We have located links that may give you full text access.
Journal Article
Research Support, Non-U.S. Gov't
The anti-apoptotic effect of PI3K-Akt signaling pathway after subarachnoid hemorrhage in rats.
The serine-threonine kinase Akt plays an important role in survival pathways by inactivating downstream apoptogenic factors in many cell systems. In the following study, we investigated whether or not the activation of the Phosphatidylinositol 3-kinase (PI3K)-Akt pathway could reduce neuronal apoptosis following subarachnoid hemorrhage (SAH). Rats were randomly divided into 6 groups: control group, SAH group, SAH+ saline group, SAH+ vehicle group, SAH+ Insulin-like Growth Factor 1 (IGF-1) group, and SAH+Ly294002 (PI3K pathway inhibitor) group. All SAH animals were subjected to injection of autologous blood into the cisterna magna twice (on day 0 and on day 1). The administration was executed via cerebral ventricle 30 minutes before the induced SAH on day 0 and was continued every 24 hours for 72 hours. Whole brains were obtained on day 2. Phospho-Akt (pAkt) expression was analyzed by immunohistochemistry and western blotting. The neuronal apoptosis was evaluated by terminal deoxynucleotidyl transferase-mediated uridine 5'-triphosphate-biotin nick end-labeling (TUNEL). We found that the PI3K-Akt pathway was activated in the brain after experimental SAH. Moreover, administration of IGF-1 significantly elevated pAkt expression and decreased the percentage of apoptotic neurons following SAH, while administration of Ly294002 suppressed pAkt expression and induced increased neuronal apoptosis following SAH. Taken as a whole, our results suggested that the activation of PI3K-Akt pathway could mediate the protective effect against neuronal apoptosis after SAH.
Full text links
Related Resources
Get seemless 1-tap access through your institution/university
For the best experience, use the Read mobile app
All material on this website is protected by copyright, Copyright © 1994-2024 by WebMD LLC.
This website also contains material copyrighted by 3rd parties.
By using this service, you agree to our terms of use and privacy policy.
Your Privacy Choices
You can now claim free CME credits for this literature searchClaim now
Get seemless 1-tap access through your institution/university
For the best experience, use the Read mobile app