scholarly journals The Dose-dependent Effects of Guibi-Tang on Focal Brain Ischemic Injury in Rats

2011 ◽  
Vol 22 (4) ◽  
pp. 201-218 ◽  
Author(s):  
Yun-Jai Gug ◽  
Jang-Ho Park ◽  
Jin-Hyung Kim ◽  
Hyang-Yi Kim ◽  
Hyung-Won Kang ◽  
...  
Keyword(s):  
Ischemic Injury ◽  
Brain Ischemic Injury ◽  
Dose Dependent

Abstract WP349: L-Glutamine Induces Heat Shock Protein 70 Expression & Attenuates Brain Ischemic Injury in Mice

Stroke ◽  
2019 ◽  
Vol 50 (Suppl_1) ◽  
Author(s):  
Longlong Luo ◽  
Yongfang Li ◽  
Fang Yuan ◽  
Liping Wang ◽  
Wanlu Li ◽  
...  
Keyword(s):  
Heat Shock ◽  
Heat Shock Protein ◽  
Heat Shock Protein 70 ◽  
Ischemic Injury ◽  
Brain Ischemic Injury

scholarly journals Brain ischemic injury in COVID‐19‐infected patients: a series of 10 post‐mortem cases

2020 ◽  
Author(s):  
Viscardo P. Fabbri ◽  
Maria P. Foschini ◽  
Tiziana Lazzarotto ◽  
Liliana Gabrielli ◽  
Giovanna Cenacchi ◽  
...  
Keyword(s):  
Ischemic Injury ◽  
Post Mortem ◽  
Brain Ischemic Injury

scholarly journals Poncirin suppresses lipopolysaccharide (LPS)-induced microglial inflammation and ameliorates brain ischemic injury in experimental stroke in mice

2020 ◽  
Vol 8 (21) ◽  
pp. 1344-1344
Author(s):  
Li-Xuan Yang ◽  
Fang-Yu Chen ◽  
Hai-Long Yu ◽  
Pin-Yi Liu ◽  
Xin-Yu Bao ◽  
...  
Keyword(s):  
Ischemic Injury ◽  
Experimental Stroke ◽  
Brain Ischemic Injury ◽  
Microglial Inflammation

Erythropoietin protects against brain ischemic injury by inhibition of nitric oxide formation

2000 ◽  
Vol 401 (3) ◽  
pp. 349-356 ◽  
Author(s):  
Gioacchino Calapai ◽  
Maria C Marciano ◽  
Francesco Corica ◽  
Alessandro Allegra ◽  
Alessandra Parisi ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Ischemic Injury ◽  
Oxide Formation ◽  
Nitric Oxide Formation ◽  
Brain Ischemic Injury

scholarly journals CX3CL1/CX3CR1-Mediated Microglia Activation Plays a Detrimental Role in Ischemic Mice Brain via p38MAPK/PKC Pathway

2015 ◽  
Vol 35 (10) ◽  
pp. 1623-1631 ◽  
Author(s):  
Yong Liu ◽  
Xiao-Mei Wu ◽  
Qian-Qian Luo ◽  
Suna Huang ◽  
Qing-Wu Qian Yang ◽  
...  
Keyword(s):  
White Matter ◽  
Protein Kinase ◽  
Inflammatory Cytokines ◽  
White Matter Lesions ◽  
Ischemic Injury ◽  
Microglia Activation ◽  
Tnf Α ◽  
Brain Ischemic Injury ◽  
Mice Brain

The exact roles of activated microglia and fractalkine (CX3CL1)/fractalkine receptor (CX3CR1) signaling are not fully understood in brain ischemic injury and the findings reported are controversial. Here, we investigated the effects of CX3CR1 siRNA on the expression of CX3CR1, p38 mitogen-activated protein kinase (p38MAPK), Protein Kinase C (PKC) and inflammatory cytokines, microglia activation, white matter lesions, and cognitive function in mice treated with bilateral common carotid artery stenosis (BCAS) in vivo as well as effects of exogenous CX3CL1, CX3CR1 siRNA, and SB2035080 on expression of inflammatory cytokines in BV2 microglia treated with oxygen–glucose deprivation (OGD) in vitro. We showed that CX3CR1 siRNA significantly inhibited the increased expression of CX3CR1, p38MAPK, PKC as well as tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, and IL-6, and also attenuated microglia activation, white matter lesions, and cognitive deficits induced by BCAS in mice brain. We also showed that exogenous CX3CL1 could induce a further enhancement in TNF-α and IL-1β expression, which could be suppressed by CX3CR1 siRNA or by the p38MAPK inhibitor in OGD-treated BV2 microglial cells in vitro. Our findings indicated that CX3CL1/CX3CR1-mediated microglial activation plays a detrimental role in ischemic brain via p38MAPK/PKC signaling and also suggested that CX3CL1/CX3CR1 axis might be a putative therapeutic target to disrupt the cascade of deleterious events that lead to brain ischemic injury.

scholarly journals Hydroxysafflor Yellow A Blocks HIF-1α Induction of NOX2 and Protects ZO-1 Protein in Cerebral Microvascular Endothelium

2021 ◽  
Author(s):  
Yi Li ◽  
Xiaotian Liu ◽  
Peilin Zhang ◽  
Yuchen Li ◽  
Mengru Sun ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Ischemic Injury ◽  
Carthamus Tinctorius ◽  
Ros Generation ◽  
Hydroxysafflor Yellow A ◽  
Microvascular Endothelium ◽  
Von Hippel Lindau ◽  
Gene Assay ◽  
Brain Ischemic Injury ◽  
Endothelial Integrity

Abstract Background: Zonula occludens-1 (ZO-1) protein ensures cerebrovascular integrity against brain ischemic injury. Hydroxysafflor yellow A (HSYA) is a major ingredient of safflower (Carthamus tinctorius L.) with anti-oxidative activity. Because conventional ROS scavengers display poor reactivity with endogenous ROS, this study investigated whether HSYA protected ZO-1 by targeting the enzymes responsible for ROS generation.Methords: Photothrombotic stroke model was prepared in mice to evaluate the protective effect of HSYA on cerebrovascular endothelium. The molecular regulation was investigated in cultured cerebral microvascular endothelial cells (bEnd.3 cells).Results: Oral administration of HSYA (50 mg/kg) reduced cerebral vascular leakage with ZO-1 protection in mice after stroke, largely due to suppression of ROS-associated inflammation. In LPS-stimulated bEnd.3 cells, HSYA increased the ratio of NAD+/NADH to restore Sirt1 induction, which bound to Von Hippel-Lindau (VHL) to ensure HIF-1α protein degradation. Although both NOX1 and NOX2 isoforms were inducible in endothelial cells, we identified NOX2 as the driving force of ROS production. Chromatin immunoprecipitation and luciferase report gene assay revealed that HIF-1α transcriptionally regulated p47phox and Nox2 subunits for the assembly of NOX2 complex, which was blocked by HSYA treatment, largely by reducing HIF-1α accumulation. Inflammation-associated lipid peroxidation impaired ZO-1 protein, but HSYA treatment attenuated carbonyl modification and thus prevented ZO-1 protein from 20S proteasome-mediated degradation, eventually protecting endothelial integrity. In microvascular ZO-1 deficient mice, we further confirmed that HSYA protected cerebrovascular integrity and attenuated ischemic injury dependent on ZO-1 protection. Conclusions: HSYA blocked HIF-1α/NOX2 signaling cascades to protect ZO-1 from proteasomal degradation, suggesting that targeting NOX2 in endothelium is a potential therapeutic strategy to protect against ischemic brain injury.

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