Abstract:
OBJECTIVE To explore the effect and mechanism of warming channels and activating blood circulation external treatment to alleviate peripheral hyperalgesia in knee osteoarthritis (KOA) based on NGF/TrKA signaling pathway.
METHODS 30 SD rats were randomly divided into normal group, KOA group and Yiceng group. KOA model was established by anterior cruciate ligament transection (ACLT). 14 days after model establishment, rats in Yiceng group were treated with Yiceng patch. The peripheral pain threshold of rats was measured at different time points. The cartilage sections were stained with HE, Aggrecan and type Ⅱ collagen. The synovial sections were stained with HE, Sirius red, silver and performed with immunostaining. The protein expression of key molecules NGF and TrKA of NGF/TrKA signaling pathway, inflammatory index IL-1β, pain mediator TRPV1, pan-neural markers PGP9.5 and S100 in synovium and complexes transported to dorsal root ganglia (DRG) tissues via nerve endings was determined by Western Blot. The corresponding gene expression was determined by qPCR. The levels of NGF and SP in peripheral blood of rats were determined by ELISA.
RESULTS Compared with the KOA group, the cold allodynia and mechanical allodynia thresholds of the rats in the Yiceng group increased (P < 0.05, P < 0.01); the protein and gene expression of NGF, TrKA, TRPV1, IL-1β, PGP9.5 in the synovial tissue decreased (P < 0.05, P < 0.01); the protein and gene expression levels of TRPV1, PGP9.5, S100 in the DRG tissue were downregulated (P < 0.05, P < 0.01).
CONCLUSION The warming channels and activating blood circulation external treatment can inhibit the NGF/TrKA signaling pathway, downregulate the gene and protein expressions of NGF, TrKA, TRPV1, IL-1β, PGP9.5, and may inhibit the sprouting of sensory nerve fibers and improve the peripheral hyperalgesia state of rats with KOA.