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. Arctigenin is mainly from Arctium lappa extract. It has been shown to induce autophagy in various cancers. However, as for whether arctigenin induces autophagy in gliomas or not, the specific mechanism is still worth exploring. Methods. Using CCK8, the monoclonal experiment was made to detect the proliferation ability. The scratch experiment and the transwell experiment were applied to the migration and invasion ability. PI/RNase and FITC-conjugated anti-annexin V were used to detect the cell cycle and apoptosis. 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) and arrested the cell cycle and induced apoptosis. Interestingly, ARG induced autophagy in a dose-dependent manner. We applied Western blotting to measure the increase in the key autophagy protein LC3B, as well as some other autophagy-related proteins (increase in Beclin-1 and decrease in P62). 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 reversed. And interestingly, the protein of apoptosis was also reversed along with autophagy. Conclusions. We thought ARG inhibited the proliferation of glioma cells by inducing autophagy and apoptosis through the AKT/mTOR pathway.

中文翻译：

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Arctigenin 通过 AKT/mTOR 通路抑制胶质母细胞瘤增殖并诱导自噬

目的。牛蒡子苷元（ARG）是从牛蒡子中提取的天然木脂素化合物，在多种癌症中显示出抗癌作用和治疗作用。牛蒡子素主要来自牛蒡子提取物。它已被证明在各种癌症中诱导自噬。然而，牛蒡子苷元是否诱导胶质瘤自噬，具体机制仍值得探索。方法. 使用CCK8进行单克隆实验检测增殖能力。划痕实验和transwell实验用于迁移和侵袭能力。PI/RNase 和 FITC 偶联的抗膜联蛋白 V 用于检测细胞周期和细胞凋亡。采用Western blotting测定指定蛋白水平，构建的LC3B-GFP质粒用于自噬分析。结果. 我们的研究表明，ARG以剂量依赖性方式（U87MG和T98G）抑制胶质瘤细胞的生长增殖和侵袭迁移，并抑制细胞周期并诱导细胞凋亡。有趣的是，ARG 以剂量依赖性方式诱导自噬。我们应用蛋白质印迹来测量关键自噬蛋白 LC3B 以及其他一些自噬相关蛋白（Beclin-1 增加和 P62 减少）的增加。为了进一步探索 ARG 通过启动自噬抑制细胞生长的机制，我们通过 Western blotting 进一步发现 ARG 处理后 AKT 和 mTOR 磷酸化蛋白（P-AKT，P-mTOR）减少，我们使用 AKT 激动剂救援，AKT和mTOR的磷酸化蛋白增加，我们发现自噬相关蛋白也被逆转。结论。我们认为 ARG 通过 AKT/mTOR 通路诱导自噬和细胞凋亡来抑制胶质瘤细胞的增殖。