Melatonin Rescues Human Dental Pulp Cells from Premature Senescence Induced by H₂O₂.
10.11620/IJOB.2017.42.3.091
- Author:
Sera PARK
1
;
Kwang Je BAK
;
Chang Youp OK
;
Hyun Joo PARK
;
Hye Ock JANG
;
Moon Kyoung BAE
;
Soo Kyung BAE
Author Information
1. Department of Dental Pharmacology, Pusan National University, Yangsan 626-870, South Korea. skbae@pusan.ac.kr
- Publication Type:Original Article
- Keywords:
Melatonin;
premature senescence;
human dental pulp cells;
H₂O₂
- MeSH:
Aging*;
Animals;
Dental Pulp Diseases;
Dental Pulp*;
Humans*;
Hydrogen Peroxide;
JNK Mitogen-Activated Protein Kinases;
MAP Kinase Signaling System;
Melatonin*;
Mice;
Oral Health;
Phosphorylation;
Pineal Gland;
Up-Regulation
- From:International Journal of Oral Biology
2017;42(3):91-97
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Although anti-aging activities of melatonin, a hormone secreted by the pineal gland, have been reported in senescence-accelerated mouse models and several types of cells, its impact and mechanism on the senescence of human dental pulp cells (HDPCs) remains unknown. In this study, we examined the impact of melatonin on cellular premature senescence of HDPCs. Here, we found that melatonin markedly inhibited senescent characteristics of HDPCs after exposure to hydrogen peroxide (H₂O₂), including the increase in senescence-associated β-galactosidase (SA-β-gal)-positive HDPCs and the upregulation of p21 protein, an indicator for senescence. In addition, as melatonin attenuated H₂O₂-stimulated phosphorylation of c-Jun N-terminal kinase (JNK), while selective inhibition of JNK activity with SP600125 significantly attenuated H₂O₂-induced increase in SA-beta-gal activity. Results reveal that melatonin antagonizes premature senescence of HDPCs via JNK pathway. Thus, melatonin may have therapeutic potential to prevent stress-induced premature senescence, possibly correlated with development of dental pulp diseases, and to maintain oral health across the life span.
