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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MDPI AG
2021-08-01
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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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id | doaj.art-802a1cc32bb84bbca49146bb280c23bb |
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issn | 2076-3921 |
language | English |
last_indexed | 2024-03-10T09:03:24Z |
publishDate | 2021-08-01 |
publisher | MDPI AG |
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series | Antioxidants |
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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