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异丙酚对大鼠局灶性脑缺血再灌注时TGF-β1表达的影响

冯春生1，李春玲2，仇金鹏1，麻海春1*，孙发武△   

  1. 1.　吉林大学第一医院麻醉科，吉林 长春130021；2. 吉林大学第一医院手术室，吉林 长春130021
  • 收稿日期:2003-08-23 修回日期:1900-01-01 出版日期:2005-07-28 发布日期:2005-07-28
  • 通讯作者: 麻海春

Effect of propofol on expression of TGF-β1 in cerebral cortexduring transient focal cerebral ischemia-reperfusion in rats

FENG Chun-sheng1, LI Chun-ling2, QIU Jin-peng1, MA Hai-chun1*,SUN Fa-wu△   

  1. 1. Department of Anesthesiology，First Hospital, Jilin University, Changchun 130021，China;2. Department of Operating Room，First Hospital, Jilin University, Changchun 130021，China
  • Received:2003-08-23 Revised:1900-01-01 Online:2005-07-28 Published:2005-07-28
  • Contact: MA Hai-chun

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摘要： 目的：观察异丙酚对大鼠局灶性脑缺血再灌注时TGF-β1表达的影响，并探讨其脑保护的 机制。 方法：采用线栓法建立大鼠局灶性脑缺血再灌注模型。45只雄性Wistar大鼠，随机分为假手术组、缺血再灌注组(I/R)和缺血再灌注-异丙酚治疗组，大鼠经历2 h脑缺血，然后实行再灌注。分别于再灌注后3、6、24、72 h断头取脑，用免疫组化法检测脑组织TGF-β1的表达；再灌注后24 h做神经功能缺陷评估及HE染色观察缺血皮层组织形态学变化。 结果：局灶性脑缺血再灌注后TGF-β1明显表达， 24 h后达高峰(P<0.01)， 72 h后降至正常。大鼠神经功能缺陷评分明显升高，组织形态学观察可见皮层水肿、淤血，神经细胞明显变性坏死；应用异丙酚能显著地促进TGF-β1的表达，与脑缺血再灌注组比较，异丙酚治疗组TGF-β1释放增多、高峰提前、延缓下降（P<0.05），同时显著降低大鼠神经功能缺陷评分和减轻缺血皮层组织形态学损伤（P<0.05）。 结论：异丙酚的脑保护作用可能与促进TGF-β1的表达有关。

关键词: 药理学, 脑缺血, 再灌注损伤, 转化生长因子β, 疾病模型, 动物

Abstract: Objective To investigate the effect of propofol on the expression of TGF-β1 in cerebral cortex during focal cerebral ischemia-reperfusion in rats. Methods The focal cerebral ischemia-reperfusion model was established by thread embolism of middle cerebral artery. Forty-five male Wistar rats were randomly allocated to sham-operation group (n=5), ischemia-reperfusion group (n=20) and propofol group (n=20), rats were subjected to 2 h of focal ischemia by left middle cerebral artery occlusion and then reperfused. At 3, 6, 24, and 72 h after reperfusion the rats were decapitated, the expressions of TGF-β1 in ischemic cortex were tested by immunohistochemical method. At 24 h after reperfusion, scores of neurological deficit were estimated and the change of histomorphology in ischemic cortex was observed under the light microscope by using HE staining. Results The expression of TGF-β1 increased significantly after focal cerebral ischemia-reperfusion, reached to maximal expression at 24 h after reperfusion (P<0.01), and decreased to normal at 72 h after reperfusion. The scores of neurological deficit in rats increased significant ly. The followings were observed in histomorphology: congestion and edema in ischemic cort ex, degeneration and necrosis of neuron. Expression of TGF-β1 in pro pofol gr oup increased significantly than that in ischemia-reperfusion group (P<0.05). The scores of neurological deficit and the damage of histomorphology in ischemic cortex lowered than that in propofol group. Conclusion The results show that propofol can stimulate the expression of TGF-β1 to produce neuroprotection. Key words：propofol/pharmacology; cerebral ischemia; reperfusi on injury; transforming growth factor beta; disease models,animal

Key words: pharmacology, cerebral ischemia, reperfusi on injury, transforming growth factor beta, disease models, animal

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  • R614.1
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