Standardized Ginkgo biloba extract EGb 761® attenuates early brain injury following subarachnoid hemorrhage via suppressing neuronal apoptosis through the activation of Akt signaling - 20/09/18
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Graphical abstract |
Highlights |
• | EGb 761 attenuated brain edema and neurological deficits after SAH. |
• | EGb 761 alleviated SAH-induced neuronal apoptosis. |
• | EGb 761 activated the Akt signaling pathway after SAH. |
• | EGb 761 might be a promising therapeutic agent for SAH. |
Abstract |
Background |
Early brain injury (EBI) plays a critical role in determining the outcome of subarachnoid hemorrhage (SAH). The present study was designed to investigate the role of EGb 761, a standardized extract of Ginkgo biloba, in SAH-induced EBI and to explore its potential mechanism of action.
Method |
A rat SAH model was established by the endovascular perforation process. Doses of 10, 50 and 100 mg/kg EGb 761 were injected intraperitoneally 2 h after SAH was induced. Mortality, SAH grade, neurological score and brain water content were measured 24 h after SAH was induced. A Western blot assay was performed to assess the expression of the apoptosis-related proteins Bax, Bcl-2, cleaved caspase-3, Akt and phosphorylated Akt (p-Akt). Terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) and neuronal nuclei (NeuN) double immunofluorescence staining were used to detect apoptotic neurons.
Results |
Animals suffered from serious neurological deficits and increased brain water content after induction of SAH. Rats treated with EGb 761 experienced dose-dependent attenuation of neurological dysfunction and decreased brain water content. In addition, EGb 761 significantly activated Akt signaling accompanied by increased Bcl-2 levels and decreased expression of Bax and cleaved caspase-3. Moreover, EGb 761 decreased the number of TUNEL/NeuN-positive cells in a dose-dependent manner. However, all the beneficial effects of EGb 761 for SAH were abolished by the Akt inhibitor MK2206.
Conclusion |
Our results indicated that EGb 761 could ameliorate SAH-induced EBI and that the neuroprotective effects of EGb 761 against SAH were exerted via suppression of neuronal apoptosis through activation of the Akt pathway.
Le texte complet de cet article est disponible en PDF.Keywords : Early brain injury, Subarachnoid hemorrhage, Apoptosis, Akt
Plan
Vol 107
P. 329-337 - novembre 2018 Retour au numéro
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