丝裂原活化蛋白激酶和核因子-κB激活在一氧化氮诱导人牙髓细胞白细胞介素-8表达中的作用

Involvement of mitogen-activated protein kinases and nuclear factor-kappa B activation in nitric oxide-induced interleukin-8 expression in human pulp cells.

作者信息

Min Kyung-San, Kim Hyun-Il, Chang Hoon-Sang, Kim Hyung-Ryong, Pae Hyun-Ock, Chung Hun-Taeg, Hong Seung-Heon, Shin Hong-In, Hong Chan-Ui, Lee Suk-Keun, Kim Eun-Cheol

机构信息

Department of Conservative Dentistry, College of Dentistry, Wonkwang University, Iksan, South Korea.

出版信息

Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2008 May;105(5):654-60. doi: 10.1016/j.tripleo.2007.11.011.

Abstract

OBJECTIVE

This study examined the effect of nitric oxide (NO) on interleukin-8 (IL-8) production and the involvement of mitogen-activated protein kinase (MAPK) and nuclear factor-kappa B (NF-kappaB) signaling pathways in primary cultured human pulp cells.

STUDY DESIGN

IL-8 production was measured using enzyme-linked immunosorbent assay (ELISA) and reverse transcriptase-polymerase chain reaction (RT-PCR) analysis. MAPK activation and IkappaB degradation and phosphorylation were determined by western blotting.

RESULTS

Sodium nitroprusside (SNP), an NO donor, has increased IL-8 secretion and mRNA expression in a dose- and time-dependent manner. SNP induced the phosphorylation of p38 MAPK and extracellular-regulated kinase (ERK), degradation and phosphorylation of IkappaB, and activation of NF-kappaB. Furthermore, inhibition of the ERK, p38, and NF-kappaB pathways blocked SNP-induced IL-8 secretion.

CONCLUSION

Human pulp cells showed NO-induced IL-8 expression via the MAPK and NF-kappaB pathways, which may play an important role in the inflammatory responses of pulp and periapical lesions.

摘要

目的

本研究检测了一氧化氮(NO)对原代培养的人牙髓细胞中白细胞介素-8(IL-8)产生的影响以及丝裂原活化蛋白激酶(MAPK)和核因子-κB(NF-κB)信号通路的参与情况。

研究设计

采用酶联免疫吸附测定(ELISA)和逆转录聚合酶链反应(RT-PCR)分析检测IL-8的产生。通过蛋白质印迹法测定MAPK激活以及IκB降解和磷酸化情况。

结果

NO供体硝普钠(SNP)以剂量和时间依赖性方式增加了IL-8的分泌和mRNA表达。SNP诱导p38 MAPK和细胞外调节激酶(ERK)磷酸化、IκB降解和磷酸化以及NF-κB激活。此外,ERK、p38和NF-κB通路的抑制阻断了SNP诱导的IL-8分泌。

结论

人牙髓细胞通过MAPK和NF-κB通路表现出NO诱导的IL-8表达,这可能在牙髓和根尖周病变的炎症反应中起重要作用。

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