Publication: Apoptotic effect of astaxanthin from white shrimp shells on lung cancer A549 cells
Issued Date
2020-09-01
Resource Type
ISSN
15969827
15965996
15965996
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2-s2.0-85092675146
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Mahidol University
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SCOPUS
Bibliographic Citation
Tropical Journal of Pharmaceutical Research. Vol.19, No.9 (2020), 1835-1842
Suggested Citation
Supita Tanasawet, Wanida Sukketsiri, Pennapa Chonpathompikunlert, Wanwimol Klaypradit, Morakot Sroyraya, Pilaiwanwadee Hutamekalin Apoptotic effect of astaxanthin from white shrimp shells on lung cancer A549 cells. Tropical Journal of Pharmaceutical Research. Vol.19, No.9 (2020), 1835-1842. doi:10.4314/tjpr.v19i9.6 Retrieved from: https://repository.li.mahidol.ac.th/handle/123456789/60089
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Title
Apoptotic effect of astaxanthin from white shrimp shells on lung cancer A549 cells
Abstract
© 2020 The authors. Purpose: To investigate the anti-cancer potential of astaxanthin from Litopenaeus vannamei encapsulated in liposomes (ASX) to treat lung cancer A549 cells. Methods: Lung adenocarcinoma A549 cells were cultured and treated with ASX, following which cell viability and nuclear staining were performed. Generation of ROS was identified by the DCFH-DA assay while tetramethylrhodamine ethyl ester was used to determine the mitochondrial membrane potential. Flow cytometry was applied to investigate caspase-3/7 activity and cell cycle distribution. Results: ASX inhibited growth of A549 in a concentration- and time- dependent manner. The IC50 values at 24, 48 and 72 h were 53.73, 22.85, 17.46 μg/mL, respectively (p < 0.05). After incubation with ASX, the morphological changes were observed in A549 cells following Hoechst 33342/PI fluorescent staining. ASX increased ROS generation and was associated with the collapse of mitochondrial membrane potential, which subsequently triggered the activation of caspase-3/7 activity leading to apoptosis (p < 0.05). In addition, A549 cells accumulated in the G0/G1 phase. Conclusion: The results suggest that ASX is a valuable nutraceutical agent to target A549 lung cancer cells via ROS-dependent pathway as well as blockage of cell cycle progression.