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.