期刊文献+

督脉穴位电针对暂时性脑缺血所致神经细胞死亡的影响 被引量:17

Effect of Electroacupuncture on Neuronal Death Induced by Cerebral Ischemia-reperfusion and Its Mechanisms
下载PDF
导出
摘要 目的 :观察电针对神经细胞死亡、DNA损伤及凋亡相关基因蛋白 (Bcl 2、Bax、P53 )表达的影响。方法 :采用短暂脑缺血再灌注 (MCAo)模型 ,应用HE、TUNEL、免疫组织化学等实验技术进行观察。结果 :大脑中动脉阻塞 2hr后 ,随着再灌时间的增加梗塞灶面积进行性发展 ,在不同再灌时间点 ,电针均能减小梗塞面积 ,而且电针可明显减少短暂脑缺血再灌注后细胞坏死和DNA损伤 ,并上调Bcl 2 /Bax比值 ,和减少P53的表达。结论 :电针具有神经保护作用 。 Objective: To observe the protective effect of electroacupuncture (EA) against rat's cerebral ischemia induced by middle cerebral artery occlusion (MCAo). Methods: 30 SD rats were randomized into ischemia (2 hr) and reperfusion (IR) control group, and IR+EA group. Each group was further divided into three subgroups respectively according to the different time course of reperfusion: IR 24 hr group, IR 48 hr group, IR 72 hr group, and EA+IR 24 hr group, EA+IR 48 hr group and EA+IR 72 hr group, with 5 rats in each group. EA was applied to 'Baihui' (GV 20) and 'Renzhong' (GV 26) for 1 hr beginning from 15 min on after ischemia. After 24 hours' reperfusion, EA was performed on the same two points for 45 min everyday. Neuronal death and apoptosis associated proteins (Bcl 2, Bax,P53) expressions of the cerebral tissue sections were observed using HE staining, TUNEL (TdT mediated dUTP Nick End Labeling) and immunohistochemistry. Results: After IR, the cerebral infarction area increased progressively along with the increase of duration of the reperfusion, while that of 3 EA groups was smaller. There were significant differences between IR 24 hr group and EA+IR 24 hr group, between IR 48 hr group and EA+IR 48 hr group, and between IR 72 hr group and EA+IR 72 hr group ( P <0.05~0.01).The surviving rates of neurons in the striate body of the brain of EA+IR 24 hr group and in the cerebral cortex of EA+IR 48 hr group and EA+IR 72 hr group were significantly higher than those of the corresponding IR control groups respectively ( P <0.05).The TUNEL positive cell ratio of the cerebral cortex in each one of 3 EA groups was significantly lower than that of each corresponding IR control group ( P <0.05~0.001). The ratio values of Bcl 2 positive cells/Bax positive cells of 3 EA groups were all significantly higher than those of the 3 corresponding IR control groups ( P <0.05~0.001). P53 immuno reaction positive neurons of EA+IR 24 hr group and EA+IR 48 hr group were markedly fewer than those of IR 24 hr group and IR 48 hr group respectively ( P <0.05). It showed that EA could evidently reduce the neuronal death and apoptosis, up regulated Bcl 2/Bax and down regulated the expression of P53 in cerebral IR rats. Conclusion: The protective effect of EA on cerebral ischemic neurons may be related with the resultant regulation of the expression of apoptosis associated proteins (Bcl 2, Bax, P53).
出处 《针刺研究》 CAS CSCD 2003年第1期10-16,共7页 Acupuncture Research
基金 国家自然科学基金重点项目 (No.39730 5 10 )
关键词 督脉穴位 电针 暂时性脑缺血 神经细胞死亡 Cerebral ischemia Acupuncture Neuronal damage Apoptosis
  • 相关文献

参考文献11

  • 1Zhao Peng, Cheng Jieshi. Effects of electroacupuncture on extracellular contents of amino acid neurotransmitters in rat striatum following transient focal cerebral ischemia. Acupunct Electrother Res, 1997, 22(2) : 119.
  • 2Zhao Peng, Huang Zhinong, Cheng Jieshi. Electro-acupuncture attennuates nitric oxide release from rat striatum after transient middle cerebral artery occlusion. Acupunct Electrother Res, 2000, 25 : 101.
  • 3McConkey DJ. The role of calcium in the regulation of apoptosis. Scanning Microsc, 1996, 10(3): 777.
  • 4Zhang H, Heim J, Meyhack B. Redistribution of Bax from cytosol to membranes is induced by apoptotic stimuli and is an early step in the apoptotic pathway. Biochem Biophys Res Commun, 1998, 251:454.
  • 5Li P, Nijhawan D, Budihardio I, et al. Cytochrome C and dATP-dependent formation of APAF-1/caspase-9 complex initiates an apoptotic protease cascade. Cell, 1997, 91:479.
  • 6Sakhi S, Bruce A, Sun N, et al. P53 induction is associated with neuronal damage in the central nervous system. Proc Natl Acad Sci USA, 1994, 91:7525.
  • 7Hughes PE, Alexi T, Yoshida T, et al. Excitotoxic lesion of rat brain with quinolinic acid induces expression of P53 messenger RNA and protein and P53-inducible genes Bax and Gadd-45 in brain areas showing DNA fragmentation.Neumscience, 1996, 74:1143.
  • 8Shimizu S, Eguchi Y, Kamiike W, et al. Retardation of chemical h3rpoxia-induced necrotic cell death by Bcl-2 and ICE inhibitors: Possible involvement of common mediators in apoptotic and necrotic signal transductions. Oncogene,1996, 12:2045.
  • 9Morrison RS, Jurgen Wenzel H, Kinoshita Y, et al. Loss of the P53 tumor suppressor gene protects neurons from kainite-induced cell death. J Neurosci, 1996, 16:1337.
  • 10Leist M, Single B, Castoldi AF, et al. Intracellular adenosine triphosphate (ATP) concentration: A switch in the decision between apoptosis and necrosis. J Exp Med, 1997,185:1481.

同被引文献235

引证文献17

二级引证文献152

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部