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

Park, Sera; Bak, Kwang Je; Ok, Chang Youp; Park, Hyun-Joo; Jang, Hye-Ock; Bae, Moon‐Kyoung; Bae, Soo-Kyung

doi:10.11620/ijob.2017.42.3.091

Cited by 4 publications

(6 citation statements)

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“…In addition, the levels of visfatin mRNA and protein were increased in a time-dependent manner and peaked at 4 (Figure 2e senescence (Figure 2a, b), which is consistent with our previous study [33]. Next, the expression pattern of visfatin following H2O2-induced premature senescence was evaluated.…”

Section: Visfatin Expression Is Upregulated In Premature Senescent Desupporting

confidence: 90%

“…To examine the effect of H 2 O 2 on dental pulp cells, hDPCs were treated for 24 h with different concentrations of H 2 O 2 , then SA-β-galactosidase staining was assayed. H 2 O 2 treatment enhanced the percentage of cells expressing SA-β-galactosidase (SA-β-gal), a marker of cellular senescence (Figure 2a,b), which is consistent with our previous study [33]. Next, the expression pattern of visfatin following H 2 O 2 -induced premature senescence was evaluated.…”

Section: Visfatin Expression Is Upregulated In Premature Senescent Desupporting

confidence: 90%

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Visfatin Induces Senescence of Human Dental Pulp Cells

Park

Jang

et al. 2020

Cells

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Dental pulp plays an important role in the health of teeth. The aging of teeth is strongly related to the senescence of dental pulp cells. A novel adipokine, visfatin, is closely associated with cellular senescence. However, little is known about the effect of visfatin on the senescence of human dental pulp cells (hDPCs). Here, it was found that in vivo visfatin levels in human dental pulp tissues increase with age and are upregulated in vitro in hDPCs during premature senescence activated by H2O2, suggesting a correlation between visfatin and senescence. In addition, visfatin knockdown by small interfering RNA led to the reduction in hDPC senescence; however, treatment with exogenous visfatin protein induced the senescence of hDPCs along with increased NADPH consumption, which was reversed by FK866, a chemical inhibitor of visfatin. Furthermore, visfatin-induced senescence was associated with both the induction of telomere damage and the upregulation of senescence-associated secretory phenotype (SASP) factors as well as NF-κB activation, which were all inhibited by FK866. Taken together, these results demonstrate, for the first time, that visfatin plays a pivotal role in hDPC senescence in association with telomere dysfunction and the induction of SASP factors.

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Section: Visfatin Expression Is Upregulated In Premature Senescent Desupporting

confidence: 90%

Section: Visfatin Expression Is Upregulated In Premature Senescent Desupporting

confidence: 90%

Visfatin Induces Senescence of Human Dental Pulp Cells

Park

Jang

et al. 2020

Cells

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“…We recently reported that 400 nM H 2 O 2 did not affect the survival of hDPCs and induced premature senescence of immortalized hDPCs [ 24 ]. In this study, we confirmed that H 2 O 2 increased the fraction of cells that was stained positive for SA-β-galactosidase (SA-β-gal), a marker of cellular senescence ( Figure 1 A,B).…”

Section: Resultsmentioning

confidence: 99%

“…Moreover, H 2 O 2 activates the signaling pathways to promote ROS production and thus, induces premature cellular premature senescence via oxidative stress in various cells, such as human retinal epithelial cells, hippocampal neurons, vascular endothelial cells, and human periodontal ligament cells [ 25 , 34 , 35 , 36 , 37 ]. In previous studies, we reported that H 2 O 2 caused premature senescence in hDPCs; however, the involvement of oxidative stress in this process was not elucidated [ 24 ]. In the present study, we demonstrated that H 2 O 2 induces senescence in hDPCs by stimulating NADPH consumption and increasing ROS generation, whereas pretreatment with FK866 significantly abrogated this effect, suggesting that FK866 acts as an antioxidant against oxidative stress-induced senescence in hDPCs during H 2 O 2 treatment.…”

Section: Discussionmentioning

confidence: 99%

FK866 Protects Human Dental Pulp Cells against Oxidative Stress-Induced Cellular Senescence

Park

Jang

et al. 2021

Antioxidants

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FK866 possesses various functional properties, such as anti-angiogenic, anti-cancer, and anti-inflammatory activities. We previously demonstrated that premature senescence of human dental pulp cells (hDPCs) was induced by hydrogen peroxide (H2O2). The present study aimed to investigate whether H2O2-induced premature senescence of hDPCs is affected by treatment with FK866. We found that FK866 markedly inhibited the senescent characteristics of hDPCs after exposure to H2O2, as revealed by an increase in the number of senescence-associated β-galactosidase (SA-β-gal)-positive hDPCs and the upregulation of the p21 and p53 proteins, which acts as molecular indicators of cellular senescence. Moreover, the stimulatory effects of H2O2 on cellular senescence are associated with oxidative stress induction, such as excessive ROS production and NADPH consumption, telomere DNA damage induction, and upregulation of senescence-associated secretory phenotype factors (IL-1β, IL-6, IL-8, COX-2, and TNF-α) as well as NF-κB activation, which were all blocked by FK866. Thus, FK866 might antagonize H2O2-induced premature senescence of hDPCs, acting as a potential therapeutic antioxidant by attenuating oxidative stress-induced pathologies in dental pulp, including inflammation and cellular senescence.

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“…Suppression of -galactosidase activity in cultured cells suggests an extension of cellular lifespan [28]. Many researchers have studied substances that extend cellular lifespan and have made efforts to identify safe substances that inhibit -galactosidase [29][30][31]. These results showed suppression of -galactosidase activity in response to treatment with active saponins.…”

Section: Discussionmentioning

confidence: 99%

Pharmacological effects of active saponins from Panax ginseng Meyer

Bae¹,

Rho²,

Kim³

et al. 2021

Trop. J. Pharm Res

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Purpose: To investigate the pharmacological effects of the active saponins isolated from Panax ginseng Meyer (P. ginseng) via extraction, heat treatment, and enzyme conversion. Methods: The effects of active saponins on rat blood were determined using a multichannel analyzer. The population doubling time (PDT) of mesenchymal stem cells (MSCs) and human-derived leukocyte cancer cells (A549) was determined by cell counting. b-galactosidase was measured in human toothderived stem cells (HTS) using a β-galactosidase ELISA kit. Results: Intraperitoneal administration of active saponins resulted in 30.09 % increase in red blood cell count and 55.55 % decrease in blood triglyceride concentrations. The stimulatory effect of active saponins (10 ng/mL) on cellular differentiation was determined based on PDT of MSCs, which decreased by 33.82 % compared to control. A 22.29 % increase in PDT of A549 cells demonstrated the suppressive effects of active saponins on cancer cell growth. Active saponins (10 ng/mL) also decreased intracellular β-galactosidase concentration by 20.42 % in HTS cells. Conclusion: Administration of active saponins to rats extends the lifespan, promotes differentiation in MSCs, suppresses A549 cell differentiation, and reduces TG and b-galactosidase associated with aging in HTS. Thus, active saponins have potentially beneficial effects in humans.

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

Cited by 4 publications

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Visfatin Induces Senescence of Human Dental Pulp Cells

Visfatin Induces Senescence of Human Dental Pulp Cells

FK866 Protects Human Dental Pulp Cells against Oxidative Stress-Induced Cellular Senescence

Pharmacological effects of active saponins from Panax ginseng Meyer

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