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<blockquote data-quote="KJ" data-source="post: 69025" data-attributes="member: 1">[URL unfurl=&quot;true&quot;]https://pubmed.ncbi.nlm.nih.gov/36034475/[/URL]Results: The results showed that 25-50 μ·g/mL ASA promoted mitochondrial activity of HDPCs at 72 h (P &lt; 0.05) and yielded significantly higher proliferation rates of HDPCs than the control at 14d and 21d (P &lt; 0.001). All concentrations of ASA promoted odontogenic differentiation of HDPCs by enhancing the levels of DSP and RUNX2, their mRNA expression, and mineralization in a dose-dependent manner. Also, ASA yielded significantly higher TGF-β1 liberation after conditioning dentin for 5 min (25, 200 μ·g/mL; P &lt; 0.001) and 10 min (200 μ·g/mL; P &lt; 0.05).Conclusions: This in vitro study demonstrated that ASA, especially in high concentrations, promoted the odontogenesis of HDPCs and TGF-β1 liberation from dentin, showing the potential of being incorporated into the novel pulp capping materials for dental tissue regeneration.</blockquote>

[QUOTE="KJ, post: 69025, member: 1"] [URL unfurl="true"]https://pubmed.ncbi.nlm.nih.gov/36034475/[/URL] [B]Results: [/B]The results showed that 25-50 [I]μ[/I]·g/mL ASA promoted mitochondrial activity of HDPCs at 72 h ([I]P[/I] < 0.05) and yielded significantly higher proliferation rates of HDPCs than the control at 14d and 21d ([I]P[/I] < 0.001). All concentrations of ASA promoted odontogenic differentiation of HDPCs by enhancing the levels of DSP and RUNX2, their mRNA expression, and mineralization in a dose-dependent manner. Also, ASA yielded significantly higher TGF-[I]β[/I]1 liberation after conditioning dentin for 5 min (25, 200 [I]μ[/I]·g/mL; [I]P[/I] < 0.001) and 10 min (200 [I]μ[/I]·g/mL; [I]P[/I] < 0.05). [B]Conclusions: [/B]This [I]in vitro[/I] study demonstrated that ASA, especially in high concentrations, promoted the odontogenesis of HDPCs and TGF-[I]β[/I]1 liberation from dentin, showing the potential of being incorporated into the novel pulp capping materials for dental tissue regeneration. [/QUOTE]

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