Influencing mechanism of magnolol on expression of BDNF and Bax in rats with cerebral ischemic stroke

Liu,Zhenbo; Xie,Jun; Lin,Kai; Qi,Liguo

doi:10.3892/etm.2018.6807

Influencing mechanism of magnolol on expression of BDNF and Bax in rats with cerebral ischemic stroke

Authors:
- Zhenbo Liu
- Jun Xie
- Kai Lin
- Liguo Qi
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Affiliations: The Second Department of Neurosurgery, Xingtai People's Hospital, Xingtai, Hebei 054031, P.R. China, Department of Neurosurgery, Tongchuan People's Hospital, Tongchuan, Shaanxi 727000, P.R. China, Department of Neurosurgery, Liaocheng People's Hospital, Liaocheng, Shandong 252004, P.R. China, Department of Neurosurgery, Taian City Central Hospital, Taian, Shandong 271000, P.R. China
Published online on: September 28, 2018 https://doi.org/10.3892/etm.2018.6807
Pages: 4423-4428
Copyright: © Liu et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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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.

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