Correlation between emodin-mediated promotion of odontogenic differentiation of dental pulp cells and CD44/ERK
10.19405/j.cnki.issn1000–1492.2026.09.011
- VernacularTitle:大黄素促牙髓细胞成牙本质向分化与CD44/ERK的相关性
- Author:
Xiaolei ZHANG
1
;
Wuli LI
1
;
Yuanyin WANG
1
Author Information
1. College & Hospital of Stomatology， Anhui Medical University， Anhui Provincial Key Laboratory of Oral Diseases Research， Hefei 230032
- Publication Type:Journal Article
- Keywords:
odontoblastic differentiation;
emodin;
CD44/ERK signaling pathway;
human dental pulp cells;
pulpitis;
dental pulp regeneration
- From:
Acta Universitatis Medicinalis Anhui
2026;61(9):1594-1602
- CountryChina
- Language:Chinese
-
Abstract:
ObjectiveTo investigate the effect of emodin on the odontoblastic differentiation of human dental pulp cells （HDPCs） induced by lipopolysaccharide （LPS）. MethodsHDPCs were isolated， cultured and pretreated with LPS and emodin at gradient concentrations. The protein expression levels of odontoblastic differentiation markers （ALP， RUNX2， DMP-1 and DSPP） were detected by Western blot. Bioinformatics analysis and small interfering RNA （siRNA） transfection were performed to identify and verify the downstream signaling pathways and targets of emodin. ResultsCompared with the LPS group， the protein expression levels of ALP， RUNX2， DMP-1 and DSPP significantly increased in the Emodin group （all P<0.05）. GO and KEGG enrichment analysis showed that the MAPK signaling pathway was the most significantly enriched pathway. Western blot results demonstrated that the p-ERK/ERK expression ratio was elevated in the OIM+LPS+Emodin group compared with the OIM+LPS group （P<0.05）. The top 10 hub genes associated with emodin-mediated promotion of HDPC odontoblastic differentiation under inflammatory conditions were screened via bioinformatics， including CD44， ITGB2， SP1， TLR2， CCL2， CCL5， ITGAX， CD86， ICAM1 and SYK. RT-qPCR results revealed that the mRNA expression of CD44 was upregulated in the OIM group compared to the CON group （P<0.01）. After CD44 knockdown， the protein levels of ALP， RUNX2， DMP-1 and DSPP decreased in the si-CD44 group compared to the si-NC group （all P<0.05）. ConclusionEmodin can significantly promote odontoblastic differentiation of LPS-challenged HDPCs， and its regulatory effect is closely related to the upregulation of CD44 expression and activation of the ERK signaling pathway.
