自噬与七氟醚诱发的发育期大鼠神经毒性有关
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Autophagy is involved in sevoflurane-induced developmental neurotoxicity in the developing rat brain
背景与目的：七氟醚可诱发新生儿广泛的神经退行性病变和导致啮齿动物空间学习能力的严重缺陷，但其具体机制尚不清楚。本研究试图通过观察接触七氟醚后新生SD大鼠海马组织自噬水平的变化，探讨自噬在七氟醚诱发神经毒性中的可能作用。
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方法：我们采用接触七氟醚7天后的72只SD大鼠来探讨海马神经元自噬和细胞凋亡。
结果：结果表明，通过蛋白质印迹对发育大脑进行检测，发现七氟醚以时间依赖性方式增加Beclin-1、微管相关蛋白轻链3II（LC3-II）蛋白的水平和降低螯体1的水平。且该结果通过透射电镜、定量逆转录聚合酶链反应、免疫组化和免疫荧光进一步证实。雷帕霉素是一种自噬激活剂，可增加Beclin-1和LC3-II蛋白的水平，同时，自噬抑制剂3-甲基腺嘌呤可降低Beclin-1和LC3-II蛋白的水平。
结论：综上所述，自噬可能与七氟醚诱发的发育期神经毒性有关，并且促进保护性自噬可能是预防七氟醚诱发发育期神经毒性的潜在途径。
Xu L1, Shen J2, Yu L2, Sun J3, Yan M4.
Autophagy is involved in sevoflurane-induced developmental neurotoxicity in the developing rat brain.
Brain Res Bull. May 24，2018;140:226-232. doi: 10.1016/j.brainresbull.2018.05.014. [Epub ahead of print].
BACKGROUND:Sevoflurane can induce neonatal wide neurodegenerative and serious deficit to space learning tasks in rodents, however, the specific mechanism is still unclear. At present, the study tried to explore the possible role of autophagy in sevoflurane-induced neurotoxicity through observing the changes in the levels of autophagy in the newborn SD rat hippocampus tissue after sevoflurane exposure.
METHODS:We used seventy-two SD rats of seven days receiving sevoflurane exposure to explore hippocampus neuron autophagy and apoptosis.
RESULTS:Our results indicated that sevoflurane increased the levels of Beclin-1, microtubule-associated protein light chain 3II protein and decreased sequestosome 1 levels in a time-dependent manner by Western blot in the developing brain. These results were further substantiated by transmission electron microscopy, quantitative reverse transcription polymerase chain reaction, immunohistochemistry and immunofluorescence. Rapamycin,an activator of autophagy, increased the levels of Beclin-1and LC3-II protein, meanwhile, 3-methyladenine, an inhibitor of autophagy, decreased Beclin-1and LC3-II protein levels.
CONCLUSIONS:Taken together, autophagy may be involved in sevoflurane-induced developmental neurotoxicity and promoting protective autophagy may be a potential way of preventing developmental sevoflurane-induced neurotoxicity.
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