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Abstract Title:Arctigenin Inhibits Glioblastoma Proliferation through the AKT/mTOR Pathway and诱导自噬。
摘要来源：
生物形成res int。 2020; 2020：3542613。 EPUB 2020年9月15日。PMID： 33015162 Hong, Xiaowei Fei, Ruen Liu
Article Affiliation:Yongan Jiang
Abstract:Purpose: Arctigenin (ARG) is a natural lignan compound extracted from Arctium lappa and has displayed anticancer function and therapeutic effect in a variety of cancers.阿氏纤维素主要来自北极提取物。已证明它会在各种癌症中诱导自噬。但是，至于亚氏霉素是在神经胶质瘤中诱导自噬t，特定机制仍然值得探索。
方法： 使用CCK8，进行单克隆实验以检测增殖能力。将刮擦实验和Transwell实验应用于迁移和入侵能力。 PI/RNase和FITC偶联的抗动脉蛋白V用于检测细胞周期和凋亡。 Western blotting was used to determine the specified protein level, and constructed LC3B-GFP plasmid was used for analysis of autophagy.
Results: Our research showed that ARG inhibited the growth and proliferation and invasion and migration of glioma cells in a dose-dependent manner (U87MG and T98G）并阻止了细胞周期并诱导凋亡。有趣的是，Arg以剂量依赖性的方式引起了自噬。我们应用了Western印迹以测量关键自噬蛋白LC3B的增加以及其他一些自噬可能ATED蛋白（beclin-1的增加，p62减少）。 In order to further explore the mechanism that ARG passed initiating autophagy to inhibit cell growth, we further found by Western blotting that AKT and mTOR phosphorylation proteins (P-AKT, P-mTOR) were reduced after ARG treatment, and we used AKT agonists to rescue, and the phosphorylated proteins of AKT and mTOR increased, and we found that the autophagy-related proteins were also逆转。有趣的是，凋亡的蛋白质也与自噬一起逆转。
结论： 我们认为，我们认为通过通过akt/mtor