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Resuscitation from experimental traumatic brain injury by magnolol therapy
Che-Chuan Wang1, Kao-Chang Lin, Bor-Shyh Lin
1Department of Neurosurgery, Chi-Mei Medical Center, Tainan, Taiwan; Institute of Imaging and Biomedical Photonics, National Chiao-Tung University, Tainan, Taiwan.
Background:
The purpose of the present study was to determine whether magnolol, a free radical scavenger, mitigates the deleterious effects of traumatic brain injury (TBI).
Material And Methods:
Traumatic brain injuries were induced in anesthetized male Sprague-Dawley rats using fluid percussion, and the rats were divided into groups treated with magnolol (2 mg/kg, intravenously) or vehicle. A group of rats that did not undergo TBI induction was also studied as controls. Biomarkers of TBI, including glycerol and 2,3-dihydroxybenzoic acid, were evaluated by microdialysis. Infraction volume, extent of neuronal apoptosis, and antiapoptosis factor transforming growth factor β1 (TGF-β1) were also measured. Functional outcomes were assessed by motor assays.
Results:
Compared with the rats without TBI, the animals with TBI exhibited higher hippocampal glycerol and 2,3-dihydroxybenzoic acid. Relative to the vehicle-treated group, the magnolol-treated group showed decreased hippocampal levels of glycerol and hydroxyl radical levels. The magnolol-treated rats also exhibited decreased cerebral infarction volume and neuronal apoptosis and increased antiapoptosis-associated factor TGF-β1 expression. These effects were translated into improved motor function post TBI.
Conclusions:
Our results suggest that intravenous magnolol injection mitigates the deleterious effects of TBI in rats based on its potent free radical scavenging capability, and the mechanism of anti-neuronal apoptosis is partly due to an increase in TGF-β1 expression in the ischemic cortex.
