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Dexmedetomidine suppresses sevoflurane anesthesia-induced neuroinflammation through activation of the PI3K/Akt/mTOR pathway
背景与目的
七氟醚是一种吸入性全身麻醉剂，已经成为外科中应用最广泛的吸入性麻醉剂之一。然而，先前的研究已经发现七氟醚麻醉能引起炎症反应，导致二次伤害。右美托咪定(DEX)是一种高选择性α肾上腺素受体激动剂，作为一种麻醉辅助药广泛应用于临床。在这项研究中，我们研究了DEX是否能够抑制七氟醚引起的神经炎症反应。
方 法
本研究的目的是用大鼠模型确定DEX产生抑制影响的作用机制。大鼠随机分为对照组（n=10），低浓度七氟醚组（L-Sev；n=10），高浓度七氟醚组（H-Sev；n=10），溶酶组（n=10）、DEX组（n=10）和DEX+LY294002（PI3K特异性抑制剂）组（n=10）。溶酶组，DEX组和DEX+LY294002组都进行高浓度七氟醚暴露。用Western blotting 法测量促炎症细胞因子（IL-6, IL-8, TNF-α）的表达和磷脂酰肌醇3-羟基激酶/蛋白激酶B/哺乳动物靶向雷帕霉素（PI3K/AKT/MTOR）通道的活性水平。
结 果
七氟醚麻醉引起促炎症细胞因子水平的增加，同时降低了大鼠皮层和海马中PI3K/AKT/MTOR通路的激活。DEX处理可降低促炎症细胞因子并阻止PI3K/AKT/MTOR途径失活。此外，PI3K/AKT/MTOR途径的抑制剂ly294002降低了DEX的抗炎活性。
结 论
PI3K/Akt/mTOR 途径有助于七氟醚引起的神经炎症，DEX引起的PI3K/Akt/mTOR信号激活能帮助减少七氟醚导致的神经炎症的影响。
原始文献摘要
Nan Wang and Mingyu Wang. Dexmedetomidine suppresses sevoflurane anesthesia-induced neuroinflammation through activation of the PI3K/Akt/mTOR pathway[J].BMC Anesthesiol 2019 Jul 27;19(1)DOI：10.1186/s12871-019-0808-5.
Background: Sevoflurane, an inhalational general anesthetic, has become one of the most widely used inhalational anesthetics in surgery. However, previous studies have found that sevoflurane anesthesia can trigger an inflammatory response, resulting in secondary damage. Dexmedetomidine (DEX), a highly-selective α adrenergic receptor agonist, is widely used as an anesthetic adjuvant in the clinic. In this study we investigated whether DEX was able to suppress sevoflurane-induced neuroinflammation.
Methods: The aim was to determine the mechanism of action of the suppressive effect of DEX using a rat model.
Rats were randomly divided into a control group (n = 10), low-dose sevoflurane group (L-Sev; n = 10), high-dose sevoflurane group (H-Sev; n = 10), vehicle group (n = 10), DEX group (n = 10) and DEX + LY294002 (a specific inhibitor of PI3K) group (n = 10). The rats in vehicle, DEX and DEX + LY294002 groups were in the presence of highdose sevoflurane exposure. Western blotting was used to measure the expression of proinflammatory cytokines (IL-6, IL-8, TNF-α) and the activity level of the phosphatidylinositol 3-hydroxy kinase/protein kinase B/mammalian target of rapamycin (PI3K/Akt/mTOR) pathway.
Results: We found that sevoflurane anesthesia induced an increase in the levels of pro-inflammatory cytokines,while decreasing activation of the PI3K/Akt/mTOR pathway in both the cortex and hippocampus of rats. Treatment with DEX reduced pro-inflammatory cytokine levels and prevented inactivation of the PI3K/Akt/mTOR pathway.Moreover, LY294002, an inhibitor of the PI3K/Akt/mTOR pathway, reduced the anti-inflammatory activity of DEX.
Conclusions: These data suggest that the PI3K/Akt/mTOR pathway contributes to sevoflurane-induced neuroinflammation and that activation of PI3K/Akt/mTOR signaling by DEX could help reduce the neuroinflammatory effects of sevoflurane.
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翻译：牛振瑛 编辑：何幼芹 审校：王贵龙
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