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首页> 外文期刊>Journal of biochemical and molecular toxicology >Abamectin induces apoptosis and autophagy by inhibiting reactive oxygen species‐mediated PI3K/AKT signaling in MGC803 cells
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Abamectin induces apoptosis and autophagy by inhibiting reactive oxygen species‐mediated PI3K/AKT signaling in MGC803 cells

机译：Abamectin通过抑制MgC803细胞中的反应性氧物质介导的PI3K / AKT信号传导来诱导细胞凋亡和自噬

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Abstract Abamectin (ABA) is one of the most widely used compounds in agriculture and veterinary medicine. However, the cytotoxicity of ABA in human gastric cells is utterly unknown. In this study, ABA suppressed the proliferation of MGC803 cells by arresting the cell cycle at the G0/G1‐phase. Moreover, ABA induced mitochondrial‐mediated apoptosis by inducing?the loss of mitochondrial membrane potential, upregulation?of Bax/Bcl‐2, and activation of caspase‐3. ABA significantly improved the LC3‐II/LC3‐I ratio and reduced P62 protein expression in a dose‐dependent manner. Through detection of the reactive oxygen species (ROS) levels, we found ABA induced the accumulation of intracellular ROS and then reduced PI3K/AKT signaling activation related?to MGC803 cell?apoptosis and autophagy. Our results indicate that ABA exerts cytotoxic effects on human MGC803 cells through apoptosis and autophagy by inhibiting ROS‐mediated PI3K/AKT signaling. Furthermore, ABA may be a potential risk to human gastric health.
机译：摘要Abamectin（ABA）是农业和兽医中使用最广泛的化合物之一。然而，ABA在人胃细胞中的细胞毒性完全未知。在本研究中，ABA通过在G0 / G1相处捕获细胞周期来抑制MGC803细胞的增殖。此外，ABA通过诱导诱导线粒体介导的细胞凋亡诱导的线粒体膜电位，上调？BAX / BCL-2的活化，并激活Caspase-3。 ABA以剂量依赖性方式显着改善LC3-II / LC3-I比率和降低的P62蛋白表达。通过检测反应性氧物种（ROS）水平，我们发现ABA诱导细胞内RO的积累，然后减少了PI3K / AKT信号传导激活相关的α对MGC803细胞？凋亡和自噬。我们的结果表明，通过抑制ROS介导的PI3K / AKT信号传导，ABA通过凋亡和自噬对人MGC803细胞产生细胞毒性作用。此外，ABA可能是人类胃病健康的潜在风险。

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