Immunopathologic effects of scorpion venom on hepato-renal tissues: Involvement of lipid derived inflammatory mediators

摘要: Scorpion venoms are known to cause different inflammatory disorders through complex mechanisms in various tissues. In the study here, involvement of phospholipase A2 (PLA2) and cyclo-oxygenase (COX)-derived metabolites hepatic renal inflammation responses were examined. Mice envenomed with Androctonus australis hector scorpion venom absence or presence inhibitors that can interfere lipid mediator synthesis, i.e., dexamethasone (PLA2 inhibitor), indomethacin (non-selective COX-1/COX-2 celecoxib (selective COX-2 inhibitor). The response was assessed by evaluating vascular permeability changes, cell infiltration, oxidative/nitrosative stress marker levels, histologic functional analyses liver kidney. Results revealed alone induced an this tissues marked increased microvascular increases levels nitric oxide peroxidation, decreases antioxidant defense. Moreover, significant alterations histological architecture these organs associated serum some metabolic enzymes, as well urea uric acid. Pre-treatment mice led parenchyma; pre-treatment seemed be more effective against inflammation. Indomethacin only slightly reduced These results suggest mediated mainly PLA2 activation, while process prostaglandin formation COX-2. findings provide additional insight toward understanding activated pathways related involved envenoming syndrome.