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首页> 外文期刊>Cellular Physiology and Biochemistry >Isoflavones Induce BEX2-Dependent Autophagy to Prevent ATR-Induced Neurotoxicity in SH-SY5Y Cells
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Isoflavones Induce BEX2-Dependent Autophagy to Prevent ATR-Induced Neurotoxicity in SH-SY5Y Cells

机译：异黄酮诱导依赖BEX2的自噬以预防ATR诱导的SH-SY5Y细胞神经毒性

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>Background/Aims: Atrazine (ATR) is a broad-spectrum herbicide in wide use around the world. However, ATR is neurotoxic and can cause cell death in dopaminergic neurons, leading to neurodegenerative disorders. Autophagy is the basic cellular catabolic process involving the degradation of proteins and damaged organelles. Studies have shown that certain plant compounds can induce autophagy and prevent neuronal cell death. This prompted us to investigate plant compounds that might reduce the neurotoxic effects of ATR. Methods: By CCK-8 and flow cytometry, we tested the ability of five candidate compoundsa€”isoflavones, resveratrol, quercetin, curcumin, and green tea polyphenolsa€”to protect cells from ATR. Changes in the expression of tyrosine hydroxylase (TH) and brain-expressed X-linked 2 (BEX2), autophagy-related proteins and key factors in mTOR signaling, were detected by Western blotting. Results: Isoflavones had the strongest activity against ATR-induced neuronal apoptosis. ATR reduced the expression of TH and BEX2, whereas isoflavones increased TH and BEX2 expression. In addition, ATR inhibited autophagy, whereas isoflavones induced autophagy through the accumulation of LC3-II and decreased expression of p62; this effect was abolished by 3-methyladenine (3-MA). Furthermore, BEX2 siRNA abolished isoflavone-mediated autophagy and neuroprotection in vitro. Conclusion: Isoflavones activate BEX2-dependent autophagy, protecting against ATR-induced neuronal apoptosis.
机译：> 背景/目的： 阿特拉津（ATR）是一种广谱除草剂，在世界范围内得到广泛使用。但是，ATR具有神经毒性，可导致多巴胺能神经元细胞死亡，从而导致神经退行性疾病。自噬是基本的细胞分解代谢过程，涉及蛋白质的降解和受损的细胞器。研究表明某些植物化合物可以诱导自噬并防止神经元细胞死亡。这促使我们研究可能降低ATR的神经毒性作用的植物化合物。 方法： 通过CCK-8和流式细胞仪，我们测试了五种候选化合物“异黄酮，白藜芦醇，槲皮素，姜黄素和绿茶多酚”的保护能力。来自ATR的单元格。蛋白质印迹法检测了酪氨酸羟化酶（TH）和脑表达的X连锁2（BEX2），自噬相关蛋白和mTOR信号传导关键因子的表达变化。 结果： 异黄酮对ATR诱导的神经元凋亡具有最强的活性。 ATR降低TH和BEX2的表达，而异黄酮增加TH和BEX2的表达。此外，ATR抑制自噬，而异黄酮通过LC3-II的积累和p62的表达降低诱导自噬。 3-甲基腺嘌呤（3-MA）消除了这种作用。此外，BEX2 siRNA在体外消除了异黄酮介导的自噬和神经保护作用。 结论： 异黄酮可激活BEX2依赖性自噬，从而防止ATR诱导的神经元凋亡。

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