大鼠全脑缺血再灌注损伤对海马CA1区胶质细胞谷氨酸转运体1表达的影响

doi:10.3969/j.issn.1002-1949.2019.09.017

摘要
图/表
参考文献(13)
相关文章 (15)

全文: PDF (1978 KB) HTML (1 KB)
输出: BibTeX | EndNote (RIS)

摘要目的观察大鼠全脑缺血再灌注损伤对海马CA1区胶质细胞谷氨酸转运体1（glial glutamate transporter-1， GLT-1)表达的影响。方法雄性Wistar大鼠90只，随机分为三组：对照组（C组, n=6），不做处理；假手术组（S组, n=42），凝闭双侧椎动脉,48 h后假手术操作；缺血再灌注组（I/R组, n=42），采用四血管阻断法制备大鼠全脑缺血再灌注模型。于缺血再灌注即刻（0 h)、8 h、16 h、1 d、3 d、5 d、7 d断头取材，通过硫堇染色观察海马病理学变化和免疫组化及Western blot技术观察GLT-1、Bax和Bcl-2蛋白的表达情况。结果与C组比较，S组大鼠海马CA1区7 d病理分级（HG）和神经元密度（ND）差异无统计学意义（0级 vs. 0～Ⅰ级，214±3.7 vs. 206±4.6，P>0.05）; 各时间点S组大鼠海马CA1区GLT-1、Bcl-2、 Bax增多(P<0.05)。与S组比较，I/R组大鼠海马CA1区7 d HG显著升高（0～Ⅰ级 vs. Ⅲ级）, ND显著降低（206±4.6 vs. 42±3.4,P<0.05)；各时间点I/R组GLT-1、Bcl-2表达和Bcl-2/Bax比值降低，而Bax表达增加 (P<0.05)。结论大鼠脑缺血再灌注损伤引起海马CA1区GLT-1表达下调，该作用可能是缺血再灌注损伤作用机制之一。

	服务

	把本文推荐给朋友
	加入我的书架
	加入引用管理器
	E-mail Alert
	RSS
	作者相关文章
	马东阳
	李艳丽
	张志强
	边庆虎
	李亚男
	安琪
	张山

关键词 ：缺血再灌注, 凋亡, 脑保护, 胶质细胞, 谷氨酸转运体1(GLT-1)

基金资助:河北省自然科学基金（H2018206345）

通讯作者: 张山（1964-），男，博士，主任医师，教授，硕士生导师，E-mail：zhangshan18531135269@126.com。

作者简介: 马东阳（1988-），男，硕士，医师，E-mail：madongyang1988@126.com。

引用本文:

马东阳，李艳丽，张志强，边庆虎，李亚男，安琪，张山. 大鼠全脑缺血再灌注损伤对海马CA1区胶质细胞谷氨酸转运体1表达的影响[J]. 中国急救医学, 2019, 39(9): 887-892.
Ma Dong-yang, Li Yan-li, Zhang Zhi-qiang, Bian Qing-hu, Li Ya-nan, An Qi, Zhang Shan. Effect of glial glutamate transporter-1 expression in hippocampal CA1 region during global cerebral ischemia reperfusion injury in rats. Chinese Journal of Critical Care Medicine, 2019, 39(9): 887-892.

链接本文:

http://www.cnemergency.org.cn/CN/10.3969/j.issn.1002-1949.2019.09.017 或 http://www.cnemergency.org.cn/CN/Y2019/V39/I9/887

［1］Shigeri Y, Seal RP, Shimamoto K. Molecular pharmacology of glutamate transporters, EAATs and VGLUTs［J］. Brain Res Brain Res Rev, 2004, 45(3): 250-265. ［2］Zhang M, Li WB, Geng JX, et al. The upregulation of glial glutamate transporter-1 participates in the induction of brain ischemic tolerance in rats［J］. J Cereb Blood Flow Metab, 2007, 27(7): 1352-1368.  ［3］Shimizu S, Nagayama T, Jin KL, et al. Bcl-2 Antisense treatment prevents induction of tolerance to focal ischemia in the rat brain［J］. J Cereb Blood Flow Metab, 2001, 21(3): 233-243.  ［4］Gustavsson M, Wilson MA, Mallard C, et al. Global gene expression in the developing rat brain after hypoxic preconditioning: involvement of apoptotic mechanisms［J］. Pediatr Res, 2007, 61(4): 444-450.  ［5］Hu XL, Olsson T, Johansson IM, et al. Dynamic changes of the anti- and pro-apoptotic proteins Bcl-w, Bcl-2, and Bax with SmacDiablo mitochondrial release after photothrombotic ring stroke in rats［J］. Eur J Neurosci, 2004, 20(5): 1177-1188.  ［6］Solaroglu I, Tsubokawa T, Cahill J, et al. Anti-apoptotic effect of granulocyte-colony stimulating factor after focal cerebral ischemia in the rat［J］. Neuroscience, 2006, 143(4): 965-974.  ［7］Jackson JG, Robinson MB. Reciprocal regulation of mitochondrial dynamics and calcium signaling in astrocyte processes［J］. J Neurosci, 2015, 35(45): 15 199-15 213.  ［8］He L, Lemasters JJ. Regulated and unregulated mitochondrial permeability transition pores: a new paradigm of pore structure and function［J］. FEBS Letters, 2002, 512(1-3): 1-7. ［9］Kim JS, Wang JH, Lemasters JJ. Mitochondrial permeability transition in rat hepatocytes after anoxia/reoxygenation: role of Ca2+-dependent mitochondrial formation of reactive oxygen species［J］. Am J Physiol Gastrointest Liver Physiol, 2012, 302(7): G723-G731. ［10］Harris MH, Thompson CB. The role of the Bcl-2 family in the regulation of outer mitochondrial membrane permeability［J］. Cell Death Differ, 2000, 7(12): 1182-1191.  ［11］O"Donnell JC, Jackson JG, Robinson MB. Transient oxygen/glucose deprivation causes a delayed loss of mitochondria and increases spontaneous calcium signaling in astrocytic processes［J］. J Neurosci, 2016, 36(27): 7109-7127. ［12］Dienel GA. Astrocytic energetics during excitatory neurotransmission: What are contributions of glutamate oxidation and glycolysis［J］. Neurochem Int, 2013, 63(4): 244-258.  ［13］Karaca M, Frigerio F, Migrenne S, et al. GDH-dependent glutamate oxidation in the brain dictates peripheral energy substrate distribution［J］. Cell Rep, 2015, 13(2): 365-375.