Abstract
The impact of magnolol on cerebral ischemic stroke in rats and the molecular mechanism were explored. Sprague-Dawley rat models were studied. Cerebral indexes, hematoxylin and eosin staining, TUNEL staining assay, reverse transcription-polymerase chain reaction (RT-PCR) and western blotting were applied. The cerebral index in model group was significantly higher than that in sham operation group, and the cerebral index was obviously decreased after magnolol administration. Inflammatory cells accumulated in the brain tissue of rats in the model group. Abundant apoptotic cells were produced in the model group, which was overtly improved after rats were given magnolol. RT-PCR and western blot analysis showed that expression of mRNA and protein of brain-derived neurotrophic factor (BDNF) were distinctly decreased in model group, and increased after rats were given magnolol; while mRNA and protein expression of Bcl-2-associated X protein (Bax) were significantly raised in model group, and reduced after rats were given magnolol. The results showed that there were statistically significant differences in expression of BDNF and Bax among sham operation, model and magnolol administration groups (p<0.01). In conclusion, magnolol can increase the expression of BDNF and decrease the expression of Bax, thereby inhibiting apoptosis to protect the nerves, and magnolol can improve cerebral ischemic stroke in rats.