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三氧化矿物凝聚体对大鼠克隆性牙髓细胞的影响:通过核因子κB信号系统表达环氧合酶-2 mRNA和炎症相关蛋白

Effect of mineral trioxide aggregate on rat clonal dental pulp cells: expression of cyclooxygenase-2 mRNA and inflammation-related protein via nuclear factor kappa B signaling system.

作者信息

Minamikawa Hajime, Deyama Yoshiaki, Nakamura Kouichi, Yoshimura Yoshitaka, Kaga Masayuki, Suzuki Kuniaki, Yawaka Yasutaka

机构信息

Department of Pediatric Dentistry, Graduate School of Dental Medicine, Hokkaido University, Sapporo, Japan.

出版信息

J Endod. 2009 Jun;35(6):843-6. doi: 10.1016/j.joen.2009.03.008.

DOI:10.1016/j.joen.2009.03.008
PMID:19482183
Abstract

INTRODUCTION

Recently, mineral trioxide aggregate (MTA) has been routinely used for endodontic treatment. It is well-known that MTA induced secondary dentin formation in pulp cavity when it was applied to dentin, whereas its cytotoxicities were unclear. The purpose of this study was to evaluate the effect of MTA on rat clonal dental pulp cells, RPC-C2A.

METHODS

This study was conducted to observe the response of RPC-C2A cells on MTA with reverse-transcriptase polymerase chain reaction, Western blot analysis, and enzyme immunoassay. Data were compared by analysis of variance. Statistical significance was established at P <.01.

RESULTS

MTA significantly caused an up-regulation of cyclooxygenase-2 (COX-2) and inducible form of nitric oxide synthase (iNOS) mRNA expression. Furthermore, MTA caused inhibitory kappa B (IkappaB) phosphorylation and translocation of nuclear factor-kappa B (NF-kappaB) subunits to nucleus. Curucumin, an inhibitor of NF-kappaB activation, suppressed MTA-induced COX-2 and iNOS mRNA expressions. In addition, MTA increased the production of prostaglandin E(2) in comparison with the controls.

CONCLUSIONS

MTA induces inflammation via NF-kappaB signaling system.

摘要

引言

最近,三氧化矿物凝聚体(MTA)已常规用于牙髓治疗。众所周知,MTA应用于牙本质时会诱导牙髓腔中继发性牙本质形成,但其细胞毒性尚不清楚。本研究的目的是评估MTA对大鼠克隆牙髓细胞RPC-C2A的影响。

方法

本研究通过逆转录聚合酶链反应、蛋白质印迹分析和酶免疫测定来观察RPC-C2A细胞对MTA的反应。数据通过方差分析进行比较。P <.01时具有统计学意义。

结果

MTA显著导致环氧合酶-2(COX-2)和诱导型一氧化氮合酶(iNOS)mRNA表达上调。此外,MTA导致抑制性κB(IkappaB)磷酸化以及核因子κB(NF-κB)亚基向细胞核的易位。姜黄素是一种NF-κB激活抑制剂,可抑制MTA诱导的COX-2和iNOS mRNA表达。此外,与对照组相比,MTA增加了前列腺素E2的产生。

结论

MTA通过NF-κB信号系统诱导炎症。

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