Curcumin attenuates replicative senescence in human dental follicle cells and restores their osteogenic differentiation.

J Oral Biosci

Department of Biochemistry, Narayana Medical College and Hospital, Nellore, Andhra Pradesh, India; Central Research Laboratory (Dept of ARC), Narayana Medical College and Hospital, Nellore, Andhra Pradesh, India; Narayana College of Pharmacy, Nellore, Andhra Pradesh, India. Electronic address:

Published: December 2023

Objective: This study aimed to examine the therapeutic effects of curcumin against replicative senescence in dental follicle cells (DFCs).

Methods: Human DFCs were cultured in Dulbecco's Modified Eagle Medium with growth supplements. Replicative senescence in DFCs at different passages was assessed using β-galactosidase activity assay. Cell proliferation and size of DFCs at different passages were determined by CCK-8 kit and microscopy method, respectively. In addition, curcumin's effect on replicative senescence, cell proliferation, and size of DFCs at different passages was analyzed. Using western-blot analysis and siRNA-mediated gene silencing, we determined the molecular mechanisms involved in curcumin's effect against replicative senescence and osteogenic differentiation in DFCs at different passages.

Results: We observed decreased proliferation and increased cell size and replicative senescence in cultured human DFCs at higher passages. Intriguingly, despite not showing any effect on cell size, curcumin (50 μM) significantly restored proliferation ability in DFCs and inhibited their replicative senescence. Concerning mechanisms, we found that curcumin inhibits replicative senescence in DFCs via down-regulation of senescence markers (P16 & P21) and restoration of proliferation markers (E2F1 & P53). Additionally, curcumin also rescued the osteogenic differentiation potential in higher-passage DFCs via restoration of osteogenic markers RUNX2 and OPN.

Conclusion: Our findings reveal for the first time that curcumin could act as a potential anti-senescence therapeutic for DFCs via regulation of proliferation, senescence, and osteogenic differentiation markers.

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Source
http://dx.doi.org/10.1016/j.job.2023.10.001DOI Listing

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