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Evidence that enolase-phosphatase 1 exacerbates early cerebral ischemia injury and blood-brain barrier breakdown by enhancing extracellular matrix destruction and inhibiting the interaction between ADI1 and MT1-MMP
In this study, we systematically provide mechanistic insights into the regulation of ENOPH1 in blood-brain barrier (BBB) dysfuction induced by early ischemia. ENOPH1 knockout mice (ENOPH1 KO) and wild type (WT) mice were exposed to transient middle cerebral artery occlusion (tMCAO) for 90 min followed by 3 h of reperfusion in vivo, and brain microvascular endothelial cell lines (bEnd.3 cells) were exposed to oxygen-glucose deprivation (OGD) in vitro. BEnd.3 cells were transfected with ENOPH1 shRNA to knockdown ENOPH1 expression. Brain ischemic damage and nerve function was assessed with 2, 3, 5-triphenyltetrazolium chlorid...
Source: Experimental Neurology - April 17, 2023 Category: Neurology Authors: Dexin Yang Li Su Xiaofeng Li Cong Xie Yuan Zhang Source Type: research

Pseudoginsenoside F11 ameliorates the dysfunction of the autophagy-lysosomal pathway by activating calcineurin-mediated TFEB nuclear translocation in neuron during permanent cerebral ischemia.
Abstract We have previously found that transcription factor EB (TFEB), as a master regulator of autophagy and lysosome biogenesis, provides neuroprotective effects on cerebral ischemia-induced neuronal damage by activation of autophagy-lysosomal pathway (ALP). We have also reported that Pseudoginsenoside F11 (PF11), an ocotillol-type saponin isolated from Panax quinquefolium L., significantly attenuates the ischemic injury of rats subjected to permanent middle cerebral artery occlusion (pMCAO), possibly by alleviating the autophagic/lysosomal defects. The present study aims to investigate whether the beneficial ef...
Source: Experimental Neurology - January 7, 2021 Category: Neurology Authors: Fu X, Liu Y, Zhang H, Yu X, Wang X, Wu C, Yang J Tags: Exp Neurol Source Type: research

NPD1 rapidly targets mitochondria-mediated apoptosis after acute injection protecting brain against ischemic injury.
Abstract Mitochondria-related cell death pathways play a major role in ischemic brain injury. Thus, mitochondrial "protective" molecules could be considered for new therapeutic regimens. We recently reported that acute administration of docosahexaenoic acid (DHA) triglyceride lipid emulsion, immediately after hypoxic-ischemic (HI) insult, markedly attenuated brain infarct size. This was associated with an early change of DHA-derived specialized pro-resolving mediator (SPM) profiles. Specifically, DHA treatment induced a 50% increase of neuroprotectin D1 (NPD1) levels in ischemic brain. Based on these findings, we ...
Source: Experimental Neurology - October 7, 2020 Category: Neurology Authors: Zirpoli H, Sosunov SA, Niatsetskaya ZV, Mayurasakorn K, Kollareth DJM, Serhan CN, Ten VS, Deckelbaum RJ Tags: Exp Neurol Source Type: research

Astrocytic Yes-associated protein attenuates cerebral ischemia-induced brain injury by regulating signal transducer and activator of transcription 3 signaling.
In this study, we investigated whether the expression of nuclear YAP in the astrocytes of rats increased significantly after middle cerebral artery occlusion (MCAO) and its effect on cerebral ischemic injury. We used XMU-MP-1 to trigger localization of YAP into the nucleus and found that XMU-MP-1 treatment decreased ischemia/stroke-induced brain injury including reduced neuronal death and reactive astrogliosis, and extenuated release of interleukin-1β (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α). Mechanically, XMU-MP-1 treatment suppressed the expression of phospho-STAT3 (P-STAT3). We established ...
Source: Experimental Neurology - July 31, 2020 Category: Neurology Authors: Huang L, Li S, Dai Q, Zhang A, Yu Q, Du W, Zhao P, Mo Y, Xu K, Chen S, Wang J Tags: Exp Neurol Source Type: research

Adiponectin peptide alleviates oxidative stress and NLRP3 inflammasome activation after cerebral ischemia-reperfusion injury by regulating AMPK/GSK-3 β.
Adiponectin peptide alleviates oxidative stress and NLRP3 inflammasome activation after cerebral ischemia-reperfusion injury by regulating AMPK/GSK-3β. Exp Neurol. 2020 Apr 07;:113302 Authors: Liu H, Wu X, Luo J, Zhao L, Li X, Guo H, Bai H, Cui W, Guo W, Feng D, Qu Y Abstract The effects of current treatment strategies for ischemic stroke are weakened by ischemia-reperfusion (I/R) injury. Effective treatments targeting I/R injury are still insufficient. Adiponectin (APN), a fat-derived hormone, has a wide range of antioxidative and anti-inflammatory effects. However, the application of APN to the cen...
Source: Experimental Neurology - April 6, 2020 Category: Neurology Authors: Liu H, Wu X, Luo J, Zhao L, Li X, Guo H, Bai H, Cui W, Guo W, Feng D, Qu Y Tags: Exp Neurol Source Type: research

Botch protects neurons from ischemic insult by antagonizing Notch-mediated neuroinflammation.
In conclusion, we found that Botch exerts neuroprotective effects via antagonizing the maturation of Notch1-induced neuronal injury and neuroinflammation, which may provide insights into novel therapeutic targets for the treatment of I/R injury. PMID: 31377404 [PubMed - as supplied by publisher]
Source: Experimental Neurology - July 31, 2019 Category: Neurology Authors: Li H, Ma J, Fang Q, Li H, Shen H, Li X, Xue Q, Zhu J, Chen G Tags: Exp Neurol Source Type: research

High-mobility group box-1 translocation and release after hypoxic ischemic brain injury in neonatal rats.
Abstract Inflammation contributes to neonatal brain injury. Pro-inflammatory cytokines represent key inflammatory meditators in neonatal hypoxic-ischemic (HI) brain injury. The high mobility group box-1 (HMGB1) protein is a nuclear protein with pro-inflammatory cytokine properties when it is translocated from the nucleus and released extracellularly after stroke in adult rodents. We have previously shown that HMGB1 is translocated from the nucleus to cytosolic compartment after ischemic brain injury in fetal sheep. In the current study, we utilized the Rice-Vannucci model to investigate the time course of HMGB1 tr...
Source: Experimental Neurology - September 11, 2018 Category: Neurology Authors: Chen X, Zhang J, Kim B, Jaitpal S, Meng SS, Adjepong K, Imamura S, Wake H, Nishibori M, Stopa EG, Stonestreet BS Tags: Exp Neurol Source Type: research

Sigma-1 receptor activation alleviates blood-brain barrier dysfunction in vascular dementia mice.
Abstract Sigma-1 receptor (Sig-1R) activation has been shown to decrease infarct volume and enhance neuronal survival after brain ischemia-reperfusion (IR) in rodent models. The present study aims to investigate first the effect of Sig-1R activation on blood-brain barrier (BBB) disruption during experimental stroke. Male C57BL/6 mice were subjected to bilateral common carotid artery occlusion (BCCAO) for 15 min, and the worst BBB leakage was observed on the 7th day after brain IR. To confirm the BBB protective role of Sig-1R, mice were divided into five groups (sham group, BCCAO group, PRE084 group, BD1047 group...
Source: Experimental Neurology - July 10, 2018 Category: Neurology Authors: Liu DY, Chi TY, Ji XF, Liu P, Qi XX, Zhu L, Wang ZQ, Lin-Li, Chen L, Zou LB Tags: Exp Neurol Source Type: research