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.