Molecular mechanisms underlying the pharmacological activities of Naja Sputatrix venom

Abstract

Various clinical manifestations leading to death have been documented in most cases ofbites caused by venomous snakes. Cobra envenomation is an extremely variable process and known to cause profound neurological abnormalities. The complexity of cobra venom, can induce multiple-organ failure leading to death in case of severe envenomation. Microarray analysis revealed the heart to be most susceptible to gene expression changes. The most abundant toxic protein in cobra venom is cardiotoxin. Exposure of rat cardiomyocyte cells to Naja sputatrix cardiotoxin resulted in cell death via a necrotic pathway. Another major component of Naja sputatrix venom is phospholipase A2. It induced pulmonary inflammation and edema when administered intravenously and intratracheally to rats. Interestingly, Naja sputatrix phospholipase A2 was found to be neuroprotective in a rat model of transient focal ischemia. It is likely that phospholipase A2 exerts its neuroprotective effect by targeting upstream events in the development of ischemic damage.