Abstract

BackgroundMigraine is one of the most common neurological diseases which has been treated by active substances from traditional Chinese medicine (TCM), such as ligustrazine, an extract of the Chinese herb Chuanxiong. However, the pathogenesis of migraine and the curative mechanisms of ligustrazine have remained unclear. The genes P2X3, TRPV1, ERK, and c-fos have been implicated to play a role. In this work, we attempted to elucidate the analgesic mechanism of ligustrazine using a classic migraine-representative rat model.MethodsThe migraine rat model was established by administration of nitroglycerin (NTG). Ligustrazine treatment was administered by intravenous injection. The animal’s behavior was continuously recorded, and then trigeminal ganglions (TGs) were isolated. Total RNA was extracted from cells and total protein was extracted from TG. Quantitative real-time polymerase chain reaction (qRT-PCR) and western blot analyses were used to detect the levels of P2X3, TRPV1, c-Fos, and ERK in TG.ResultsLigustrazine could reduce the neurological activities of NTG-induced migraine rats. The rats TG nerve showed varying degrees of expression of P2X3, TRPV1, c-Fos and ERK expression element. Ligustrazine could inhibit over-expression of P2X3, TRPV1, c-fos, and ERK in the TG nerve of NTG-induced migraine rats.ConclusionsOur results demonstrated that ligustrazine had potent activity against NTG-induced migraine rats through inhibition of the c-fos/ERK signaling pathway. This work may provide a comprehensive basis for a better understanding of the pathogenesis of migraine and the curative mechanisms of ligustrazine.

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