GPER agonist G1 suppresses neuronal apoptosis mediated by endoplasmic reticulum stress after cerebral ischemia/reperfusion injury

Neural Regeneration Research
Ziwei HanLi Li

Abstract

Studies have confirmed a strong association between activation of the endoplasmic reticulum stress pathway and cerebral ischemia/reperfusion (I/R) injury. In this study, three key proteins in the endoplasmic reticulum stress pathway (glucose-regulated protein 78, caspase-12, and C/EBP homologous protein) were selected to examine the potential mechanism of endoplasmic reticulum stress in the neuroprotective effect of G protein-coupled estrogen receptor. Female Sprague-Dawley rats received ovariectomy (OVX), and then cerebral I/R rat models (OVX + I/R) were established by middle cerebral artery occlusion. Immediately after I/R, rat models were injected with 100 μg/kg E2 (OVX + I/R + E2), or 100 μg/kg G protein-coupled estrogen receptor agonist G1 (OVX + I/R + G1) in the lateral ventricle. Longa scoring was used to detect neurobehavioral changes in each group. Infarct volumes were measured by 2,3,5-triphenyltetrazolium chloride staining. Morphological changes in neurons were observed by Nissl staining. Terminal dexynucleotidyl transferase-mediated nick end-labeling staining revealed that compared with the OVX + I/R group, neurological function was remarkably improved, infarct volume was reduced, number of normal Nissl bodies was d...Continue Reading

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Citations

Nov 1, 2020·The Journal of Pharmacology and Experimental Therapeutics·Eman Y Gohar, David M Pollock
Dec 16, 2020·The Journal of Pharmacology and Experimental Therapeutics·Qian WangBing Xue
Aug 28, 2020·Pharmacological Research : the Official Journal of the Italian Pharmacological Society·Zeinab VahidiniaMohammad Taghi Joghataei
May 6, 2021·British Journal of Pharmacology·Quynh Nhu DinhChristopher G Sobey

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Methods Mentioned

BETA
protein assay
electrophoresis
X-ray
Fluorescence
hormone replacement therapy

Software Mentioned

ImageJ
SPSS

Related Concepts

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Apoptosis

Apoptosis is a specific process that leads to programmed cell death through the activation of an evolutionary conserved intracellular pathway leading to pathognomic cellular changes distinct from cellular necrosis