International immunopharmacology · 2025
Artemisinin regulates cell proliferation, apoptosis, and the inflammatory response of human dental pulp stem cells through the p53 signaling pathway under LPS-induced inflammation.
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Sui Yuan, Dong Xiaofei, Tong Enkang, Zhao Cuicui, Nie Rongrong, Meng Xiangfeng
Аннотация
OBJECTIVE: The purpose of this study was to investigate the effects and mechanism of artemisinin (ART) on the proliferation, apoptosis, and inflammatory response of human dental pulp stem cells (HDPSCs) under lipopolysaccharide (LPS)-induced inflammation.
METHODS: HDPSCs were isolated, cultured, and identified by flow cytometry and three-directional differentiation induction. A suitable concentration of LPS was selected to mimic the inflammatory condition in vitro. After culturing with ART and LPS for 48 h, cell proliferation was observed by CCK-8 assay; cell apoptosis was observed by flow cytometry, western blot, and Caspase-3 activity; and the inflammatory response was observed by qRT-PCR and ELISA. Transcriptome sequencing, immunofluorescence staining, qRT-PCR, western blot, and RITA were used to explore the underlying mechanism.
RESULTS: HDPSCs were successfully isolated and exhibited the potential for multilineage differentiation. 0.1 μg/mL of LPS was utilized to mimic the inflammatory condition. ART promoted HDPSCs proliferation but repressed apoptosis and the inflammatory response under LPS-induced inflammation. Further, ART exerted its effect through the p53 signaling pathway.
CONCLUSION: ART inhibited the p53 signaling pathway to promote HDPSCs proliferation, but hinder apoptosis and the inflammatory response under LPS-induced inflammation.
CLINICAL SIGNIFICANCE: This study demonstrates that ART facilitates the alleviation of inflammation and preserves the viability of HDPSCs. Therefore, ART may serve as a promising therapeutic drug for the repair and regeneration of dental pulp in the treatment of deep caries and reversible pulpitis.
METHODS: HDPSCs were isolated, cultured, and identified by flow cytometry and three-directional differentiation induction. A suitable concentration of LPS was selected to mimic the inflammatory condition in vitro. After culturing with ART and LPS for 48 h, cell proliferation was observed by CCK-8 assay; cell apoptosis was observed by flow cytometry, western blot, and Caspase-3 activity; and the inflammatory response was observed by qRT-PCR and ELISA. Transcriptome sequencing, immunofluorescence staining, qRT-PCR, western blot, and RITA were used to explore the underlying mechanism.
RESULTS: HDPSCs were successfully isolated and exhibited the potential for multilineage differentiation. 0.1 μg/mL of LPS was utilized to mimic the inflammatory condition. ART promoted HDPSCs proliferation but repressed apoptosis and the inflammatory response under LPS-induced inflammation. Further, ART exerted its effect through the p53 signaling pathway.
CONCLUSION: ART inhibited the p53 signaling pathway to promote HDPSCs proliferation, but hinder apoptosis and the inflammatory response under LPS-induced inflammation.
CLINICAL SIGNIFICANCE: This study demonstrates that ART facilitates the alleviation of inflammation and preserves the viability of HDPSCs. Therefore, ART may serve as a promising therapeutic drug for the repair and regeneration of dental pulp in the treatment of deep caries and reversible pulpitis.