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首页> 外文期刊>Brain research >The role of phosphoinositide-3-kinase/Akt pathway in propofol-induced postconditioning against focal cerebral ischemia-reperfusion injury in rats.
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The role of phosphoinositide-3-kinase/Akt pathway in propofol-induced postconditioning against focal cerebral ischemia-reperfusion injury in rats.

机译：磷酸肌醇-3-激酶/ Akt通路在异丙酚诱导的后处理中对抗大鼠局灶性脑缺血再灌注损伤的作用。

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The aim of this study was to investigate whether propofol could provide postconditioning to ischemic brain injury and the role of phosphoinositide-3-kinase/Akt (PI3K/Akt) pathway in this phenomenon. Rats underwent 2 h of middle cerebral artery occlusion (MCAO) followed by 22 h of reperfusion were randomly divided into nine groups (n=15 each): sham-operated group, MCAO group, propofol 10, 20 and 35 mg x kg(-1) x h(-1) group (propofol 10, 20, 35 mg x kg(-1) x h(-1) infused at the onset of reperfusion for 30 min), wortmannin group (wortmannin 0.6 mg/kg administered 30 min before MCAO), and the other three groups received wortmannin followed by 10, 20 and 35 mg x kg(-1) x h(-1) propofol respectively. Propofol at doses of 10 and 20 mg x kg(-1) x h(-1) significantly reduced infarct volume, decreased neurological deficit scores and attenuated neuron apoptosis compared with MCAO group alone. Increased phosphorylated Akt (P-Akt) was observed in the ischemic penumbra of propofol 10 and 20 mg x kg(-1) x h(-1) group after transient MCAO. The selective PI3K inhibitor, wortmannin partly eliminated the neuroprotective effect and the elevation of P-Akt expression in ischemic penumbra induced by propofol. Propofol at dose of 35 mg x kg(-1) x h(-1) did not affect infarct volume, neurological deficit scores, neuronal apoptosis and the level of P-Akt in transient MCAO rats. Taken together, these results demonstrated that propofol at doses of 10 or 20 mg x kg(-1) x h(-1) infused at the onset of reperfusion for 30 min could provide neuroprotection to transient MCAO rats, and the postconditioning effect induced by propofol partly through maintaining the activity of PI3K/Akt pathway.
机译：这项研究的目的是调查丙泊酚是否可以为缺血性脑损伤提供后处理，以及在这种现象中磷酸肌醇-3-激酶/ Akt（PI3K / Akt）通路的作用。将大鼠大脑中动脉闭塞2 h（MCAO），然后再灌注22 h，随机分为9组（每组15只）：假手术组，MCAO组，异丙酚10、20和35 mg x kg（- 1）xh（-1）组（异丙酚10、20、35 mg x kg（-1）xh（-1）在再灌注开始时输注30分钟），渥曼青霉素组（渥曼青霉素0.6 mg / kg，在30分钟前给药） MCAO），其他三组分别接受渥曼青霉素，10、20和35 mg x kg（-1）xh（-1）异丙酚。与单独的MCAO组相比，丙泊酚10和20 mg x kg（-1）x h（-1）的剂量可显着减少梗塞体积，降低神经功能缺损评分并减弱神经元凋亡。短暂MCAO后，在异丙酚10和20 mg x kg（-1）x h（-1）组的缺血半影中观察到磷酸化Akt（P-Akt）增加。选择性PI3K抑制剂渥曼青霉素部分消除了异丙酚诱导的缺血性半影​​中的神经保护作用和P-Akt表达的升高。 35 mg x kg（-1）x h（-1）剂量的丙泊酚不会影响短暂MCAO大鼠的梗塞面积，神经功能缺损评分，神经元凋亡和P-Akt水平。综上所述，这些结果表明，在再灌注开始30分钟后注入10或20 mg x kg（-1）xh（-1）的丙泊酚剂量可以为短暂的MCAO大鼠提供神经保护作用，并且由丙泊酚诱导的后适应作用部分是通过维持PI3K / Akt途径的活性。

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