Ginkgolide B Modulates BDNF Expression in Acute Ischemic Stroke.
10.3340/jkns.2016.1010.018
- Author:
Hu WEI
1
;
Tao SUN
;
Yanghua TIAN
;
Kai WANG
Author Information
1. Department of Neurology, Affiliated Provincial Hospital of Anhui Medical University, Hefei, China.
- Publication Type:Original Article
- Keywords:
Stroke;
Ginkgolide B;
Brain-derived neurotrophic factor;
Apoptosis
- MeSH:
Animals;
Apoptosis;
Blotting, Western;
Brain;
Brain-Derived Neurotrophic Factor*;
Caspase 3;
In Vitro Techniques;
Infarction, Middle Cerebral Artery;
Mice;
Neurons;
Neuroprotective Agents;
Stroke*;
Up-Regulation;
Water
- From:Journal of Korean Neurosurgical Society
2017;60(4):391-396
- CountryRepublic of Korea
- Language:English
-
Abstract:
OBJECTIVE: To investigate the neuroprotective effects of Ginkgolide B (GB) against ischemic stroke-induced injury in vivo and in vitro, and further explore the possible mechanisms concerned. METHODS: Transient middle cerebral artery occlusion (tMCAO) mice and oxygen-glucose deprivation/reoxygenation (OGD/R)-treated N2a cells were used to explore the neuroprotective effects of GB. The expression of brain-derived neurotrophic factor (BDNF) was detected via Western blot and qRT-PCR. RESULTS: GB treatment (4 mg/kg, i. p., bid) significantly reduced neurological deficits, water content, and cerebral infarct volume in tMCAO mice. GB also significantly increased Bcl-2/Bax ratio, reduced the expression of caspase-3, and protected against OGD/R-induced neuronal apoptosis. Meanwhile, GB caused the up-regulation of BDNF protein in vivo and in vitro. CONCLUSION: Our data suggest that GB might protect the brain against ischemic insult partly via modulating BDNF expression.
