动物造模 z-bio 2021-07-22 424

　　OBJECTIVE: To explore the role of peripheral neuroprotease activated receptor 2-protein kinase A/protein kinase Cε (PAR2-PKA/PKCε) pathway in pain changes and possible interventions for acute and chronic pain at the same time.

　　Method: SD rats were randomly divided into blank group, sham induction group, induction group, inhibitor group 1, and inhibitor 2 groups. Except for the blank group and the sham induction group, all rats were injected with carrageenan and prostaglandin E2 (PGE2) to establish a hyperalgesia model. 7 days after carrageenan injection, PGE2 was injected into the foot. The rats in the inhibitor 1 group and the inhibitor 2 group received PAR2 inhibitor treatment before and after PGE2 injection. Observe the mechanical pain threshold (PWT) changes of rats before injection, 5 hours, 3 days, 6 days, 7 days 0.5 hours, 7 days 4 hours, 7 days 24 hours, and 7 test the dorsal model one day after 24 hours. Injection of carrageenan PAR2, protein kinase A (PKA) and protein kinase (PKCε) are expressed in the dorsal root ganglia (DRG).

　　Result: We successfully established a pain sensitization induction model. PGE2 was given 7 days after carrageenan injection and significantly prolonged the presence of pain caused by PGE2. The PWT of rats in the sham operation induction group 7d24h after carrageenan injection was not significantly different from that of the blank group during the same period (P\u003c0.05). On the other hand, the PWT of rats in the induction group was significantly lower than that of the blank group and sham induction group (Pu003c0.01). The expression of PAR2 and PKCε in the model DRG of the induction group increased significantly at 7d24h after carrageenan injection, and was higher than that of the sham induction group and the blank group during the same period (Pu003c0.05). The inhibition of PAR2 was significantly reversed at 7d24h after carrageenan injection. Regardless of time, it induced pain in rats in the PGE2-induced group (Pu003c0.05) and inhibited the expression of PKCε in DRG. .. However, the use of PAR2 inhibitors can affect the pain caused by acute PGE2 and cannot regulate the PKA content of DRG.

　　Conclusion: Inhibition of PAR2 expression may prevent the transformation of acute pain to chronic pain. This may be related to the inhibition of the activation of the PAR2-PKCε pathway in DRG. However, the inhibition of PAR2 cannot prevent acute pain. This may be because the PAR2-related pathways of DRG are not involved in the development of acute pain.