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一氧化氮合酶/一氧化氮在大鼠慢性牙齿炎性疼痛发展中的作用

Involvement of NOS/NO in the development of chronic dental inflammatory pain in rats.

作者信息

Fan Wenguo, Huang Fang, Li Cuixia, Qu Huaigang, Gao Zhixiong, Leng Shuilong, Li Dongpei, He Hongwen

机构信息

Department of Oral Anatomy and Physiology, Guanghua School of Stomatology, Sun Yat-sen University, 74 Zhongshan Road 2, Guangzhou, 510080, China.

出版信息

Brain Res Rev. 2009 Mar;59(2):324-32. doi: 10.1016/j.brainresrev.2008.10.002. Epub 2008 Nov 5.

DOI:10.1016/j.brainresrev.2008.10.002
PMID:19013482
Abstract

Nitric oxide (NO) is believed to be an important messenger molecule in nociceptive transmission. To assess the possible roles of NO in trigeminal sensory system, we examined the distribution and density of histochemical staining for nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-d), a marker for nitric oxide synthase (NOS), and immunohistochemical staining for c-Fos, a neuronal activity marker, in the trigeminal ganglion (TG) and trigeminal nucleus caudalis (Vc) following pulp exposure (PX) injured rats. The neurons innervating injured tooth in TG were labeled by the retrograde transport of fluoro-gold (FG). Teeth were processed for H&E staining. We found that NADPH-d activity increased significantly in the TG and Vc following PX pretreatment (7-28 days, especially in 21-28 days). Such changes were closely corresponding to the pattern of c-Fos detected by immunocytochemistry. The results demonstrate that PX-induced chronic pulpal inflammation results in significant alterations in the TG cells and in the Vc, and such changes may underlie the observed NADPH-d activity. It suggests that NOS/NO may play an active role in both peripheral and central processing of nociceptive information following chronic tooth inflammation.

摘要

一氧化氮(NO)被认为是伤害性感受传递中的一种重要信使分子。为了评估NO在三叉神经感觉系统中的可能作用,我们在牙髓暴露(PX)损伤的大鼠中,检测了烟酰胺腺嘌呤二核苷酸磷酸黄递酶(NADPH-d,一氧化氮合酶(NOS)的标志物)的组织化学染色分布和密度,以及神经元活性标志物c-Fos的免疫组织化学染色,观察其在三叉神经节(TG)和三叉神经尾核(Vc)中的变化。通过荧光金(FG)逆行转运标记TG中支配受损牙齿的神经元。对牙齿进行苏木精-伊红(H&E)染色。我们发现,在PX预处理后(7 - 28天,尤其是21 - 28天),TG和Vc中的NADPH-d活性显著增加。这种变化与免疫细胞化学检测到的c-Fos模式密切对应。结果表明,PX诱导的慢性牙髓炎症导致TG细胞和Vc发生显著改变,而这种变化可能是观察到的NADPH-d活性的基础。这表明,在慢性牙齿炎症后,NOS/NO可能在伤害性信息的外周和中枢处理中发挥积极作用。

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