Thesis (M.Sc.) - Cairo University - Faculty of Pharmacy - Department of Pharmacology and Toxicology

In the kidney, endocannabinoid anandamide (AEA) regulates renal blood flow, while its analogs were shown to ameliorate renal ischemia/reperfusion injury in mice. However, AEA modulatory effect on mercuric chloride-induced renal damage has not been evaluated. In the present study, AEA reduced serum creatinine, cystatin-C, blood urea nitrogen, interleukin-18, and kidney injury molecule-1. Additionally, it suppressed renal caspase-1, inositol trisphosphate, and nuclear factor of activated T-cells 1. AEA also decreased the inflammatory cascade evidenced by the suppression of renal high mobility group box protein- 1 , receptor of glycated end products, peroxisome proliferator-activated receptor- {uF067} , and nuclear factor-kB p65. Moreover, AEA boosted renal WNT-5A, glutathione (GSH) and B-cell lymphoma (BCL)-2, while reducing malondialdehyde, and caspase-3. The selective cannabinoid (CB)2 receptor antagonist, AM630, in part, antagonized the effect of AEA on all previous parameters. Accordingly, AEA partially acts by CB2R dependent anti- inflammatory, antioxidant, and anti-apoptotic mechanisms to ameliorate mercuric chloride-induced kidney injury

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