Honokiol, a constituent of Magnolia obovata, has various pharmacological effects, including protection against
cerebral ischemia. However, few studies have been conducted to evaluate the possible
neuroprotective effects of
honokiol against
cerebral ischemia. We recently reported that cerebral ischemic neuronal damage could be triggered by
glucose intolerance that develops after the onset of ischemic stress (i.e., post-ischemic
glucose intolerance). In addition, suppression of post-ischemic
glucose intolerance significantly ameliorated ischemic neuronal damage. Here, we investigated the effects of
honokiol on the development of post-ischemic
glucose intolerance and neuronal damage. Mice were subjected to
middle cerebral artery occlusion (MCAO) for 2 h. The development of post-ischemic
glucose intolerance on day 1 and neuronal damage on day 3 after MCAO were significantly reduced by intraperitoneal administration of
honokiol (10 mg/kg) compared with the vehicle-treated group.
Honokiol did not affect serum
insulin or
adiponectin levels. However,
honokiol significantly decreased the expression of
phosphoenolpyruvate carboxykinase and increased the expression of
5'-AMP-activated protein kinase (AMPK) on day 1 after MCAO, compared with the vehicle-treated MCAO group. The results of this study suggest that
honokiol could prevent post-ischemic
glucose intolerance in an AMPK-dependent manner, which may be involved in the
neuroprotective effects of
honokiol against
cerebral ischemia.