NDLI: Astaxanthin Inhibits Autophagic Cell Death Induced by Bisphenol A in Human Dermal Fibroblasts

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Astaxanthin Inhibits Autophagic Cell Death Induced by Bisphenol A in Human Dermal Fibroblasts

Content Provider	MDPI
Author	Lim, Seong-Ryeong Kim, Do-Wan Sung, Junghee Kim, Tae Hoon Choi, Chang-Hyung Lee, Sei-Jung
Copyright Year	2021
Description	Astaxanthin, a natural antioxidant carotenoid, is a nutrient with diverse health benefits, given that it decreases the risk of oxidative stress-related diseases. In the present study, we investigate the functional role of astaxanthin during autophagic cell death induced by the estrogenic endocrine-disrupting chemical bisphenol A (BPA) in normal human dermal fibroblasts (NHDF). BPA significantly induced apoptotic cell death and autophagy in NHDF. Autophagic cell death evoked by BPA was significantly restored upon a treatment with astaxanthin (10 μM) via the inhibition of intracellular reactive oxygen species (ROS) production. Astaxanthin inhibited the phosphorylation of extracellular signal-regulated kinases (ERK) stimulated by ROS production, but it did not influence the activation of c-Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (MAPK) in BPA-treated NHDF. Astaxanthin abrogated the ERK-mediated activation of nuclear factor-kappa B (NF-κB), which is responsible for the mRNA expression of LC3-II, Beclin-1, Atg12, and Atg14 during apoptotic cell death induced by BPA. These results indicate that astaxanthin is a pharmacological and nutritional agent that blocks the skin fibroblastic autophagic cell death induced by BPA in human dermal fibroblasts.
Starting Page	1273
e-ISSN	20763921
DOI	10.3390/antiox10081273
Journal	Antioxidants
Issue Number	8
Volume Number	10
Language	English
Publisher	MDPI
Publisher Date	2021-08-11
Access Restriction	Open
Subject Keyword	Antioxidants Dermatology Astaxanthin Autophagic Cell Death Bisphenol A Normal Human Dermal Fibroblasts Reactive Oxygen Species
Content Type	Text
Resource Type	Article

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