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  2. Abamectin induces apoptosis and autophagy by inhibiting reactive oxygen species-mediated PI3K/AKT signaling in MGC803 cells

Abamectin induces apoptosis and autophagy by inhibiting reactive oxygen species-mediated PI3K/AKT signaling in MGC803 cells

  • J Biochem Mol Toxicol. 2019 Jul;33(7):e22336. doi: 10.1002/jbt.22336.
Shanshan Zhu 1 2 3 Jing Zhou 2 3 Zhonglou Zhou 2 3 Qiqi Zhu 1
Affiliations

Affiliations

  • 1 Department of Anesthesiology, The Second Affiliated Hospital and Yuying Children's Hospital, Wenzhou Medical University, Wenzhou, Zhejiang, China.
  • 2 Department of Scientific Research, School of Optometry and Ophthalmology and The Eye Hospital, Wenzhou Medical University, Wenzhou, Zhejiang, China.
  • 3 Department of Scientific Research, State Key Laboratory of Optometry, Ophthalmology and Vision Science, Wenzhou, Zhejiang, China.
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.

Keywords

AKT; PI3K; abamectin; apoptosis; autophagy; reactive oxygen species.

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