Aged Garlic Extract Attenuates Cerebral Damage and Cyclooxygenase-2 Induction after Ischemia and Reperfusion in Rats

• DOI: 10.1007/s11130-011-0251-3
• Publication Date: 2011-08-17T12:42:32Z
• Authors: Ana Laura Colín-G...; Alma Ortiz-Plata; Juana Villeda-Her...; Diana Barrera; Eduardo Molina-Jijón; José Pedraza-Chav...; Perla D. Maldonado
• Keywords: Male; 0303 health sciences; Time Factors; Plant Extracts; Tumor Necrosis Factor-alpha; Anti-Inflammatory Agents; Deoxyguanosine; Cerebral Infarction; Antioxidants; Brain Ischemia; Rats; Oxidative Stress; Random Allocation; 03 medical and health sciences; 8-Hydroxy-2'-Deoxyguanosine; Cyclooxygenase 2; Models, Animal; Reperfusion; Animals; Rats, Wistar; Garlic

Different garlic products reduce the cerebral ischemic damage due to their antioxidant properties. In this work, we investigated the effect of aged garlic extract (AGE) on cyclooxygenase-2 (COX-2) protein levels and activity, and its role as a possible mechanism of neuroprotection in a cerebral ischemia model. Animals were subjected to 1 h of ischemia plus 24 h of reperfusion. AGE (1.2 ml/kg weight, i.p.) was administered at onset of reperfusion. To evaluate the damage induced by cerebral ischemia, the neurological deficit, the infarct area, and the histological alterations were measured. As an oxidative stress marker to deoxyribonucleic acid, 8-hydroxy-2-deoxyguanosine (8-OHdG) levels were determined. Finally, as inflammatory markers, TNFα levels and COX-2 protein levels and activity were measured. AGE treatment diminished the neurological alterations (61.6%), the infarct area (54.8%) and the histological damage (37.7%) induced by cerebral ischemia. AGE administration attenuated the increase in 8-OHdG levels (77.8%), in TNFα levels (76.6%), and in COX-2 protein levels (73.6%) and activity (30.7%) induced after 1 h of ischemia plus 24 h of reperfusion. These data suggest that the neuroprotective effect of AGE is associated not only to its antioxidant properties, but also with its capacity to diminish the increase in TNFα levels and COX-2 protein expression and activity. AGE may have the potential to attenuate the cerebral ischemia-induced inflammation.