[1]杨红宁,吕兰欣,颜晓庆,等.全脑缺血再灌注诱导大鼠海马CA1区 GluR6巯基亚硝基化的机制[J].医学信息,2019,(18):51-54.[doi:10.3969/j.issn.1006-1959.2019.18.017]
 YANG Hong-ning,LYU Lan-xin,YAN Xiao-qing,et al.Mechanism of Nitrosation of GluR6 Thiol in Rat Hippocampal CA1 Region Induced by Global Cerebral Ischemia-reperfusion[J].Medical Information,2019,(18):51-54.[doi:10.3969/j.issn.1006-1959.2019.18.017]
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全脑缺血再灌注诱导大鼠海马CA1区 GluR6巯基亚硝基化的机制()
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医学信息[ISSN:1006-1959/CN:61-1278/R]

卷:
期数:
2019年18期
页码:
51-54
栏目:
论著
出版日期:
2019-09-15

文章信息/Info

Title:
Mechanism of Nitrosation of GluR6 Thiol in Rat Hippocampal CA1 Region Induced by Global Cerebral Ischemia-reperfusion
文章编号:
1006-1959(2019)18-0051-04
作者:
杨红宁吕兰欣颜晓庆韩 东胡书群许 铁
江苏省卫生应急研究所/徐州医学院附属医院急诊医学实验室,江苏 徐州 221002
Author(s):
YANG Hong-ningLYU Lan-xinYAN Xiao-qingHAN DongHU Shu-qunXU Tie
Jiangsu Provincial Health Emergency Research Institute/Emergency Medical Laboratory, Affiliated Hospital of Xuzhou Medical College,Xuzhou 221002,Jiangsu,China
关键词:
谷氨酸受体6亚基巯基亚硝基化全脑缺血再灌注
Keywords:
Key words:Glutamate receptor 6 subunitSulfhydryl nitrosylationGlobal cerebral ischemia reperfusion
分类号:
R364.1+2;Q71
DOI:
10.3969/j.issn.1006-1959.2019.18.017
文献标志码:
A
摘要:
目的 用大鼠全脑缺血模型探讨全脑缺血再灌注诱导大鼠海马CA1区GluR6巯基亚硝基化的机制。方法 将78只雄性SD大鼠随机分为假手术组(Sham组)、全脑缺血再灌注组(I/R组)、给药组(7-NI组、GSNO组、SNP组、NS102组)及溶剂对照组[生理盐水(Saline)组、DMSO组],每组6只。采用四动脉结扎去结扎法构建大鼠全脑缺血再灌注模型。运用生物素转化法检测蛋白质的巯基亚硝基化,聚丙烯酰胺凝胶电泳、免疫印迹方法对GluR6巯基亚硝基化水平进行分析研究。结果 全脑缺血再灌注后,I/R组GluR6巯基亚硝基化水平高于Sham组,差异有统计学意义(P<0.05),7-NI组GluR6巯基亚硝基化水平相比I/R组明显降低,差异有统计学意义(P<0.05),溶剂DMSO组与I/R组相比差异无统计学意义(P>0.05);GSNO组和SNP组GluR6巯基亚硝基化水平比I/R组明显降低,差异有统计学意义(P<0.05),溶剂Saline组与I/R组相比差异无统计学意义(P>0.05);NS102预处理组GluR6巯基亚硝基化水平比I/R组明显降低,差异有统计学意义(P<0.05),溶剂DMSO组与I/R组相比差异无统计学意义(P>0.05)。结论 7-NI、GSNO、SNP 和NS102都能抑制脑缺血再灌注诱导的GluR6巯基亚硝基化。nNOS介导产生的内源性NO介导全脑缺血再灌注诱导的大鼠海马CA1区GluR6巯基亚硝基化,并受外源性NO影响;全脑缺血再灌注通过激活KA受体诱导大鼠海马CA1区GluR6发生巯基亚硝基化。
Abstract:
Abstract:Objective To investigate the mechanism of GluR6 thiol nitrosylation in rat hippocampal CA1 region induced by global cerebral ischemia-reperfusion in a rat model of global cerebral ischemia.Methods 78 male Sprague-Dawley rats were randomly divided into sham operation group (Sham group), global cerebral ischemia-reperfusion group (I/R group), and drug-administered group (7-NI group, GSNO group, SNP group, NS102 group). And the solvent control group [saline group, DMSO group], 6 in each group. A rat model of global cerebral ischemia-reperfusion was established by four-arterial ligation and ligation. The biotin-transformation method was used to detect the sulfhydryl nitrosylation of proteins, and the phosphination level of GluR6 thiol was analyzed by polyacrylamide gel electrophoresis and immunoblotting.Results After global cerebral ischemia-reperfusion, the level of GluR6 thiol nitrosylation in the I/R group was higher than that in the Sham group,the difference was statistically significant (P<0.05). The level of GluR6 thiol nitrosylation in 7-NI group was significantly lower than that in I/R group, the difference was statistically significant (P<0.05). Solvent DMSO group and I/R group There was no significant difference between the two groups (P>0.05). The nitrosation level of GluR6 in the GSNO group and the SNP group was significantly lower than that in the I/R group,the difference was statistically significant (P<0.05).There was no significant difference between the Saline group and the I/R group (P>0.05). The GluR6 sulfhydryl nitrosylation level in the NS102 pretreatment group was significantly lower than that in the I/R group,the difference was statistically significant (P<0.05). There was no significant difference between the solvent DMSO group and the I/R group (P>0.05).Conclusion 7-NI, GSNO, SNP and NS102 can inhibit GluR6 sulfhydryl nitrosylation induced by cerebral ischemia-reperfusion. nNOS-mediated endogenous NO mediates GluR6 sulfhydryl nitrosylation in rat hippocampal CA1 region induced by global cerebral ischemia-reperfusion and is affected by exogenous NO; global cerebral ischemia-reperfusion activates KA receptor Induction of thiol nitrosylation of GluR6 in the hippocampal CA1 region of rats.

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更新日期/Last Update: 2019-09-15