Analgesic Action of Catechin on Chronic Constriction Injury-Induced Neuropathic Pain in Sprague-Dawley Rats

Chronic neuropathy is a common and debilitating problem that poses a significant challenge to health care worldwide. Natural compounds have received considerable attention as potential sources of new drugs for the treatment of neuropsychiatric pain. Catechin is a well-known novel flavonoid with several therapeutic properties, notably in neurodegenerative diseases. The current study is designed to investigate the role of catechin in neuroprotective activity in the chronic constriction injury (CCI) model. Apparently, healthy adult male Sprague-Dawley rats weighing 160-190 g (8 weeks old) were selected and grouped into the following: sham (distilled water), CCI group (CCI), standard [CCI + pregabalin (10 mg/kg, p.o.)], and test catechin [CCI + catechin (50 and 100 mu g/kg p.o.)] for 28 days. Behavioral, thermal, and mechanical changes were evaluated. The results showed that mechanical allodynia and thermal hyperalgesia were reduced in the catechin-treated group when compared with the CCI group. In addition, the relationship between the analgesic effect of catechin and the expressions of TNF-alpha, IL-6, and IL-beta was established. The results showed that catechin reversed the signs of neuropathic pain. It also decreased the levels of TNF-alpha, IL-6, and IL-beta in the rat brain. Therefore, the results suggested that catechin has promising potential in the treatment and management of neuropathic pain by decreasing the levels of NF-kappa beta-regulated inflammatory cytokines in the chronic constriction injury model.

Automated summary

This study demonstrates that catechin has neuroprotective activity in the chronic constriction injury (CCI) model and can reduce mechanical allodynia and thermal hyperalgesia. Additionally, the analgesic effect of catechin may be related to the expressions of TNF-alpha, IL-6, and IL-beta. Therefore, catechin shows promising potential in the treatment and management of neuropathic pain by decreasing the levels of NF-kappa beta-regulated inflammatory cytokines in the CCI model.