Pharmacological Evaluation of CB2 Receptor Modulator in the Treatment of Neuropathic Pain

Abstract

Neuropathic pain (NP), a complex and incapacitating chronic condition, significantly affects patients' quality of life and poses a significant challenge to healthcare systems across the world. Through the CB1 and CB2 pathways, cannabinoids successfully lessen hyperalgesia and allodynia in animal models of neuropathic pain. Numerous cannabinoids, such as synthetic endocannabinoids, cannabinoid agonists (CB1), cannabinoid receptor antagonists (CB2), and endocannabinoid modulators, have been shown in animal experiments to lessen neuropathic pain behaviour. Animal models of traumatic nerve damage, including chronic constriction injury, partial nerve ligation, and spinal nerve ligation models, as well as neuropathy models brought on by metabolic issues or toxins, such as streptozotocin- and chemotherapy-induced neuropathy, have shown effectiveness. In this study, we examine the pharmacological and molecular impacts of cannabinoid receptor agonists on rats' neuropathic pain caused by paclitaxel. A range of biochemical indicators, including as CRP, and catalase activity, were assessed in close proximity to behavioural responses using the acetone drop, pin prick, and tail flick tests. The findings demonstrated that CB2 modulation eased pain while lowering pro-inflammatory cytokines and oxidative stress. These results show that cannabinoid receptor agonists are a viable treatment option for chemotherapy-induced peripheral neuropathy and have the potential to reduce neuropathic pain.