scholarly journals Homocysteine Aggravates Cortical Neural Cell Injury through Neuronal Autophagy Overactivation following Rat Cerebral Ischemia-Reperfusion

2016 ◽  
Vol 17 (8) ◽  
pp. 1196 ◽  
Author(s):  
Yaqian Zhao ◽  
Guowei Huang ◽  
Shuang Chen ◽  
Yun Gou ◽  
Zhiping Dong ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Cell Injury ◽  
Ischemia Reperfusion ◽  
Neural Cell ◽  
Cerebral Ischemia Reperfusion ◽  
Neuronal Autophagy

scholarly journals Inhibition of GPR4 attenuates SH-SY5Y cell injury in cerebral ischemia/reperfusion via anti-apoptotic pathways

2021 ◽  
Author(s):  
Chunli Xing ◽  
Guizhen Yan ◽  
Qishuai Liu
Keyword(s):  
Cerebral Ischemia ◽  
Cell Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Ph Sensor ◽  
Cell Activity ◽  
Endothelial Permeability ◽  
Glucose Deprivation ◽  
Cerebral Ischemia Reperfusion ◽  
Ldh Release

Cerebral ischemia/reperfusion injury (CIRI) can lead to increased vascular endothelial permeability and blood-brain barrier damage in patients with stroke. G protein-coupled receptor 4 (GPR4) is a functional pH sensor that plays a key role in renal ischemia-reperfusion-induced apoptosis. However, whether GPR4 has a role in cerebral ischemia remains to be further studied. Our study found that after oxygen-glucose deprivation/reoxygenation (OGD/R) treatment, the levels of GPR4 and CHOP in SH-SY5Y cells were significantly increased, which was accompanied by a decrease in cell viability, and an increase in LDH release and apoptosis. After knockdown of GPR4 using shRNA, CHOP levels in SH-SY5Y cells were also decreased, which unexpectedly increased cell activity and decreased LDH release and apoptosis rate. Interestingly, CHOP overexpression reversed the effect of GPR4 knockdown, suggesting that OGD/R-induced CIRI may involve endoplasmic reticulum stress-related apoptosis. In conclusion, our study provided a basis for further research on the mechanism of CIRI.

scholarly journals Protective Action of Betulinic Acid on Cerebral Ischemia/Reperfusion Injury through Inflammation and Energy Metabolic Homeostasis

2020 ◽  
Vol 10 (7) ◽  
pp. 2578
Author(s):  
Wenjiao Jiang ◽  
Kun Hao
Keyword(s):  
Cerebral Ischemia ◽  
Betulinic Acid ◽  
Cell Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Protective Action ◽  
Enzyme Linked Immunosorbent Assay ◽  
Protective Effects ◽  
Cerebral Ischemia Reperfusion

This work evaluated the protective effects of betulinic acid (BA) in vitro cerebral ischemia/reperfusion and provides clues about its pharmacological mechanism. A rat model of middle cerebral artery occlusion (MCAO) was established to investigate the effects of BA on cerebral ischemia. SHSY5Y cell injury was induced by oxygen–glucose deprivation and recovery (OGD/R) to further verify the action of BA in vitro. Our data show a significant improvement in infarct size, neurological score, and cerebral edema after BA treatment. Enzyme linked immunosorbent assay (ELISA) data show that BA inhibited interleukin-1β (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α) in vivo and in vitro. Protein expression results show that BA down-regulated hypoxia-inducible factor-1α (HIF-1α), up-regulated adenosine monophosphate activated protein kinase (AMPK), peroxisome proliferative activated receptor (PPAR)-α, and PPAR-γ coactivator-1α (PGC-1α), and blocked phosphorylation of IκBα and nuclear factor kappa Bp65 (NF-κB-p65) in the brains of MCAO rats and OGD/R-stimulated SHSY5Y cells. The results reveal the potent effects of BA on cerebral ischemia, suggesting that HIF-1α might be a crucial therapeutic target to regulate energy metabolism and inflammation.

Bardoxolone Ameliorates Cerebral Ischemia/ Reperfusion Injury in Male Rats

2019 ◽  
Vol 22 (04) ◽  
pp. 122-130
Author(s):  
Rihab H Al-Mudhaffer ◽  
Laith M Abbas Al-Huseini ◽  
Saif M Hassan ◽  
Najah R Hadi
Keyword(s):  
Cerebral Ischemia ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Male Rats ◽  
Cerebral Ischemia Reperfusion ◽  
Cerebral Ischemia Reperfusion Injury
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