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Effect of Acetyl‐L‐Carnitine on Infarct Size in Multiple Models of Experimental Focal Cerebral Ischemia in Rats
Author(s) -
Jalal Fakhreya Yousuf,
Maher Timothy John
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.716.14
Subject(s) - neuroprotection , medicine , ischemia , stroke (engine) , anesthesia , internal carotid artery , infarction , middle cerebral artery , myocardial infarction , mechanical engineering , engineering
Acetyl‐L‐carnitine (ALCAR), an acetyl ester of carnitine present in brain, is involved in many aspects of neuronal activity, e.g., energy metabolism, phospholipid synthesis for membrane formation/integrity, and modulation of neurotrophic factors and neurohormones. Aberrant neuronal activity occurs following stroke, and ALCAR has been shown to provide some neuroprotection in a few rat studies. This study determined the neuroprotective effect of ALCAR in multiple rat models of ischemic stroke. Focal cerebral ischemia was induced using distal permanent middle cerebral artery occlusion (MCAO) combined with bilateral carotid artery occlusion (BCCO), proximal permanent MCAO, and both permanent and transient intraluminal suture models. Rats were subjected to distal permanent MCAO combined with BCCO and treated with acute or chronic doses of ALCAR 30 min prior the MCAO. Acute doses of 50, 200, 400 mg/kg I.P. did no affect infarct size, while chronic ALCAR (400mg/kg X 5 days) significantly reduced in infarct size (p< 0.001). Lower doses ALCAR (50 and 200 mg/kg X 5 days) failed to alter infarct size. The effective dose of ALCAR (400 X 5 days) also produced a significant reduction in infarct size in rats subjected to proximal permanent MCAO, permanent, and transient intraluminal suture models. ALCAR might exert its neuroprotection via a host of different mechanistic pathways.