Kinin B2 Receptor Mediates Cisplatin-Induced Painful Peripheral Neuropathy by Intracellular Kinase Pathways and TRPA1 Channel Sensitisation

Chemotherapy-induced peripheral neuropathy is a severe clinical problem frequently associated with cisplatin use. Although its pathophysiology poorly understood, it known that kinin receptors and the transient receptor potential ankyrin 1 (TRPA1) channel play significant role in induced by rodents. However, of signalling pathways downstream from B2 activation sensitisation TRPA1 remains unknown this model. The cisplatin-induced model caused mechanical cold allodynia male Swiss mice. Antagonists for B1 attenuated painful parameters. Local sub-nociceptive doses (bradykinin) (allyl isothiocyanate; AITC) agonists enhanced parameters cisplatin-treated mice, which their respective antagonists attenuated. Furthermore, we demonstrated interaction between since phospholipase C (PLC) protein kinase epsilon (PKCε) inhibitors increase evoked bradykinin AITC Therefore, regulating can mitigate decurrent oncology treatment cisplatin.