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

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-d...

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Main Authors: Seong-Ryeong Lim, Do-Wan Kim, Junghee Sung, Tae Hoon Kim, Chang-Hyung Choi, Sei-Jung Lee
Format: Article
Language:English
Published: MDPI AG 2021-08-01
Series:Antioxidants
Subjects:
Online Access:https://www.mdpi.com/2076-3921/10/8/1273
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author Seong-Ryeong Lim
Do-Wan Kim
Junghee Sung
Tae Hoon Kim
Chang-Hyung Choi
Sei-Jung Lee
author_facet Seong-Ryeong Lim
Do-Wan Kim
Junghee Sung
Tae Hoon Kim
Chang-Hyung Choi
Sei-Jung Lee
author_sort Seong-Ryeong Lim
collection DOAJ
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.
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spelling doaj.art-802a1cc32bb84bbca49146bb280c23bb2023-11-22T06:36:43ZengMDPI AGAntioxidants2076-39212021-08-01108127310.3390/antiox10081273Astaxanthin Inhibits Autophagic Cell Death Induced by Bisphenol A in Human Dermal FibroblastsSeong-Ryeong Lim0Do-Wan Kim1Junghee Sung2Tae Hoon Kim3Chang-Hyung Choi4Sei-Jung Lee5Department of Pharmaceutical Engineering, Daegu Haany University, Gyeongsan 38610, KoreaDepartment of Pharmaceutical Engineering, Daegu Haany University, Gyeongsan 38610, KoreaResearch Center, Reanzen Co., Ltd., Anyang 14056, KoreaFoodyWorm Inc., Yancheongsongdae-gil 10, Ochang-eup, Cheongwon-gu, Choenju-si 28118, KoreaDivision of Cosmetic Science and Technology, Daegu Haany University, Gyeongsan 38610, KoreaDepartment of Pharmaceutical Engineering, Daegu Haany University, Gyeongsan 38610, KoreaAstaxanthin, 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.https://www.mdpi.com/2076-3921/10/8/1273astaxanthinautophagic cell deathbisphenol Anormal human dermal fibroblastsreactive oxygen species
spellingShingle Seong-Ryeong Lim
Do-Wan Kim
Junghee Sung
Tae Hoon Kim
Chang-Hyung Choi
Sei-Jung Lee
Astaxanthin Inhibits Autophagic Cell Death Induced by Bisphenol A in Human Dermal Fibroblasts
Antioxidants
astaxanthin
autophagic cell death
bisphenol A
normal human dermal fibroblasts
reactive oxygen species
title Astaxanthin Inhibits Autophagic Cell Death Induced by Bisphenol A in Human Dermal Fibroblasts
title_full Astaxanthin Inhibits Autophagic Cell Death Induced by Bisphenol A in Human Dermal Fibroblasts
title_fullStr Astaxanthin Inhibits Autophagic Cell Death Induced by Bisphenol A in Human Dermal Fibroblasts
title_full_unstemmed Astaxanthin Inhibits Autophagic Cell Death Induced by Bisphenol A in Human Dermal Fibroblasts
title_short Astaxanthin Inhibits Autophagic Cell Death Induced by Bisphenol A in Human Dermal Fibroblasts
title_sort astaxanthin inhibits autophagic cell death induced by bisphenol a in human dermal fibroblasts
topic astaxanthin
autophagic cell death
bisphenol A
normal human dermal fibroblasts
reactive oxygen species
url https://www.mdpi.com/2076-3921/10/8/1273
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