This Article Full Text Full Text (PDF) All Versions of this Article: 38/11/3023    most recent STROKEAHA.107.488502v1 Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Rajanikant, G.K. Articles by Majid, A. Search for Related Content PubMed PubMed Citation Articles by Rajanikant, G.K. Articles by Majid, A. Pubmed/NCBI databases Compound via MeSH Substance via MeSH Related Collections Animal models of human disease Acute Cerebral Infarction

(Stroke. 2007;38:3023.)
© 2007 American Heart Association, Inc.

Original Contributions

Carnosine Is Neuroprotective Against Permanent Focal Cerebral Ischemia in Mice

G.K. Rajanikant, PhD; Daniel Zemke, PhD; Marie-Claude Senut, PhD; Mark B. Frenkel; Alex F. Chen, MD, PhD; Rishi Gupta, MD Arshad Majid, MD

From the Department of Neurology and Ophthalmology, Michigan State University, East Lansing, Mich.

Correspondence to Arshad Majid, MD, Associate Professor, Department of Neurology and Ophthalmology., Director, Division of Cerebrovascular Diseases., A-217 Clinical Center, Michigan State University, East Lansing, MI 48824. E-mail arshad.majid{at}ht.msu.edu

Background and Purpose— Carnosine is a naturally occurring dipeptide with multiple neuroprotective properties. In addition, it is well tolerated in high doses with minimal side effects. The purposes of this study were to determine whether carnosine is neuroprotective in permanent focal cerebral ischemia and to determine potential mechanisms of neuroprotection.

Methods— We investigated the efficacy of carnosine in a mouse model of permanent focal cerebral ischemia. The effects of carnosine were investigated with respect to neuronal damage and infarct formation, endogenous antioxidant status, and matrix metalloproteinase activity.

Results— Carnosine significantly decreased infarct size and neuronal damage when administered at time points both before and after the induction of ischemia. Carnosine also decreased reactive oxygen species levels in the ischemic brain, preserved normal glutathione levels, and decreased matrix metalloproteinase protein levels and activity.

Conclusions— Carnosine is neuroprotective in focal cerebral ischemia and appears to influence deleterious pathological processes that are activated after the onset of ischemia.

Key Words: brain ischemia • carnosine • neuroprotective agents

This article has been cited by other articles:

				J. Min, M. U. Farooq, E. Greenberg, F. Aloka, A. Bhatt, M. Kassab, J. P. Morgan, and A. Majid Cardiac Dysfunction After Left Permanent Cerebral Focal Ischemia: The Brain and Heart Connection Stroke, July 1, 2009; 40(7): 2560 - 2563. [Abstract] [Full Text] [PDF]

				M. A. Kamal, H. Jiang, Y. Hu, Richard. F. Keep, and D. E. Smith Influence of genetic knockout of Pept2 on the in vivo disposition of endogenous and exogenous carnosine in wild-type and Pept2 null mice Am J Physiol Regulatory Integrative Comp Physiol, April 1, 2009; 296(4): R986 - R991. [Abstract] [Full Text] [PDF]