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Melatonin Rescues Human Dental Pulp Cells from Premature Senescence Induced by H2O2

  • Park, Sera (Department of Dental Pharmacology, Pusan National University) ;
  • Bak, Kwang Je (Department of Dental Pharmacology, Pusan National University) ;
  • Ok, Chang Youp (Department of Dental Pharmacology, Pusan National University) ;
  • Park, Hyun-Joo (Department of Oral Physiology, Pusan National University) ;
  • Jang, Hye-Ock (Department of Dental Pharmacology, Pusan National University) ;
  • Bae, Moon-Kyoung (Department of Oral Physiology, Pusan National University) ;
  • Bae, Soo-Kyung (Department of Dental Pharmacology, Pusan National University)
  • Received : 2017.08.09
  • Accepted : 2017.09.08
  • Published : 2017.09.30

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 ($H_2O_2$), including the increase in senescence-associated ${\beta}$-galactosidase (SA-${\beta}$-gal)-positive HDPCs and the upregulation of p21 protein, an indicator for senescence. In addition, as melatonin attenuated $H_2O_2$-stimulated phosphorylation of c-Jun N-terminal kinase (JNK), while selective inhibition of JNK activity with SP600125 significantly attenuated $H_2O_2$-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.

Keywords

References

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