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Condition: Ischemic Stroke
Cancer: Neuroblastoma

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Total 54 results found since Jan 2013.

SIRT1/PGC-1 α signaling activation by mangiferin attenuates cerebral hypoxia/reoxygenation injury in neuroblastoma cells
This study is designed to investigate the protective effect of MGF treatment in the setting of cerebral IRI and to elucidate the potential mechanisms. We first evaluated the toxicity of MGF and chose the safe concentrations for the following experiments. MGF exerted obvious neuroprotection against hypoxia/reoxygenation (HR)-induced injury, indicated by restored cell viability and cell morphology, decreased lactate dehydrogenase (LDH) release and reactive oxygen species generation. MGF also restored the protein expressions of SIRT1, PGC-1α, Nrf2, NQO1, HO-1, NRF1, UCP2, and Bcl2 down-regulated by HR treatment. However, SIR...
Source: European Journal of Pharmacology - June 11, 2021 Category: Drugs & Pharmacology Authors: Mengfan Chen Zheng Wang Wenying Zhou Chenxi Lu Ting Ji Wenwen Yang Zhenxiao Jin Ye Tian Wangrui Lei Songdi Wu Qi Fu Zhen Wu Xue Wu Mengzhen Han Minfeng Fang Yang Yang Source Type: research

Neuroprotective effects of Senkyunolide I against glutamate-induced cells death by attenuating JNK/caspase-3 activation and apoptosis
Biomed Pharmacother. 2021 May 24;140:111696. doi: 10.1016/j.biopha.2021.111696. Online ahead of print.ABSTRACTGlutamate-induced neurotoxicity is one of the most important pathogenic mechanisms in neurological diseases and is widely used as an in vitro model for ischemic stroke. Senkyunolide I (SEI), an active constituent derived from traditional Chinese medicine Ligusticum chuanxiong Hort. and Angelica sinensis (Oliv.) Diels, has been shown to have beneficial effects against focal cerebral ischemia-reperfusion in rats. However, the mechanisms underlying SEI-mediated neuroprotection remain not well understood. Thus, we expl...
Source: Biomedicine and pharmacotherapy = Biomedecine and pharmacotherapie - May 27, 2021 Category: Drugs & Pharmacology Authors: Min Wang Hideki Hayashi Ichiro Horinokita Mayumi Asada Yui Iwatani Jian-Xun Liu Norio Takagi Source Type: research

Increase of Cry 1 expression is a common phenomenon of the disturbed circadian clock in ischemic stroke and opioid addiction
Biochem Biophys Res Commun. 2021 Apr 21;558:8-13. doi: 10.1016/j.bbrc.2021.04.053. Online ahead of print.ABSTRACTIncreasing evidences suggest the involvement of disrupted circadian clock in various pathologies including stroke and substance abuse. Here we took an attempt to do a comparative study on the regulation of circadian clock gene expression under two pathological circumstances - Opioid addiction and Ischemic stroke in the same cell line model (human neuroblastoma SH-SY5Y cells). To mimic in vivo ischemic stroke condition cells were placed in a hypoxia chamber and incubated for 10 h in balanced salt solution lacking...
Source: Biochemical and Biophysical Research communications - April 24, 2021 Category: Biochemistry Authors: Kaninika Roy Daytee Maji Ishani Deb Source Type: research

Effects of uric acid on oxidative and nitrosative stress and other related parameters in SH-SY5Y human neuroblastoma cells.
Uric acid (UA) is the end -product of purine catabolism in humans and higher primates and comprises about 65% of the total antioxidant capacity of plasma [1]. Urate circulates in humans at concentrations that are near its limit of solubility and many times higher than those in most other mammals. In patients with ischemic stroke, the most common type of stroke which is a leading cause of disability and the second most common cause of dementia, UA reduces the incidence of early clinical deterioration and improves outcomes compared to placebo [2].
Source: Prostaglandins, Leukotrienes and Essential Fatty Acids - December 30, 2020 Category: Biomedical Science Authors: Frederic M ármol, Juan Sanchez, Albert Martínez-Pinteño Source Type: research

LncRNA FOXD3-AS1 knockdown protects against cerebral ischemia/reperfusion injury via miR-765/BCL2L13 axis.
CONCLUSIONS: We verified a critical signaling pathway of FOXD3-AS1/miR-765/BCL2L13 in regulating cerebral ischemia/reperfusion injury. PMID: 33068927 [PubMed - as supplied by publisher]
Source: Biomedicine and pharmacotherapy = Biomedecine and pharmacotherapie - October 14, 2020 Category: Drugs & Pharmacology Authors: Lu Y, Han Y, He J, Zhou B, Fang P, Li X Tags: Biomed Pharmacother Source Type: research

miR ‑183‑5p attenuates cerebral ischemia injury by negatively regulating PTEN.
miR‑183‑5p attenuates cerebral ischemia injury by negatively regulating PTEN. Mol Med Rep. 2020 Sep 07;: Authors: Zhu L, Zhou X, Li S, Liu J, Yang J, Fan X, Zhou S Abstract Cerebral ischemia is a common cerebrovascular disease caused by the occlusion of a cerebral blood vessel. MicroRNAs (miRNAs/miRs) are emerging regulators of various human diseases, including cerebral ischemia. Upregulation of miR‑183‑5p has been reported to alleviate liver injury induced by ischemia‑reperfusion (I/R). However, the effect of miR‑183‑5p on cerebral ischemia injury remains unknown. The present study evalu...
Source: Molecular Medicine Reports - September 10, 2020 Category: Molecular Biology Tags: Mol Med Rep Source Type: research

PAQR3 protects against oxygen –glucose deprivation/reperfusion-induced injury through the ERK signaling pathway in N2A cells
AbstractCerebral ischemia –reperfusion injury is pivotal in the development of multiple-subcellular organelle and tissue injury after acute ischemic stroke. Recently, the Golgi apparatus (GA) has been shown to be a key subcellular organelle that plays an important role in neuroprotection against oxygen–glucose deprivatio n/reperfusion (OGD/R) injury. PAQR3, a scaffold protein exclusively localized in the GA, was originally discovered as a potential tumor suppressor protein. PAQR3 acts as a spatial regulator of Raf-1 that binds Raf-1 and sequesters it to the GA, where it negatively modulates the Ras/Raf/MEK/ERK signa li...
Source: Journal of Molecular Histology - May 24, 2020 Category: Laboratory Medicine Source Type: research

Upregulation of miR-219a-5p Decreases Cerebral Ischemia/Reperfusion Injury In Vitro by Targeting Pde4d
In this study, we explored the neuroprotective effects of miR-219a-5p on brain using an in vitro ischemia model (mouse neuroblastoma N2a cells treated with oxyglucose deprivation and reperfusion), and in vivo cerebral I/R model in mice.
Source: Journal of Stroke and Cerebrovascular Diseases - April 1, 2020 Category: Neurology Authors: Min-Yi Lu, Jin-Rong Wu, Rui-Bing Liang, Yu-Peng Wang, You-Cai Zhu, Zi-Ting Ma, Hao Zhang, Jie Zan, Wen Tan Source Type: research

Neuroprotective effects of miR-532-5p against ischemic stroke
In this study, we established anin vivo middle cerebral artery occlusion (MCAO) model in mice. The expression level of miR-532-5p, neurological score, infarct area, neuronal apoptosis, and phosphoinositide 3-kinase (PI3K)/Akt signaling pathway-related molecules were examined. Low miR-532-5p levels and high phosphatase and tensin homolog deleted on chromosome 10 (PTEN) levels were detected in the mouse MCAO model. MiR-532-5p overexpression improved neurological dysfunction, reduced the infarct area, attenuated neuronal injury and apoptosis, and promoted the activation of the PI3K/Akt signaling pathway in MCAO mice. In vitro...
Source: Metabolic Brain Disease - February 20, 2020 Category: Neurology Source Type: research

Early Transplantation of Human Cranial Bone-derived Mesenchymal Stem Cells Enhances Functional Recovery in Ischemic Stroke Model Rats.
Authors: Oshita J, Okazaki T, Mitsuhara T, Imura T, Nakagawa K, Otsuka T, Kurose T, Tamura T, Abiko M, Takeda M, Kawahara Y, Yuge L, Kurisu K Abstract We analyzed the cell characteristics, neuroprotective, and transplantation effects of human cranial bone-derived mesenchymal stem cells (hcMSCs) in ischemic stroke model rats compared with human iliac bone-derived mesenchymal stem cells (hiMSCs). The expressions of brain-derived neurotrophic factor (BDNF) and vascular endothelial growth factor (VEGF ) as neurotrophic factors were analyzed in both MSCs. hiMSCs or hcMSCs were intravenously administered into ischemic st...
Source: Neurologia Medico-Chirurgica - January 22, 2020 Category: Neurosurgery Tags: Neurol Med Chir (Tokyo) Source Type: research

Orexin-A protects against oxygen-glucose deprivation/reoxygenation-induced cell damage by inhibiting endoplasmic reticulum stress-mediated apoptosis via the Gi and PI3K signaling pathways.
Abstract The neuropeptide orexin-A (OXA) has a neuroprotective effect, acting as an anti-apoptotic factor in response to multiple stimuli. Apoptosis induced by endoplasmic reticulum stress (ERS) underlies oxygen-glucose deprivation and reoxygenation (OGD/R)-induced cell damage, an in vitro model of ischemia/reperfusion injury. However, that OXA inhibits ERS-induced apoptosis in the OGD/R model has not been reported. In the present study, we investigated the neuroprotective effect of OXA (0.1 μM) on OGD/R-induced damage in the human neuroblastoma cell line SH-SY5Y. After OXA treatment following 4 h oxygen-gluc...
Source: Cellular Signalling - June 20, 2019 Category: Cytology Authors: Kong T, Qiu K, Liu M, Cheng B, Pan Y, Yang C, Chen J, Wang C Tags: Cell Signal Source Type: research

The Effects of Intelectin-1 on Antioxidant and Angiogenesis in HUVECs Exposed to Oxygen Glucose Deprivation
Conclusion: These results suggest intelectin-1 promotes angiogenesis, inhibits oxidative stress and reduces apoptosis by stimulating the Akt-eNOS signaling pathway in response to ischemia in vitro. Introduction Stroke is a main reason of human neurological disability, ischemic stroke (IS) accounts for almost 80–90% of all strokes. IS occurs after a cerebral blood flow disruption, leading to cellular death and tissue damage by restricting glucose and oxygen supplies (1). Ischemic vascular diseases cause substantial vascular valve and vascular endothelial cell injuries, eventually damaging the surrounding tis...
Source: Frontiers in Neurology - April 15, 2019 Category: Neurology Source Type: research

Connecting Metainflammation and Neuroinflammation Through the PTN-MK-RPTP β/ζ Axis: Relevance in Therapeutic Development
Conclusion The expression of the components of the PTN-MK-RPTPβ/ζ axis in immune cells and in inflammatory diseases suggests important roles for this axis in inflammation. Pleiotrophin has been recently identified as a limiting factor of metainflammation, a chronic pathological state that contributes to neuroinflammation and neurodegeneration. Pleiotrophin also seems to potentiate acute neuroinflammation independently of the inflammatory stimulus while MK seems to play different -even opposite- roles in acute neuroinflammation depending on the stimulus. Which are the functions of MK and PTN in chronic neuroi...
Source: Frontiers in Pharmacology - April 11, 2019 Category: Drugs & Pharmacology Source Type: research