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茯苓酸的抗炎作用通过血红素加氧酶-1促进牙髓细胞的成牙本质细胞分化。

Anti-inflammatory effect of pachymic acid promotes odontoblastic differentiation via HO-1 in dental pulp cells.

作者信息

Lee Y-H, Lee N-H, Bhattarai G, Kim G-E, Lee I-K, Yun B-S, Hwang P-H, Yi H-K

机构信息

Department of Oral Biochemistry, BK21 program, Jeonju, Korea.

出版信息

Oral Dis. 2013 Mar;19(2):193-9. doi: 10.1111/j.1601-0825.2012.01970.x. Epub 2012 Jul 31.

Abstract

OBJECTIVES

Heme oxygenase-1 (HO-1) is contributed to odontoblast differentiation in human dental pulp cells (HDPCs). In this study, pachymic acid from mushroom Formitopsis niagra is examined to determine whether it affects pulpal inflammation and promotes odontogenesis via HO-1 gene expression.

MATERIALS AND METHODS

The HDPCs were given H2O2 for inflammation. The anti-inflammatory character and odontoblast differentiation by pachymic acid were analyzed by Western blotting, alkaline phosphatase activity, and alizarin red S staining. To understand the mechanism of pachymic acid via HO-1 induction, the cells were treated with zinc protoporphyrin IX (ZnPP: HO-1 inhibitor).

RESULTS

H2O2 induced pulp inflammation and disturbed odontoblast differentiation. However, the HDPCs treated with pachymic acid affected anti-inflammatory effect and induction of odontoblast differentiation through increasing HO-1 expression. In addition, pachymic acid has potent cytoprotection and mineralization under H2O2 treatment. Furthermore, pachymic acid significantly suppressed nuclear factor-kappa B (NF-κB) translocation into nucleus and induced NE-E2-related factor-2 (Nrf2) translocation into nucleus. Overall, NF-κB and Nrf2 translocation were regulated by the HO-1 pathway.

CONCLUSIONS

The pachymic acid showed anti-inflammatory function and odontoblast differentiation via HO-1 pathway. These results suggested that pachymic acid may be applicable for prevention of oral inflammation or to improve dentin mineralization against several stresses.

摘要

目的

血红素加氧酶-1(HO-1)有助于人牙髓细胞(HDPCs)向成牙本质细胞分化。在本研究中,检测了尼亚加拉拟层孔菌中的厚皮酸,以确定其是否通过HO-1基因表达影响牙髓炎症并促进牙发生。

材料与方法

用H2O2处理HDPCs以诱导炎症。通过蛋白质免疫印迹法、碱性磷酸酶活性检测和茜素红S染色分析厚皮酸的抗炎特性和成牙本质细胞分化情况。为了解厚皮酸通过诱导HO-1发挥作用的机制,用锌原卟啉IX(ZnPP:HO-1抑制剂)处理细胞。

结果

H2O2诱导牙髓炎症并干扰成牙本质细胞分化。然而,用厚皮酸处理的HDPCs通过增加HO-1表达影响抗炎作用和成牙本质细胞分化的诱导。此外,厚皮酸在H2O2处理下具有强大的细胞保护和矿化作用。此外,厚皮酸显著抑制核因子-κB(NF-κB)向细胞核的转位,并诱导核因子E2相关因子2(Nrf2)向细胞核的转位。总体而言,NF-κB和Nrf2的转位受HO-1途径调控。

结论

厚皮酸通过HO-1途径发挥抗炎功能并促进成牙本质细胞分化。这些结果表明,厚皮酸可能适用于预防口腔炎症或改善牙本质矿化以抵抗多种应激。

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