scholarly journals Propofol protects hippocampal neurons from apoptosis in ischemic brain injury by increasing GLT-1 expression and inhibiting the activation of NMDAR via the JNK/Akt signaling pathway

2016 ◽  
Vol 38 (3) ◽  
pp. 943-950 ◽  
Author(s):  
Hong-Yan Gong ◽  
Fang Zheng ◽  
Chao Zhang ◽  
Xi-Yan Chen ◽  
Jing-Jing Liu ◽  
...  
Keyword(s):  
Brain Injury ◽  
Signaling Pathway ◽  
Hippocampal Neurons ◽  
Akt Signaling ◽  
Ischemic Brain Injury ◽  
Akt Signaling Pathway ◽  
Ischemic Brain

scholarly journals RETRACTED ARTICLE:Bone mesenchymal stem cell-derived exosomal microRNA-29b-3p prevents hypoxic-ischemic injury in rat brain by activating the PTEN-mediated Akt signaling pathway

2020 ◽  
Vol 17 (1) ◽  
Author(s):  
Kun Hou ◽  
Guichen Li ◽  
Jinchuan Zhao ◽  
Baofeng Xu ◽  
Yang Zhang ◽  
...  
Keyword(s):  
Brain Injury ◽  
Signaling Pathway ◽  
Akt Signaling ◽  
Luciferase Reporter ◽  
Ischemic Brain Injury ◽  
Akt Signaling Pathway ◽  
Ischemic Brain ◽  
Hypoxic Ischemic Brain Injury ◽  
The Brain

Abstract Background Mesenchymal stem cells (MSCs) are suspected to exert neuroprotective effects in brain injury, in part through the secretion of extracellular vesicles like exosomes containing bioactive compounds. We now investigate the mechanism by which bone marrow MSCs (BMSCs)-derived exosomes harboring the small non-coding RNA miR-29b-3p protect against hypoxic-ischemic brain injury in rats. Methods We established a rat model of middle cerebral artery occlusion (MCAO) and primary cortical neuron or brain microvascular endothelial cell (BMEC) models of oxygen and glucose deprivation (OGD). Exosomes were isolated from the culture medium of BMSCs. We treated the MCAO rats with BMSC-derived exosomes in vivo, and likewise the OGD-treated neurons and BMECs in vitro. We then measured apoptosis- and angiogenesis-related features using TUNEL and CD31 immunohistochemical staining and in vitro Matrigel angiogenesis assays. Results The dual luciferase reporter gene assay showed that miR-29b-3p targeted the protein phosphatase and tensin homolog (PTEN). miR-29b-3p was downregulated and PTEN was upregulated in the brain of MCAO rats and in OGD-treated cultured neurons. MCAO rats and OGD-treated neurons showed promoted apoptosis and decreased angiogenesis, but overexpression of miR-29b-3p or silencing of PTEN could reverse these alterations. Furthermore, miR-29b-3p could negatively regulate PTEN and activate the Akt signaling pathway. BMSCs-derived exosomes also exerted protective effects against apoptosis of OGD neurons and cell apoptosis in the brain samples from MCAO rats, where we also observed promotion of angiogenesis. Conclusion BMSC-derived exosomal miR-29b-3p ameliorates ischemic brain injury by promoting angiogenesis and suppressing neuronal apoptosis, a finding which may be of great significance in the treatment of hypoxic-ischemic brain injury.

scholarly journals Hemin-mediated neuroglobin induction exerts neuroprotection following ischemic brain injury through PI3K/Akt signaling

2013 ◽  
Vol 8 (2) ◽  
pp. 681-685 ◽  
Author(s):  
BEI ZHANG ◽  
XIUPING JI ◽  
SHIJUN ZHANG ◽  
HUIYUN REN ◽  
MINJUAN WANG ◽  
...  
Keyword(s):  
Brain Injury ◽  
Akt Signaling ◽  
Ischemic Brain Injury ◽  
Ischemic Brain

scholarly journals Macamide B Pretreatment Attenuates Neonatal Hypoxic-Ischemic Brain Damage of Mice Induced Apoptosis by Regulates Autophagy Via The PI3K/AKT Signaling Pathway

2021 ◽  
Author(s):  
Xiaoxia Yang ◽  
Mengxia Wang ◽  
Qian Zhou ◽  
Yanxian Bai ◽  
Jing Liu ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Brain Damage ◽  
Infarct Volume ◽  
Neuroprotective Effect ◽  
Akt Signaling ◽  
Akt Signaling Pathway ◽  
Ischemic Brain Damage ◽  
Ischemic Brain ◽  
Induced Apoptosis ◽  
The Impact

Abstract Lepidium meyenii (Maca) is an annual or biennial herb from South America that is a member of the genus Lepidium L. in the family Cruciferae. This herb has antioxidant, anti-apoptotic, and enhances autophagy functions and can prevent cell death, and protect neurons from ischemic damage. Macamide B, an effective active ingredient of maca, has a neuroprotective role in neonatal hypoxic-ischemic brain damage (HIBD), and the underlying mechanism of its neuroprotective effect is not yet known. The purpose of this study is to explore the impact of macamide B on HIBD-induced autophagy and apoptosis and its potential mechanism for neuroprotection. The modified Rice-Vannucci method was used to induce HIBD on 7-day-old (P7) macamide B and vehicle-pretreated pups. TTC staining was used to evaluate the cerebral infarct volume of pups, brain water content was measured to evaluate the neurological function of pups, neurobehavioral testing was used to assess functional recovery after HIBD, TUNEL and FJC staining was used to detect cell autophagy and apoptosis, and western blot analysis was used to detect the expression levels of the pro-survival signaling pathway phosphatidylinositol-3-kinase/protein kinase B (PI3K/AKT) and autophagy and the apoptosis-related proteins. The results show that macamide B pretreatment can significantly decrease brain damage, improve the recovery of neural function after HIBD. At the same time, macamide B pretreatment can induce the activation of PI3K/AKT signaling pathway after HIBD, enhance autophagy, and reduce hypoxic-ischemic (HI)-induced apoptosis. In addition, 3-methyladenine (3-MA), an inhibitor of PI3K/AKT signaling pathway, significantly inhibits the increase in autophagy levels, aggravates HI-induced apoptosis, and reverses the neuroprotective effect of macamide B on HIBD. Our data indicate that macamide B pretreatment might regulate autophagy through PI3K/AKT signaling pathway, thereby reducing HIBD-induced apoptosis and exerting neuroprotective effects on neonatal HIBD. Macamide B may become a new drug for the prevention and treatment of HIBD.

scholarly journals Metformin ameliorates sepsis-induced brain injury by inhibiting apoptosis, oxidative stress and neuroinflammation via the PI3K/Akt signaling pathway

Oncotarget ◽  
2017 ◽  
Vol 8 (58) ◽  
pp. 97977-97989 ◽  
Author(s):  
Guangming Tang ◽  
Huiyun Yang ◽  
Jing Chen ◽  
Mengrao Shi ◽  
Lingqing Ge ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Brain Injury ◽  
Signaling Pathway ◽  
Akt Signaling ◽  
Akt Signaling Pathway

5-LOX Inhibitor Zileuton Reduces Inflammatory Reaction and Ischemic Brain Damage Through the Activation of PI3K/Akt Signaling Pathway

2016 ◽  
Vol 41 (10) ◽  
pp. 2779-2787 ◽  
Author(s):  
Xian-kun Tu ◽  
Hua-bin Zhang ◽  
Song-sheng Shi ◽  
Ri-sheng Liang ◽  
Chun-hua Wang ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Brain Damage ◽  
Inflammatory Reaction ◽  
Akt Signaling ◽  
Akt Signaling Pathway ◽  
Ischemic Brain Damage ◽  
Ischemic Brain
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