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中国应用生理学杂志 ›› 2016, Vol. 32 ›› Issue (4): 305-309.doi: 10.13459/j.cnki.cjap.2016.04.005

• 研究论文 • 上一篇    下一篇

瘦素对小鼠脑缺血/再灌注损伤神经元凋亡的影响

司艺玲, 张金英, 邓子辉, 薛辉, 颜光涛   

  1. 解放军总医院基础医学研究所生物化学研究室, 北京 100853
  • 收稿日期:2015-11-04 修回日期:2016-04-05 出版日期:2016-07-28 发布日期:2018-06-20
  • 通讯作者: 颜光涛,Tel:010-66937027;E-mail:yan301@263.net E-mail:yan301@263.net
  • 基金资助:
    国家自然科学基金资助项目(30670821)

The effects of leptin on neuron apoptosis in mice with cerebral ischemia/reperfusion injury

SI Yi-ling, ZHANG Jin-ying, DENG Zi-hui, XUE Hui, YAN Guang-tao   

  1. Research Laboratory of Biochemistry, Basic Medical Institute, General Hospital of PLA, Beijing 100853, China
  • Received:2015-11-04 Revised:2016-04-05 Online:2016-07-28 Published:2018-06-20
  • Supported by:
    国家自然科学基金资助项目(30670821)

摘要: 目的:研究Leptin在脑缺血性损伤神经元凋亡中的作用及其机制。方法:将75只雄性昆明小鼠完全随机分成3组,即假手术组、缺血/再灌注模型组、Leptin干预组;通过大脑中动脉栓塞(MCAO)复制小鼠局灶性脑缺血再灌注损伤模型,Leptin干预组在缺血0 min腹腔注射Leptin(1μg/g体重),TUNEL染色检测神经元凋亡,RT-PCR检测凋亡相关基因bcl-2和caspase-3 mRNA表达,免疫组化凋亡相关基因bcl-2和caspase-3蛋白水平的表达。结果:模型组脑缺血中心区神经元以坏死为主,与假手术组相比,其半影区神经元凋亡数量显著增多、促凋亡基因cas-pase-3和抑凋亡基因bcl-2的mRNA和蛋白表达水平均显著升高(P<0.01);与模型组比较,Leptin干预组半影区凋亡神经元数量显著减少、caspase-3 mRNA和蛋白表达水平显著降低(P<0.01),抑凋亡基因bcl-2 mRNA和蛋白表达水平显著升高(P<0.01)。结论:Leptin能够通过上调抑凋亡基因bcl-2表达,下调促凋亡基因caspase-3表达抑制神经元凋亡,在脑缺血性损伤中发挥神经保护作用。

关键词: 瘦素, 脑缺血, 神经元, 凋亡, 神经保护, 小鼠

Abstract: Objective:To study the effect of leptin on neuron apoptosis in mice with cerebral ischemia injury. Methods:Seventy-five male Kuming mice were randomly divided into 3 groups:sham, model and leptin intervention group, respectively. Focal cerebral ischemia/reperfusion injury model in mice was established by middle cerebral artery occlusion. Leptin intervention group was injected with leptin (1μg/g weight, I. P.) at 0 min of ischemic injury. Neuron apoptosis was detected by TUNEL staining. The mRNA expression of apoptosis relative gene bcl-2 and caspase-3 were detected by RT-PCR. The protein expression of bcl-2 and caspase-3 were detected by immunohistochemistry. Results:In model group, most of the neurons in the central area of cerebral ischemia had necrosis obviously, and the amount of neuron apop-tosis was much higher than that in sham group (P<0.01). Compared with sham group, both expression of pro-apoptosis gene caspase-3 and anti-apoptosis gene bcl-2 increased significantly in model group (P<0.01). Compared with model group, the amount of neuron apoptosis and expression level of caspase-3 were decreased significantly (P<0.01), whereas the mRNA and protein expression of bcl-2 were increased sig-nificantly in leptin intervention group (P<0.01). Conclusion:Leptin could reduce neuron apoptosis through down-regulation the expression of caspase-3 and up-regulation the expression of bcl-2. It suggests that leptin could play a neuroprotective role in cerebral ischemia injury.

Key words: leptin, cerebral ischemia, neuron, apoptosis, neuroprotection, mice

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