究项目（13KJD310003）；徐州市科技计划项目（KC14SH076） |
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| 中文摘要: |
| 目的：研究脑缺血再灌注以及联合给予脑缺血和NMDA（N- 甲基-D- 天冬氨酸）受体抑制剂MK801 对大鼠海马CA1 区
GluR6 巯基亚硝基化以及海马CA1 区锥体细胞凋亡的影响。方法：采用四动脉结扎法构建大鼠全脑缺血再灌注模型，给予SD 大
鼠腹腔注射NMDA受体特异性抑制剂MK801 (3 mg/kg)。主要运用' 生物素转化法'(Biotin-Switch method)、SDS-PAGE、免疫印
迹、焦油紫染色等方法对GluR6 的巯基亚硝基化（S- 亚硝基化）、蛋白表达水平以及海马CA1 区锥体细胞的凋亡水平进行研究。
结果：脑缺血／再灌注显著促进GluR6 的巯基亚硝基化以及海马CA1 区锥体细胞的凋亡，给予NMDA 受体特异性抑制剂
MK801 能够显著抑制脑缺血／复灌诱导增加的GluR6 的S- 亚硝基化以及海马CA1 区锥体细胞的凋亡。结论：脑缺血／再灌注
早期NMDA 受体介导了GluR6的巯基亚硝基化以及海马CA1区锥体细胞的凋亡，从而为临床治疗缺血再灌注脑损伤提供了理
论依据。 |
| 英文摘要: |
| Objective:The objective of this study is primarily to determine whether NMDA recepter affects GluR6 S-nitrosylation
and the survival of CA1 subfield during the early stages of ischemia-reperfusion.Methods:Transient cerebral ischemia was induced by a
four-vessel occluded (4-VO) method. Sprague-Dawley rats were treated intraperitoneally with MK801（3 mg/kg, an selective inhibitor of
NMDA recepter). We perform this study mainly by biotin switch assay, SDS-PAGE and western bloting to exam the S-nitrosylation and
expression of GluR6. Cresyl violet staining was performed to examine the survival and apoptosis neurons in the pyramidal cell layer of
the hippocamal CA1 subfield.Results:Here, we showed that S-nitrosylation of GluR6 and the apoptosis of CA1 pyramidal neuron was
dramatically induced by cerebral ischemia-reperfusion,and that administration of MK801 observably diminished the increased
S-nitrosylation of GluR6 and the apoptosis of CA1 pyramidal neuron.Conclusion:These data suggest that NMDA recepter facilitates
GluR6 S-nitrosylation and the apoptosis of CA1 pyramidal neuron in the early stages of cerebral ischemia-reperfusion. In contrast,
MK801 antagonizes the above action of cerebral ischemia-reperfusion．Thus, our results provide that NMDA recepter regulate GluR6 by
S-nitrosylation and affect the CA1 pyramidal neuron during the early stages of ischemia-reperfusion, which can be a new approach for
stroke therapy. |
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