Effect of Carnosine on Rats under Experimental Brain Ischemia

Abstract

The effect of dietary carnosine on the behavioral and biochemical characteristics of rats under experimental ischemia was studied. Carnosine was shown to improve the animals orientation and learning in "Open Field" and "T-Maze" tests, and this effect was accompanied with an increase in glutamate binding to N-methyl-D-aspartate (NMDA) receptors in brain synaptosomes. Long-term brain ischemia induced by both sides' occlusion of common carotid arteries resulted in 55% mortality of experimental rats, and those who survived were characterized by partial suppression of orientation in T-maze. In the group of rats treated with carnosine, mortality after ischemic attack was decreased (from 55% to 17%) and most of the learning parameters were kept at the pre-ischemic level. Monoamine oxidase B (MAO B) activity in brain of the carnosine treated rats was not changed by ischemia significantly (compared to that of ischemic untreated rats) but NMDA binding to brain synaptosomal membranes being increased by ischemic attack was significantly suppressed and reached the level characteristic of normal brain. The suggestion was made that carnosine possesses a dual effect on NMDA receptors resulting in increase in their amount after long-term treatment but decrease the capacity to bind NMDA after ischemic attack.

The effects of carnosine in an experimental rat model of septic shock

“…Stvolinsky et al and Gallant et al reported decreased mortality after ischemic attack in rats treated with carnosine (from 55% to 17%), with most learning parameters maintained at pre-ischemic levels [20,21]. One of the underlying mechanism of ischemic attack is thought to be oxidative damage due to the generation of free radicals.…”

Energy metabolism, proteotoxic stress and age-related dysfunction – Protection by carnosine

“…Evidence that carnosine may exert protective action against a number of conditions associated with ischaemia (see Stvolinsky and Dobrota, 2000 and Refs. therein;Gallant et al, 2000;Rajanikant et al, 2007;Tang et al, 2007;Yasuhara et al, 2008), including when added after the ischaemic episode (Dobrota et al, 2005;Tang et al, 2007;Rajanikant et al, 2007), and type-2 diabetes has been obtained mostly from the study of animal models and cell culture (Lee et al, 2005;Shi et al, 2009;Kamel et al, 2008;Tanida et al, 2004). Evidence supporting a role for carnosine in controlling diabetic kidney disease in humans has emerged from a study of carnosinase polymorphisms which suggest that lower levels of serum carnosinase activity decreases the incidence of kidney disease in type-2 diabetics (Ahluwalia et al, 2011;Janssen et al, 2005;Freedman et al, 2007;Sauerhoefer et al, 2005).…”

Safety and Efficacy Evaluation of Carnosine, an Endogenous Neuroprotective Agent for Ischemic Stroke

“…12,13 In focal ischemia, we have previously shown that intraperitoneally administrated carnosine reduced brain damage in mouse ischemia models induced by permanent middle cerebral artery occlusion (pMCAO). 14 We also showed that carnosine is the most effective among several carnosine analogues in reducing pMCAO-induced infarction volumes.…”