| Objective To investigate the pathogenesis of CM,provide a theoretical basis for its treatment with drugs,and explore the role of transient receptor potential vanilloid subfamily member-1(TRPV1)in the pathogenesis of CM.Methods A total of 72 rats were randomly divided into four groups:control group,sham operation group(saline group),operation group(CM group),and antagonist group(capsazepine group).Dura mater,trigeminal ganglion(TG),and spinal trigeminal nucleus caudalis(TNC)were dissected to detect the expression levels of TRPV1 and calcition gene-related peptide(CGRP)using immunohistochemistry and real-time PCR.Results Expression levels of TRPV1 and CGRP in the dura mater,TG,and TNC were increased in CM rats(P<0.05).Behavior of rats was significantly reduced after intracerebroventricular injection of capsazepine,and the expression of TRPV1 and CGRP were decreased(P<0.05).Conclusions TRPV1 is involved in CM neurogenic inflammatory response and pain transmission by influencing CGRP release.The results suggested that TRPV1 may be involved in the pathophysiology of CM via the TRPV1-CGRP signaling pathway. |
PDF Full Text Request