Pharmacological characterization of rat paw edema induced by Cerastes gasperettii (cerastes) venom

Abstract

Inflammatory response induced by the venom of the Arabian sand viper Cerastes gasperettii was studied by measuring rat hind-paw edema. Cerastes gasperettii venom (CgV, 3.75-240 µg/paw), heated for 30s at 97&deg;C, caused a marked dose and time-dependent edema in rat paw. Response was maximal 2h after venom administration and ceased within 24h. Heated CgV was routinely used in our experiments at the dose of 120 µg/paw. Among all the drugs and antivenoms tested, cyproheptadine and 5-nitroindazole were the most effective in inhibiting edema formation. Aprotinin, mepyramine, dexamethasone, diclofenac, dipyridamole, Nomega-nitro-L-arginine, quinacrine, and nordihydroguaiaretic acid showed statistically (p<0.001) significant inhibitory effect, but with variations in their inhibition degree. Equine polyspecific and rabbit monospecific antivenoms significantly (p<0.001) reduced edema when locally administered (subplantar) but were ineffective when intravenously injected. We can conclude that the principal inflammatory mediators were serotonin, histamine, adenosine transport factors, phosphodiesterase (PDE), cyclooxygenase, lipoxygenase and phospholipase A2 (PLA2), in addition to other prostaglandins and cytokines

Edema and Nociception Induced by Philodryas patagoniensis Venom in Mice: A Pharmacological Evaluation with Implications for the Accident Treatment

“…Regarding the time course and intensity of the edematogenic response, our results are in agreement with studies that have shown a peak of activity 30 minutes after venom injection, with a dose-effect response (Rocha and Furtado, 2007). In fact, the edema induced by PpV reached the maximal intensity faster than in edema induced by some viperid Philodryas patagoniensis Venom-Induced Edema and Nociception venoms (Chaves et al, 1995;Gonçalves and Mariano, 2000;Barbosa et al, 2003;Al-Asmari and Abdo, 2006). We also found that PpV elicits a marked dose-dependent nociceptive response, which is more intense than that described in relation to P. olfersii venom (Rocha and Furtado, 2007).…”

“…Other studies have shown that histamine does not participate in the edema induced by Bothrops jararaca or B. asper venom in mice (Perales et al, 1992;Chaves et al, 1995). However, this mediator can participate in the edema induced by other animal venoms, such as viperid venoms (Al-Asmari and Abdo, 2006;Galvão Nascimento et al, 2010;Sebia-Amrane and Laraba-Djebari, 2013), Lonomia caterpillar venom (de Castro Bastos et al, 2004), Potamotrygon motoro stingray venom (Kimura et al, 2015), and Echinometra lucunter sea urchin coelomic fluid (Sciani et al, 2014).…”

Bitis arietans Snake Venom Induces an Inflammatory Response Which Is Partially Dependent on Lipid Mediators

“…Furthermore, edema, myotoxicity and leukocyte recruitment induced by B. jararaca and B. jararacussu venoms can also be attenuated by pre-treatment with dexamethasone, an inhibitor of phospholipases A 2 (PLA 2 ), which are the enzymes responsible for membrane phospholipids hydrolysis and AA release [22]. Other works have also shown the beneficial role of drugs that block the lipid mediators' synthesis in snake envenomations [23,24], indicating that the inflammatory events promoted by snake venoms are, at least in part, dependent on these molecules.…”