〔Abstract〕 Objective To investigate the pathological role of detect protein kinase C(PKC)/transient receptor potential vanilloid subtype 1(TRPV1) pathway in trigeminal neuralgia(TN) in rats. Methods The infraorbital nerve-chronic constriction injury(ION-CCI) was used to establish a rat model of TN. The rats were randomly divided into Sham group, CCI group, CCI+DMSO group and CCI+GF109203X(a PKC inhibitor) group. The mechanical pain threshold of the rats was measured using a Von Frey brush. qRT-PCR and Western blot were used to detect PKC and TRPV1 in the trigeminal ganglion(TG). HE staining was used to observe the pathological changes of TG. Results The mechanical pain threshold significantly decreased(P<0.05), and the expression of phosphorylated PKC(p-PKC) and TRPV1 in TG significantly increased in the CCI group(P<0.05). Histopathological results showed that compared with the Sham group, the CCI group observed significant changes in TG such as increased inflammatory cell infiltration and nerve cell swelling. Injection of GF109203X effectively reduced the phosphorylation of PKC and the expression of TRPV1 in the TG of rats, and the mechanical pain threshold of the rats increased(P<0.05). Under the light microscope, cell swelling and inflammatory cells in the TG were reduced. Conclusion PKC/TRPV1 pathway may be involved in trigeminal neuralgia in rats.