Effect of NOS inhibitor on cytokine and COX2 expression in rat pulpitis
Effect of NOS inhibitor on cytokine and COX2 expression in rat pulpitis
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DOI：
10.1177/154405910508400815
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发表时间：
2005-08-01
影响因子：
7.6
通讯作者：
Suda, H
中科院分区：
文献类型：
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作者：
Kawashima, N;Kawanishi, HN;Suda, H
牙髓炎过程中合成了多种化学介质；因此，控制它们的产生将有助于诱导减少牙髓炎症。我们假设一氧化氮（NO）可能是牙髓炎症的重要介质。应用LPS诱导大鼠切牙牙髓炎症，采用逆转录/聚合酶链反应和免疫组化染色检测诱导型一氧化氮合酶（iNOS）的表达。LPS处理后，iNOS mRNA在3 h后首次检测到，6 h时达到峰值，随后逐渐下降。inos阳性细胞为巨噬细胞和中性粒细胞。NOS抑制剂引起促炎细胞因子和COX2 mRNA的表达急剧下降，在lps诱导的牙髓炎中高度诱导。这些结果表明NO的合成与介质生成的启动有关，其下调可能有助于预防促炎介质的合成。缩写：ANOVA，方差分析；COX2，环加氧酶2；乙二胺四乙酸；iNOS，诱导型一氧化氮合酶；IL,白介素;n - g -硝基l -精氨酸甲酯；有限合伙人,脂多糖;NO，一氧化氮；NOS，一氧化氮合酶；PG,前列腺素;RT-PCR，逆转录/聚合酶链反应；肿瘤坏死因子。
Various kinds of chemical mediators are synthesized in the course of pulpitis; thus, control of their production would assist in inducing a reduction in pulpal inflammation. We hypothesized that nitric oxide ( NO) would be an important mediator of pulpal inflammation. Pulpal inflammation was induced by the application of LPS in rat incisor pulp, and inducible nitric oxide synthase ( iNOS) expression was evaluated by reverse-transcription/polymerase chain-reaction and immunohistochemical staining. After LPS application, iNOS mRNA was first detected after 3 hrs, peaked at 6 hrs, and decreased thereafter. iNOS-positive cells were macrophages and neutrophils. An NOS inhibitor caused drastic decreases in the expression of pro-inflammatory cytokines and COX2 mRNA, which was highly induced in the LPS-induced pulpitis. These results indicate that NO synthesis is related to the initiation of mediator production, and that its down-regulation should contribute to the prevention of pro-inflammatory mediator synthesis. Abbreviations: ANOVA, analysis of variance; COX2, cyclo-oxygenase 2; EDTA, ethylenediaminetetraacetic acid; iNOS, inducible nitric oxide synthase; IL, interleukin; L-NAME, N-G-nitro L-arginine methyl ester; LPS, lipopolysaccharide; NO, nitric oxide; NOS, nitric oxide synthases; PG, prostaglandin; RT-PCR, reverse-transcription/polymerase chain-reaction; TNF alpha, tumor necrosis factor alpha.