Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

Estradiol prevents the injury-induced decrease of Akt activation and Bad phosphorylation.

Chung Kil Won1, Seung Jun Ha, Hae Sook Noh

  • 1Department of Anatomy, College of Veterinary Medicine and Institute of Animal Science, Gyeongsang National University, Chinju 660-701, South Korea.

Neuroscience Letters
|August 10, 2005
PubMed
Summary

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Binding affinity screening and MAPK/NF-κB mechanisms of antioxidant and anti-inflammatory phenolics compounds from Gynura procumbens stem extract (GPSE).

Scientific reports·2026
Same author

Retraction notice to "Quercetin attenuated ischemic stroke induced neurodegeneration by modulating glutamatergic and synaptic signaling pathways" [Heliyon 10 (2024) e28016].

Heliyon·2025
Same author

The HRAS-binding C2 domain of PLCη2 suppresses tumor-like synoviocytes and experimental arthritis in rheumatoid arthritis.

Experimental & molecular medicine·2025
Same author

Comprehensive analysis of Apigetrin's effects on liver cancer cells: Insights from bioinformatics, in vitro studies, and next-generation transcriptome sequencing.

Molecular and cellular probes·2025
Same author

Microglial galectin-3 increases with aging in the mouse hippocampus.

The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology·2025
Same author

Anti-Inflammatory Effects of Fermented and Aged Mountain-Cultivated Ginseng Sprouts via Suppression of MAPK-NF-κB Pathway in Lipopolysaccharide-Stimulated RAW264.7 Macrophages.

Food science & nutrition·2024

Estradiol protects brain cells from injury by activating survival signals. This study shows estradiol activates Akt and Bad phosphorylation, reducing brain infarct volume and neuronal cell death.

Area of Science:

  • Neuroscience
  • Endocrinology
  • Cell Biology

Background:

  • Neuronal cell death contributes to brain injury pathology.
  • Estradiol is known to have neuroprotective effects.
  • The specific molecular mechanisms underlying estradiol's neuroprotection require further elucidation.

Purpose of the Study:

  • To investigate the role of the Akt signaling pathway in estradiol-mediated neuroprotection.
  • To determine if estradiol modulates the phosphorylation of Akt and its downstream targets, Bad and Bcl-x(L).
  • To examine the effect of estradiol on the interaction between phosphorylated Bad (pBad) and 14-3-3 proteins.

Main Methods:

  • Ovariectomized adult female rats were subjected to middle cerebral artery occlusion (MCAO).
  • Animals were treated with estradiol or a control vehicle (oil) prior to MCAO.

Related Experiment Videos

  • Brain tissue was collected 24 hours post-MCAO for analysis of infarct volume, TUNEL staining, and Western blot analysis of phosphorylated Akt (pAkt), pBad, Bcl-x(L), and 14-3-3.

    • Main Results:

    • Estradiol treatment significantly reduced infarct volume and the number of TUNEL-positive cells in the cerebral cortex.
    • Estradiol prevented the MCAO-induced decrease in pAkt, pBad, and Bcl-x(L) levels.
    • Estradiol enhanced the interaction between pBad and 14-3-3 proteins.

    Conclusions:

    • Estradiol exerts neuroprotective effects against brain injury.
    • Activation of the Akt pathway and phosphorylation of Bad are key mechanisms mediating estradiol's protective effects.
    • Estradiol promotes neuronal survival by modulating apoptotic and anti-apoptotic signaling pathways.