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作 者:黄浩泉 刘付宁[1] 胡楚文[1] 韩智晓[1] 曹铭辉[1] HUANG Hao-quan, LIU Fu-ning, HU Chu-wen, HAN Zhi-xiao, CAO Ming-hui(Department of Anesthesiology, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, 51012)
出 处:《岭南急诊医学杂志》2018年第2期142-144,共3页Lingnan Journal of Emergency Medicine
基 金:国家自然科学基金资助项目(81471352)
摘 要:目的:探讨AMPK是否会影响七氟烷引起的细胞凋亡,为研究吸入麻醉药致神经毒性的机制提供新的靶点和思路。方法:用4.1%七氟烷处理H4人脑神经胶质瘤细胞6 h,建立七氟烷细胞毒性模型。建模前予以AMPK激动剂(二甲双胍)或AMPK抑制剂(Compound C)进行预处理。运用Westernblot检测AMPK、p AMPK、full-length caspase-3以及caspase-3 fragment的表达情况。结果:在七氟烷致H4细胞凋亡的模型中,通过AMPK激动剂进一步增加七氟烷所致的p AMPK上调,能够减少细胞凋亡。结论:在七氟烷致H4细胞凋亡的模型中,激活AMPK具有细胞保护作用。Objective: To investigate whether AMPK can affect the apoptosis induced by sevoflurane and provide new targets and ideas for the study of neurotoxicity induced by inhaled anesthetics. Methods: H4 human neuroglioma cells were treated with 4.1% sevoflurane for 6 hours, and the cytotoxic model of sevoflurne was established. Pre - modeling was pretreated with AMPK agonists (metformin) or AMPK inhibitors (Compound C ). Western blot is used to detect the expression of AMPK, pAMPK, full-length Caspase-3, and caspase-3 fragment. Results : In the model of scvoflurane inducing apoptosis in H4 cells, the increase of pAMPK induced by sevoflurane was further increased by AMPK agonists, which could reduce apoptosis. Conclusion : In the model of sevoflurane inducing apoptosis in H4 cells, the activation of AMPK has the protective effect of cells.
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