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首页> 外文期刊>Journal of stroke and cerebrovascular diseases: The official journal of National Stroke Association >Propofol Reduces Inflammatory Brain Injury after Subarachnoid Hemorrhage: Involvement of PI3K/Akt Pathway
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Propofol Reduces Inflammatory Brain Injury after Subarachnoid Hemorrhage: Involvement of PI3K/Akt Pathway

机译：PihOFol在蛛网膜下腔出血后减少炎症性脑损伤：PI3K / AKT途径的参与

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Background: Our previous study showed that propofol, one of the widely used anesthetic agents, can attenuate subarachnoid hemorrhage (SAH)-induced early brain injury (EBI) via inhibiting inflammatory and oxidative reaction. However, it is perplexing whether propofol attenuates inflammatory and oxidative reaction through modulating PI3K/ Akt pathway. The present study investigated whether PI3K/ Akt pathway is involved in propofol's anti-inflammation, antioxidation, and neuroprotection against SAH-induced EBI. Materials and methods: Adult Sprague-Dawley rats underwent SAH and received treatment with propofol or vehicle after 2 and 12 hours of SAH. LY294002 was injected intracerebroventricularly to selectively inhibit PI3K/Akt signaling. Mortality, SAH grading, neurological scores, brain water content, evans blue extravasation, myeloperoxidase, malondialdehyde, superoxide dismutase, and glutathione peroxidase were measured 24 hours after SAH. Immunoreactivity of p-Akt, t-Akt, nuclear factor- kappa B (NF-kappa B) p65, nuclear factor erythroid-related factor 2 (Nrf2), NAD(P)H:quinone oxidoreductase (NQO1), and cyclooxygenase-2 (COX-2) in rat brain was determined by western blot. Tumor necrosis factor-alpha (TNF-alpha) and interleukin-1 beta (IL-1 beta) in rat brain were examined by ELISA. Results: Propofol significantly reduces neurological dysfunction, BBB permeability, brain edema, inflammation, and oxidative stress, all of which were reversed by LY294002. Propofol significantly upregulates the immunoreactivity of p-Akt, Nrf2, and NQO1, all of which were abolished by LY294002. Propofol significantly downregulates the overexpression of NF-kappa B p65, COX-2, TNF-alpha, and IL-1 beta, all of which were inhibited by LY294002. Conclusion: These results suggest that propofol attenuates SAH-induced EBI by inhibiting inflammatory reaction and oxidative stress, which might be associated with the activation of PI3K/Akt signaling pathway.
机译：背景：我们以前的研究表明，通过抑制炎症和氧化反应，可以通过抑制炎症和氧化反应来抑制蛛网膜下腔（SAH）抑制早期脑损伤（EBI）的紫外线之一。然而，它令人困惑异丙酚通过调节PI3K / AKT途径衰减炎症和氧化反应。本研究研究了PI3K / AKT途径是否参与异丙酚的抗炎，抗氧化和针对SAH诱导的EBI的神经保护作用。材料和方法：成人Sprague-Dawley大鼠接受了Sah并在2至12小时后用异丙酚或载体接受治疗。 LY294002注入颅内闭合以选择性地抑制PI3K / AKT信号传导。 24小时后24小时测量死亡率，患有SAH分级，神经学评定，脑水含量，evans蓝渗透，麦芽糖氧化酶，丙酰基，超氧化物歧化酶和谷胱甘肽过氧化物酶。 P-AKT，T-AKT，核因子-Kappa（NF-Kappa B）P65，核因子红细胞相关因子2（NRF2），NAD（P）H：醌氧化还原酶（NQO1）和环氧氧酶-2的P65大鼠脑中的（COX-2）通过Western印迹测定。通过ELISA检查大鼠大脑中肿瘤坏死因子-α（TNF-α）和白细胞介素-1β（IL-1β）。结果：异丙酚可显着降低神经功能障碍，BBB渗透性，脑水肿，炎症和氧化应激，所有这些都是通过I294002逆转的。异丙酚显着上调了P-AKT，NRF2和NQO1的免疫反应性，所有这些都被Ly294002废除了。异丙酚显着下调NF-Kappa B p65，Cox-2，TNF-α和IL-1β的过表达，所有这些都被Ly294002抑制。结论：这些结果表明，通过抑制炎症反应和氧化应激来抑制SAH诱导的EBI，这可能与PI3K / AKT信号通路的激活相关。

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