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Propofol increases expression of basic fibroblast growth factor after transient cerebral ischemia in rats

机译:异丙酚增加了大鼠瞬时脑缺血后碱性成纤维细胞生长因子的表达

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摘要

Anesthetics such as propofol can provide neuroprotective effects against cerebral ischemia. However, the underlying mechanism of this beneficial effect is not clear. Therefore, we subjected male Sprague-Dawley rats to 2 h of middle cerebral artery occlusion and investigated how post-ischemic administration of propofol affected neurologic outcome and the expression of basic fibroblast growth factor (bFGF). After 2 h of ischemia, just before reperfusion, the animals were randomly assigned to receive either propofol (20 mg•kg−1•h−1) or vehicle (10% intralipid, 2 ml•kg−1•h−1) intravenously for 4 h. Neurologic scores, infarct volume, and brain water content were measured at different time points after reperfusion. mRNA level of bFGF was measured by real-time PCR, and the protein expression level of bFGF was analyzed by immunohistochemistry and Western blot. At 6 h, 24 h, 72 h, and 7 days of reperfusion, infarct volume was significantly reduced in the propofol-treated group compared to that in the vehicle-treated group (all P<0.05). Propofol post-treatment also attenuated brain water content at 24 and 72 h and reduced neurologic deficit score at 72 h and 7 days of reperfusion (all P<0.05). Additionally, in the peri-infarct area, bFGF mRNA and protein expression were elevated at 6, 24, and 72 h of reperfusion compared to that in the vehicle-treated group (all P<0.05). These results show that post-ischemic administration of propofol provides neural protection from cerebral ischemia-reperfusion injury. This protection may be related to an early increase in the expression of bFGF.
机译:诸如丙泊酚的麻醉剂可提供针对脑缺血的神经保护作用。但是,这种有益作用的潜在机制尚不清楚。因此,我们对雄性Sprague-Dawley大鼠进行了2 h的大脑中动脉闭塞试验,并研究了异丙酚的缺血后给药如何影响神经系统结局和碱性成纤维细胞生长因子(bFGF)的表达。缺血2小时后,即在再灌注之前,将动物随机分配为接受异丙酚(20 mg•kg -1 •h -1 )或赋形剂(10%静脉内脂质2 ml•kg -1 •h -1 )静脉注射4 h。在再灌注后的不同时间点测量神经系统评分,梗塞体积和脑含水量。通过实时PCR检测bFGF的mRNA水平,并通过免疫组织化学和Western印迹分析bFGF的蛋白表达水平。在再灌注的6 h,24 h,72 h和7天,与媒介物治疗组相比,丙泊酚治疗组的梗塞体积明显减少(所有P <0.05)。异丙酚后处理还可以在24和72 h减弱脑含水量,并在72 h和7天再灌注时降低神经功能缺损评分(所有P <0.05)。此外,与媒介物治疗组相比,在梗死周围区域,在再灌注的第6、24和72小时,bFGF mRNA和蛋白表达升高(所有P <0.05)。这些结果表明,异丙酚的缺血后给药为神经缺血再灌注损伤提供了神经保护。这种保护作用可能与bFGF表达的早期增加有关。

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