Ginkgolide B Modulates BDNF Expression in Acute Ischemic Stroke.

Area of Science:

• Neuroscience
• Pharmacology

Background:

• Ischemic stroke is a leading cause of death and disability worldwide.
• Current treatments for ischemic stroke have limitations and significant side effects.
• Ginkgolide B (GB), a compound from Ginkgo biloba, has shown potential therapeutic properties.

Purpose of the Study:

• To investigate the neuroprotective effects of Ginkgolide B (GB) against ischemic stroke.
• To explore the underlying mechanisms of GB's neuroprotection, focusing on brain-derived neurotrophic factor (BDNF).

Main Methods:

• In vivo studies utilized transient middle cerebral artery occlusion (tMCAO) in mice.
• In vitro studies employed oxygen-glucose deprivation/reoxygenation (OGD/R) in N2a cells.
• Western blot and qRT-PCR were used to assess BDNF expression.

Main Results:

• GB treatment significantly reduced neurological deficits, brain water content, and infarct volume in tMCAO mice.
• GB protected against OGD/R-induced neuronal apoptosis by increasing the Bcl-2/Bax ratio and decreasing caspase-3 expression.
• GB administration led to the up-regulation of BDNF protein levels both in vivo and in vitro.

Conclusions:

• Ginkgolide B exhibits significant neuroprotective effects against ischemic stroke.
• The mechanism involves the modulation of BDNF expression, suggesting a potential therapeutic role for GB in stroke treatment.