Filtered By:
Condition: Ischemic Stroke
Drug: Estradiol

This page shows you your search results in order of date.

Order by Relevance | Date

Total 3 results found since Jan 2013.

Elastin-derived peptide VGVAPG affects the proliferation of mouse cortical astrocytes with the involvement of aryl hydrocarbon receptor (Ahr), peroxisome proliferator-activated receptor gamma (Ppar γ), and elastin-binding protein (EBP).
Elastin-derived peptide VGVAPG affects the proliferation of mouse cortical astrocytes with the involvement of aryl hydrocarbon receptor (Ahr), peroxisome proliferator-activated receptor gamma (Pparγ), and elastin-binding protein (EBP). Cytokine. 2019 Nov 21;126:154930 Authors: Szychowski KA, Gmiński J Abstract During aging and ischemic and hemorrhagic stroke, elastin molecules are degraded and elastin-derived peptides are released into the brain microenvironment. Val-Gly-Val-Ala-Pro-Gly (VGVAPG) is a repeating hexapeptide in the elastin molecule. It is well documented that the peptide sequence binds...
Source: Cytokine - November 20, 2019 Category: Molecular Biology Authors: Szychowski KA, Gmiński J Tags: Cytokine Source Type: research

GPER expressed on microglia mediates the anti‐inflammatory effect of estradiol in ischemic stroke
ConclusionsOur studies have suggested that GPER expressed on microglia mediated the anti‐inflammatory effect of estradiol after ischemic stroke. Our studies could potentially help to develop more specific drugs to manage inflammation postischemic stroke. GPER was highly expressed in activated microglia after ischemia and estradiol. The specific GPER agonist G1 could inhibit the secretion of proinflammatory cytokines including IL‐1β and TNF‐α, which the anti‐inflammatory effect of G1 and E2 were both abolished by the specific GPER antagonist G15.
Source: Brain and Behavior - March 21, 2016 Category: Neurology Authors: Tian‐Zhi Zhao, Qian Ding, Jun Hu, Shi‐Ming He, Fei Shi, Lian‐Ting Ma Tags: Original Research Source Type: research

17-beta estradiol inhibits oxidative stress-induced accumulation of AIF into nucleolus and PARP1-dependent cell death via estrogen receptor alpha.
Abstract Oxidative stress-induced DNA damage results in over-activation of poly(ADP-ribose) polymerase 1 (PARP1), leading to parthanatos, a newly discovered cell elimination pathway. Inhibition of PARP1-dependent cell death has shown to improve the outcome of diseases, including stroke, heart ischemia, and neurodegenerative diseases. In the present study we aimed to detect whether estrogen plays a protective role in inhibiting parthanatos. We utilized human mammary adenocarcinoma cells (MCF7) that abundantly express the estrogen receptor alpha and beta (ERα and ERβ). Parthanatos was induced by challenging the ce...
Source: Toxicology Letters - September 30, 2014 Category: Toxicology Authors: Batnasan E, Wang R, Wen J, Ke Y, Li X, Bohio AA, Zeng X, Huo H, Han L, Boldogh I, Ba X Tags: Toxicol Lett Source Type: research