Black Ginseng Ameliorates Cellular Senescence via p53-p21/p16 Pathway in Aged Mice

Cellular senescence, one of the hallmarks of aging, refers to permanent cell cycle arrest and is accelerated during the aging process. Black ginseng (BG), prepared by a repeated steaming and drying process nine times from fresh ginseng (<i>Panax ginseng</i> C.A. Meyer), is garnering atte...

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Main Authors: Su-Jeong Lee, Da-Yeon Lee, Jennifer F. O’Connell, Josephine M. Egan, Yoo Kim
Format: Article
Language:English
Published: MDPI AG 2022-07-01
Series:Biology
Subjects:
Online Access:https://www.mdpi.com/2079-7737/11/8/1108
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author Su-Jeong Lee
Da-Yeon Lee
Jennifer F. O’Connell
Josephine M. Egan
Yoo Kim
author_facet Su-Jeong Lee
Da-Yeon Lee
Jennifer F. O’Connell
Josephine M. Egan
Yoo Kim
author_sort Su-Jeong Lee
collection DOAJ
description Cellular senescence, one of the hallmarks of aging, refers to permanent cell cycle arrest and is accelerated during the aging process. Black ginseng (BG), prepared by a repeated steaming and drying process nine times from fresh ginseng (<i>Panax ginseng</i> C.A. Meyer), is garnering attention for herbal medicine due to its physiological benefits against reactive oxygen species (ROS), inflammation, and oncogenesis, which are common cues to induce aging. However, which key nodules in the cellular senescence process are regulated by BG supplementation has not been elucidated yet. In this study, we investigated the effects of BG on cellular senescence using in vitro and aged mouse models. BG-treated primary mouse embryonic fibroblasts (MEFs) in which senescence was triggered by ionizing radiation (IR) expressed less senescence-associated β-galactosidase (SA-β-gal)-positive stained cells. In our aged mice (18 months old) study, BG supplementation (300 mg/kg) for 4 weeks altered hepatic genes involved in the aging process. Furthermore, we found BG supplementation downregulated age-related inflammatory genes, especially in the complement system. Based on this observation, we demonstrated that BG supplementation led to less activation of the canonical senescence pathway, p53-dependent p21 and p16, in multiple metabolic organs such as liver, skeletal muscle and white adipose tissue. Thus, we suggest that BG is a potential senolytic candidate that retards cellular senescence.
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spelling doaj.art-268878944b09474c828b2e387125421d2023-12-01T23:25:51ZengMDPI AGBiology2079-77372022-07-01118110810.3390/biology11081108Black Ginseng Ameliorates Cellular Senescence via p53-p21/p16 Pathway in Aged MiceSu-Jeong Lee0Da-Yeon Lee1Jennifer F. O’Connell2Josephine M. Egan3Yoo Kim4Department of Nutritional Sciences, Oklahoma State University, Stillwater, OK 74078, USADepartment of Nutritional Sciences, Oklahoma State University, Stillwater, OK 74078, USALaboratory of Clinical Investigation, National Institute on Aging (NIA), Baltimore, MD 21224, USALaboratory of Clinical Investigation, National Institute on Aging (NIA), Baltimore, MD 21224, USADepartment of Nutritional Sciences, Oklahoma State University, Stillwater, OK 74078, USACellular senescence, one of the hallmarks of aging, refers to permanent cell cycle arrest and is accelerated during the aging process. Black ginseng (BG), prepared by a repeated steaming and drying process nine times from fresh ginseng (<i>Panax ginseng</i> C.A. Meyer), is garnering attention for herbal medicine due to its physiological benefits against reactive oxygen species (ROS), inflammation, and oncogenesis, which are common cues to induce aging. However, which key nodules in the cellular senescence process are regulated by BG supplementation has not been elucidated yet. In this study, we investigated the effects of BG on cellular senescence using in vitro and aged mouse models. BG-treated primary mouse embryonic fibroblasts (MEFs) in which senescence was triggered by ionizing radiation (IR) expressed less senescence-associated β-galactosidase (SA-β-gal)-positive stained cells. In our aged mice (18 months old) study, BG supplementation (300 mg/kg) for 4 weeks altered hepatic genes involved in the aging process. Furthermore, we found BG supplementation downregulated age-related inflammatory genes, especially in the complement system. Based on this observation, we demonstrated that BG supplementation led to less activation of the canonical senescence pathway, p53-dependent p21 and p16, in multiple metabolic organs such as liver, skeletal muscle and white adipose tissue. Thus, we suggest that BG is a potential senolytic candidate that retards cellular senescence.https://www.mdpi.com/2079-7737/11/8/1108black ginsengcellular senescencesenolyticscomplement C1qβ-cateninp53
spellingShingle Su-Jeong Lee
Da-Yeon Lee
Jennifer F. O’Connell
Josephine M. Egan
Yoo Kim
Black Ginseng Ameliorates Cellular Senescence via p53-p21/p16 Pathway in Aged Mice
Biology
black ginseng
cellular senescence
senolytics
complement C1q
β-catenin
p53
title Black Ginseng Ameliorates Cellular Senescence via p53-p21/p16 Pathway in Aged Mice
title_full Black Ginseng Ameliorates Cellular Senescence via p53-p21/p16 Pathway in Aged Mice
title_fullStr Black Ginseng Ameliorates Cellular Senescence via p53-p21/p16 Pathway in Aged Mice
title_full_unstemmed Black Ginseng Ameliorates Cellular Senescence via p53-p21/p16 Pathway in Aged Mice
title_short Black Ginseng Ameliorates Cellular Senescence via p53-p21/p16 Pathway in Aged Mice
title_sort black ginseng ameliorates cellular senescence via p53 p21 p16 pathway in aged mice
topic black ginseng
cellular senescence
senolytics
complement C1q
β-catenin
p53
url https://www.mdpi.com/2079-7737/11/8/1108
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