Behavioral and histologic neuroprotection of aqueous garlic extract after reversible focal cerebral ischemia

• Published in: Journal of medicinal food Vol. 9; no. 4; pp. 537 - 544
• Main Authors: Saleem, S, Ahmad, M, Ahmad, A.S, Yousuf, S, Ansari, M.A, Khan, M.B, Ishrat, T, Islam, F
• Format: Journal Article
• Language: English
• Published: United States 2006
• Subjects: adenosinetriphosphatase; animal behavior; animal models; Animals; apoptosis; arteries; aspartic acid; Behavior, Animal - drug effects; blood chemistry; Brain - enzymology; Brain Chemistry; Brain Ischemia - enzymology; Brain Ischemia - metabolism; catalase; Catalase - analysis; chemoprevention; Constriction; enzyme activity; garlic; Garlic - chemistry; glutamates; glutathione; Glutathione - analysis; glutathione peroxidase; Glutathione Peroxidase - analysis; glutathione reductase (NADPH); Glutathione Reductase - analysis; glutathione transferase; Glutathione Transferase - analysis; Hand Strength; histopathology; ischemia; Male; malondialdehyde; Malondialdehyde - analysis; Middle Cerebral Artery; Motor Activity - drug effects; neurophysiology; Neuroprotective Agents - administration & dosage; plant extracts; Plant Extracts - administration & dosage; Rats; Rats, Wistar; reperfusion; Sodium-Potassium-Exchanging ATPase - analysis; stroke; superoxide dismutase; Superoxide Dismutase - analysis
• ISSN: 1096-620X; 1557-7600
• DOI: 10.1089/jmf.2006.9.537

The objective of the present study was to investigate the effects of aqueous garlic extract (AGE) on neurobehavioral activities, malondialdehyde (MDA) and reduced glutathione (GSH) levels, glutathione peroxidase (GPx), glutathione reductase (GR), glutathione S-transferase (GST), superoxide dismutase (SOD), catalase (CAT), and sodium-potassium ATPase (Na(+),K(+)-ATPase) activities, and glutamate and aspartate content in a middle cerebral artery (MCA) occlusion (MCAO) model of acute cerebral ischemia in rats. The right MCA of male Wistar rats was occluded for 2 hours using intraluminal 4-0 monofilament, and reperfusion was allowed for 22 hours. MCAO caused significant depletion in GSH and its dependent enzymes (GPx, GR, and GST) and significant elevation of MDA, glutamate, and aspartate. The activities of Na(+),K(+)- ATPase, SOD, and CAT were decreased significantly by MCAO. The neurobehavioral activities (grip strength, spontaneous motor activity, and motor coordination) were also decreased significantly in the MCAO group. All of the alterations induced by ischemia were significantly attenuated by pretreatment with AGE (500 mg/mL/kg of body weight, i.p.) 30 minutes before the induction of MCAO and correlated well with histopathology by decreasing the neuronal cell death following MCAO and reperfusion. These findings suggest that AGE effectively modulates neurobehavioral and neurochemical changes in focal ischemia, most probably by virtue of its antioxidant properties.