2018
DOI: 10.17219/acem/75776
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Simvastatin increases cell viability and suppresses the expression of cytokines and vascular endothelial growth factor in inflamed human dental pulp stem cells in vitro

Abstract: Taken together, these results suggested that simvastatin might be a potent ingredient to enhance cell proliferation, alleviate inflammation response and attune vasculogenesis in pulpitis.

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Cited by 10 publications
(10 citation statements)
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“…20% HPL increases expression of pro-angiogenic factors at both gene and protein levels, while maintaining the cell viability [ 127 ]. In LPS-induced DPSCs simvastatin inhibits the expression of proinflammatory cytokines and VEGF, blocking the MAPK signaling [ 128 ]. It also promotes proliferation and apoptosis [ 128 ].…”
Section: Resultsmentioning
confidence: 99%
See 1 more Smart Citation
“…20% HPL increases expression of pro-angiogenic factors at both gene and protein levels, while maintaining the cell viability [ 127 ]. In LPS-induced DPSCs simvastatin inhibits the expression of proinflammatory cytokines and VEGF, blocking the MAPK signaling [ 128 ]. It also promotes proliferation and apoptosis [ 128 ].…”
Section: Resultsmentioning
confidence: 99%
“…In LPS-induced DPSCs simvastatin inhibits the expression of proinflammatory cytokines and VEGF, blocking the MAPK signaling [ 128 ]. It also promotes proliferation and apoptosis [ 128 ].…”
Section: Resultsmentioning
confidence: 99%
“…Moreover, DPCs subsequently migrate to the injured site, where they differentiate into odontoblast-like cells to synthesize reparative dentin, initiating repair and regeneration [ 27 30 ]. However, antibacterial activities easily induce the inflammatory cascade and thereby propagate sustained inflammation [ 2 4 ], which not only irreversibly damages vital pulp tissue but also actively impedes the repair responses of DPCs, and these effects eventually lead to total necrosis of the pulp [ 1 , 24 ]. Hence, attenuation of inflammation is a prerequisite for the initiation of pulp healing and regeneration.…”
Section: Discussionmentioning
confidence: 99%
“…As bacteria and their toxic components penetrate into the pulp, inflammatory responses from resident cells, including dental pulp cells (DPCs), macrophages, and other immune cells, are initiated to eliminate invading microbes [ 1 ]. However, these antimicrobial activities allow the easy propagation of sustained inflammation, which is enormously destructive to the vital pulp and ultimately leads to tissue necrosis and prevention of innate self-repair of the pulp [ 2 4 ]. Hence, the attenuation of excessive inflammation and the preservation of pulp vitality have been the most substantial challenges in modern endodontics.…”
Section: Introductionmentioning
confidence: 99%
“…DPSC play an important role in pulpal defense and are recruited from their niche, migrate to the affected site and then differentiate into odontoblasts to form reparative dentine (Shi and Gronthos, 2003). Considering that DPSC are the reserve cells for pulp injury and repair, we used LPS to stimulate DPSC to establish an inflammatory dental pulp cells model (Widbiller et al, 2018;Xue et al, 2018), and explored the anti-inflammatory and differentiation inducing function of HBD4 in vitro.…”
Section: Discussionmentioning
confidence: 99%