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Anandamide (AEA), an endocannabinoid, has demonstrated analgesic and anti-inflammatory properties in various experimental models. However, the mechanisms underlying its role in neuropathic pain and inflammation remain unclear.
Carrageenan-induced inflammation and Chronic Constriction Injury (CCI) were used to model inflammatory and neuropathic pain in Wistar rats. Behavioral tests (e.g., paw edema, mechanical and thermal hyperalgesia), hematological and biochemical analyses, and molecular studies (mRNA expression of AEA pathway enzymes) were conducted to evaluate AEA’s therapeutic potential.
Anandamide significantly reduced paw edema and alleviated pain behaviors in CCI rats in a dose-dependent manner. It normalized hematological and biochemical markers and decreased levels of oxidative stress indicators (MDA, nitrite). mRNA analysis revealed upregulation of AEA degradation enzymes following CCI, indicating disrupted endocannabinoid signaling.
AEA’s analgesic and anti-inflammatory actions appear to be mediated through CB1 receptor activation and modulation of ATP-sensitive potassium channels. The observed improvements in biochemical and behavioral markers suggest its efficacy in modulating neuroinflammation and neuropathic pain.
Anandamide demonstrates significant potential as a therapeutic agent in managing neuropathic and inflammatory pain. Further studies are warranted to elucidate its mechanisms and optimize its clinical applicability.
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