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Lipotoxicity in human lung alveolar type 2 A549 cells: Mechanisms and protection by tannic acid
Kun-Feng Tsai1, Chen-Jung Shen2, Chi-Wai Cheung3, Tzong-Luen Wang4, Louis W. C. Chow5, Yuk-Man Leung6, Kar-Lok Wong7
1 Gastroenterology and Hepatology Section, Department of Internal Medicine, An Nan Hospital, China Medical University; Department of Medical Sciences Industry, Chang Jung Christian University, Tainan, Taiwan
2 Endocrinology and Metabolism Section, Department of Internal Medicine, An Nan Hospital, China Medical University, Tainan, Taiwan
3 Department of Anesthesiology, University of Hong Kong, China
4 School of Medicine, Fu-Jen Catholic University; Department of Emergency Medicine, Fu-Jen Catholic University Hospital, Taipei, Taiwan
5 State Key Laboratory of Quality Research in Chinese Medicines, Macau University of Science and Technology, Taipa, Macau; UNIMED Medical Institute, Hong Kong; Organisation for Oncology and Translational Research, Hong Kong, China
6 Department of Physiology, China Medical University, Taichung, Taiwan
7 Department of Anesthesiology, University of Hong Kong, China; Department of Anesthesiology, Kuang Tien General Hospital, Shalu, Taichung, Taiwan
Correspondence Address:
Prof. Yuk-Man Leung
Department of Physiology, China Medical University, Taichung
Taiwan
 Source of Support: None, Conflict of Interest: None
DOI: 10.4103/cjp.cjp_68_21
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Palmitic acid (PA) is a saturated free fatty acid which, when being excessive, accounts for lipotoxicity. Using human lung A549 cells as a model for lung alveolar type 2 epithelial cells, we found that challenge of A549 cells with PA resulted in apoptotic cell death, as reflected by positive annexin V and PI staining, and also appearance of cleaved caspase-3. PA treatment also caused depletion of intracellular Ca2+ store, endoplasmic reticulum (ER) stress, and oxidative stress. Tannic acid (TA), a polyphenol present in wines and many beverages, alleviated PA-induced ER stress, oxidative stress and apoptotic death. Thus, our results suggest PA lipotoxicity in lung alveolar type 2 epithelial cells could be protected by TA.
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