摘要

Inflammatory mediators play key roles in neuropathic pain of the trigeminal system. Anesthetic isoflurane (ISO) possesses anti-inflammatory activity. However, the inhibitory effects of ISO on inflammation-triggered neuropathic pain are unclear. In this study, we investigated the effects of 1.4% ISO on neuropathic pain in interleukin1 beta (IL-1 beta)-challenged primary rat trigeminal ganglia cells (TGCs). Here, we found that ISO reduced the mRNA and protein levels of cyclooxygenase-2 (COX-2) and C-C motif ligand 2 (CCL2) in IL-1 beta-stimulated TGCs, as determined by quantitative real-time PCR and Western blot, respectively. Enzyme-linked immunosorbent assays showed that IL-1 beta-induced prostaglandin E-2 (PGE(2)), CCL2, and calcitonin gene-related peptide (CGRP) release from TGCs was significantly inhibited by ISO treatment. Pretreatment with a selective inhibitor of COX-2 (parecoxib) notably attenuated IL-1 beta-induced PGE(2) and CGRP release in TGCs. Pretreatment with an inhibitor of CCL2 synthesis (bindarit) also reduced CGRP release in IL-1 beta-challenged TGCs. Collectively, ISO ameliorates neuropathic pain through reduction of CGRP release by inhibiting COX-2 activity and CCL2 production in IL-1 beta-treated TGCs.