Stroke is the second leading cause of death and permanent disability in adults worldwide. The treatment options for ischemic are very limited and new therapies are still required. Arginase is an endogenous competitor of Nitric acid Synthase (NOS) for the common substrate L-arginine, and upregulation of arginase during Ischemia/Reperfusion (I/R) compromises NO mediated effects. In this work, we focused on the inflammatory response to brain ischemia and the potential role of L-norvaline as arginase inhibitor against ischemic brain injury.  

       Rats were subjected to Middle Cerebral Artery Occlusion (MCAO) and the effects of L-Norvaline (50 mg/kg/day) on infarct volume, serum Advanced Glycation End products (AGEs), behaviour (gait score and ability to grasp), expression of Arginase (I & II), iNOS, eNOS, TNF-α and IL-1β level was compared to the standard Cerebrolysin (0.15 mg/kg, ip).  
     

The results of the current study support the involvement of inflammation in ischemic brain injury and point out a possible role of arginase in this process.