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• W1996946760 abstract "Background . Oxidative stress plays a pivotal role in the lung injuries of critical ill patients. This study investigates the protection conferred by α 2 adrenoceptor agonist dexmedetomidine (Dex) from lung alveolar epithelial cell injury induced by hydrogen peroxide (H 2 O 2 ) and the underlying mechanisms. Methods . The lung alveolar epithelial cell line, A549, was cultured and then treated with 500 μ M H 2 O 2 with or without Dex (1 nM) or Dex in combination with atipamezole (10 nM), an antagonist of α 2 receptors. Their effect on mitochondrial membrane potential (<mml:math xmlns:mml=http://www.w3.org/1998/Math/MathML id=M1><mml:mi>Δ</mml:mi><mml:msub><mml:mrow><mml:mi>ψ</mml:mi></mml:mrow><mml:mrow><mml:mtext mathvariant=normal>m</mml:mtext></mml:mrow></mml:msub></mml:math>), reactive oxygen species (ROS), and the cell cycle was assessed by flow cytometry. Cleaved-caspases 3 and 9, BAX, Bcl-2, phospho-mTOR (p-mTOR), ERK1/2, and E-cadherin expression were also determined with immunocytochemistry. Results . Upregulation of cleaved-caspases 3 and 9 and BAX and downregulation of Bcl-2, p-mTOR, and E-cadherin were found following H 2 O 2 treatment, and all of these were reversed by Dex. Dex also prevented the ROS generation, cytochrome C release, and cell cycle arrest induced by H 2 O 2 . The effects of Dex were partially reversed by atipamezole. Conclusion . Our study demonstrated that Dex protected lung alveolar epithelial cells from apoptotic injury, cell cycle arrest, and loss of cell adhesion induced by H 2 O 2 through enhancing the cell survival and proliferation." @default.
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• W1996946760 date "2015-01-01" @default.
• W1996946760 modified "2023-10-05" @default.
• W1996946760 title "Dexmedetomidine Attenuates Oxidative Stress Induced Lung Alveolar Epithelial Cell Apoptosis<i>In Vitro</i>" @default.
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• W1996946760 doi "https://doi.org/10.1155/2015/358396" @default.
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