Neuroprotective effect of chlorogenic acid in global cerebral ischemia-reperfusion rat model

Abstract BackgroundNeuroinflammation and apoptosis are involved in the pathogenesis of ischemic stroke. Alisol A 24-acetate (24A) has a strong inhibitory effect on inflammation and cell apoptosis. The neuroprotective effect of 24A in the global cerebral ischemia/ reperfusion (GCI/R) is still unclear. Methods GCI/R mice was used to investigated the neuroprotective effect of 24A. Modified neurological deficit scores, Morris Water Maze and object recognition test were used to evaluate behaviors. The metabolism in brain regions was detected by MRS. The changes of microglia, astrocytes and neurons was detected. The inflammation and apoptosis were measured.Results The results showed that 24A improved behavioral dysfunction and brain metabolism, alleviate neuroinflammation and apoptosis, inhibited microglia and astrocytes activation, which is associated with the activation of PI3K/AKT pathway. ConclusionsTaken together, our study demonstrated that 24A could alleviate GCI/R injury through anti-neuroinflammation and anti-apoptosis via regulating the PI3K/AKT pathway.

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Neuroprotective effect of menaquinone-4 (MK-4) on transient global cerebral ischemia/reperfusion injury in rat

PLoS ONE ◽

10.1371/journal.pone.0229769 ◽

2020 ◽

Vol 15 (3) ◽

pp. e0229769 ◽

Cited By ~ 3

Author(s):

Bahram Farhadi Moghadam ◽

Masoud Fereidoni

Keyword(s):

Cerebral Ischemia ◽

Reperfusion Injury ◽

Ischemia Reperfusion Injury ◽

Neuroprotective Effect ◽

Ischemia Reperfusion ◽

Global Cerebral Ischemia ◽

Transient Global Cerebral Ischemia ◽

Cerebral Ischemia Reperfusion ◽

Cerebral Ischemia Reperfusion Injury

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Modulation of Preactivation of PPAR-βon Memory and Learning Dysfunction and Inflammatory Response in the Hippocampus in Rats Exposed to Global Cerebral Ischemia/Reperfusion

PPAR Research ◽

10.1155/2012/209794 ◽

2012 ◽

Vol 2012 ◽

pp. 1-11 ◽

Cited By ~ 6

Author(s):

Ge Kuang ◽

Qin He ◽

Yunmei Zhang ◽

Ruichun Zhuang ◽

Anling Xiang ◽

...

Keyword(s):

Cerebral Ischemia ◽

Hippocampal Neurons ◽

Nuclear Translocation ◽

Ischemia Reperfusion Injury ◽

Neuroprotective Effect ◽

Ischemia Reperfusion ◽

Global Cerebral Ischemia ◽

Dependent Manner ◽

Neuroprotective Effects ◽

Cerebral Ischemia Reperfusion

The aim of this study is to investigate the neuroprotective effects and relevant mechanism of GW0742, an agonist of PPAR-β, after global cerebral ischemia-reperfusion injury (GCIRI) in rats. The rats showed memory and cognitive impairment and cytomorphological change in the hippocampus neurons following GCIRI. These effects were significantly improved by pretreatment with GW0742 in the dose-dependent manner. The expressions of IL-1β, IL-6, and TNF-αwere increased after GCIRI, while the increases in these proinflammatory cytokines by GCIRI were inhibited by GW0742 pretreatment. Similarly, GW0742 pretreatment also improved the GCIRI-induced decrease in the expression of IL-10, which can act as an inhibitory cytokine to reduce cerebral ischemic injury. For another, NF-κB p65 expression was significantly increased in hippocampal neurons with apparent nuclear translocation after global cerebral IRI, and these phenomena were also largely attenuated by GW0742 pretreatment. Moreover, the mRNA and protein expressions of PPAR-βwere significantly decreased in GCIRI + GW0742 groups when compared with those in GCIRI group. Our data suggests that the PPAR-βagonist GW0742 can exert significant neuroprotective effect against GCIRI in rats via PPAR-βactivation and its anti-inflammation effect mediated by the inhibition of expression and activation of NF-κB in the hippocampus.

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Urinary Proteome Changes in Global Cerebral Ischemia-Reperfusion Injury Rat Model Using Proteomics

10.21203/rs.3.rs-1006901/v1 ◽

2021 ◽

Author(s):

Xiaopeng Sun ◽

Qiujie Li ◽

Mingshan Wang ◽

Weiwei Qin

Keyword(s):

Cerebral Ischemia ◽

Rat Model ◽

Early Stage ◽

Ischemia Reperfusion ◽

Differentially Expressed ◽

Global Cerebral Ischemia ◽

Differentially Expressed Proteins ◽

Urinary Proteome ◽

Cerebral Ischemia Reperfusion ◽

Severe Hypotension

Abstract Background Cerebral ischemia-reperfusion (I/R) injury is the leading cause of death in severe hypotension caused by cardiac arrest, drowning, and excessive blood loss. Urine can sensitively reflect pathophysiological changes in the brain even at an early stage. Methods In this study, a rat model of global cerebral I/R injury was established via Pulsinelli’s four-vessel occlusion (4-VO) method. The proteomics techniques of data-independent acquisition (DIA) and parallel reaction monitoring (PRM) were applied to profile the urinary proteome. The differentially expressed proteins were subjected to Gene Ontology (GO) and protein-protein interaction (PPI) analysis. Results One hundred and sixty-four proteins significantly differed in the 4-VO rat urine samples compared to the control samples (1.5-fold change, p<0.05). GO analysis showed that the acute-phase response, the ERK1 and ERK2 cascade, endopeptidase activity, blood coagulation, and angiogenesis were overrepresented. After PRM validation, fifteen differentially expressed proteins were identified, and their expression was consistent with the DIA quantification. The abundance of FGG, COMP, TFF2, and HG2A was significantly changed only at 12 h after I/R injury. APOE, FAIM3, FZD1, IL1R2, UROK and CD48 were upregulated only at 48 h after I/R injury. KNG1, CATZ, PTGDS, PRVA and HEPC showed an overall trend of upregulation or downregulation at 12 and 48 h after I/R injury, reflecting the progression of cerebral I/R injury. Conclusion In this study, fifteen differentially expressed urinary proteins were identified and validated in a 4-VO rat model. Eight of these proteins were reported to be associated with cerebral I/R injury. These findings provide important clues to inform the monitoring of cerebral I/R injury and further the current understanding of its molecular biological mechanisms.

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