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Phenothiazines reduced autophagy in ischemic stroke through endoplasmic reticulum (ER) stress-associated PERK-eIF2 α pathway
CONCLUSION: The combined treatment of C + P plays a crucial role in stroke therapy by inhibiting ER stress-mediated autophagy, thereby leading to reduced apoptosis and increased neuroprotection. Our findings highlight the PERK-eIF2α pathway as a central mechanism through which C + P exerts its beneficial effects. The results from this study may pave the way for the development of more targeted and effective treatments for stroke patients.PMID:37673390 | DOI:10.1016/j.expneurol.2023.114524
Source: Experimental Neurology - September 6, 2023 Category: Neurology Authors: Shuyu Lv Xiaokun Geng Ho Jun Yun Yuchuan Ding Source Type: research

Long non-coding RNA Gm11974 aggravates oxygen –glucose deprivation-induced injury via miR-122-5p/SEMA3A axis in ischaemic stroke
This study aimed to investigate the role and potential mechanism of lncRNA Gm11974 in ischaemic stroke. Mouse  neuroblastoma N2a cells were treated with oxygen–glucose deprivation (OGD). The levels of Gm11974, microRNA-122-5p (miR-122-5p) and semaphorin 3A (SEMA3A) were detected by quantitative real-time PCR (qRT-PCR) or western blot. Cell viability and apoptosis were determined by 3-(4,5-dimethyl-2-thia zolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) assay, Caspase-3 Assay Kit and flow Cytometry. The levels of oxidative stress indicators were measured by using commercial kits. The relationship between miR-122-5p and ...
Source: Metabolic Brain Disease - August 2, 2021 Category: Neurology 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

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

Long non-coding RNA AK038897 aggravates cerebral ischemia/reperfusion injury via acting as a ceRNA for miR-26a-5p to target DAPK1.
Abstract Emerging evidence has suggested a significant role of long non-coding RNAs (lncRNAs) in ischemic stroke by acting as competing endogenous RNAs (ceRNAs) for microRNAs (miRNAs) to regulate certain RNA transcripts. AK038897 is an lncRNA that was reported to be upregulated in rat brains in response to transient focal ischemia. We aimed to investigate the possible regulatory role of AK038897 in ischemic stroke. We detected increased AK038897 and decreased miR-26a-5p levels in mouse brains following middle cerebral artery occlusion/reperfusion (MCAO/R) and in neuro-2A (N2a) neuroblastoma cells following oxygen-...
Source: Experimental Neurology - January 28, 2019 Category: Neurology Authors: Wei R, Zhang L, Hu W, Wu J, Zhang W Tags: Exp Neurol Source Type: research

Neuroprotective Effects of Isosteviol Sodium through Increasing CYLD by the Downregulation miRNA-181b.
In this study, we found that miR-181b expression was significantly decreased in N2A neuroblastoma cells after CoCl2-induced hypoxic injury in vitro. We further found, via western blot analysis and quantitative polymerase chain reaction assay, that altering miR-181b expression could induce changes in one of its target proteins, cylindromatosis (CYLD). Specifically, upregulation and downregulation of miR-181b (through transfection of either pre- or small interfering miR-181b, respectively) could negatively regulate CYLD protein levels as well as N2A cell survival rate and apoptosis following CoCl2-induced injury. Furthermore...
Source: Brain Research Bulletin - May 25, 2018 Category: Neurology Authors: Zhang H, Zan J, Zhong K, Lu M, Sun X, Tan W Tags: Brain Res Bull Source Type: research

The secretome of adipose-derived mesenchymal stem cells protects SH-SY5Y cells from arsenic-induced toxicity, independent of a neuron-like differentiation mechanism.
Abstract Arsenic exposure through contaminated food, water, and air causes irreversible neural damage and affects millions of people worldwide. Several studies have demonstrated that the secreted factors (secretome) from mesenchymal stromal/stem cells (MSCs) can promote neural recovery after several forms of injury including stroke and neurodegenerative diseases. The present study was conducted to determine if the secretome from adipose-derived MSCs (ADSCs) prevents arsenic damage to SH-SY5Y cells. To this end, human neuroblastoma cells (SH-SY5Y) were pre-treated with the secretome from ADSCs and then challenged w...
Source: Neurotoxicology - April 13, 2018 Category: Neurology Authors: Curtis TM, Hannett JM, Harman RM, Puoplo NA, Van de Walle GR Tags: Neurotoxicology Source Type: research

Curcumin protects neural cells against ischemic injury in N2a cells and mouse brain with ischemic stroke
ConclusionCurcumin promotes neuron survival in vivo and in vitro to exert neuroprotective effects against ischemia injury. Moreover, our results for the first time demonstrated curcumin inhibited ischemia‐induced mitochondrial apoptosis via restricting Bax activation, which may be one of the possible mechanisms underlying the neuroprotective effects of curcumin. Curcumin promotes neuron survival in vivo and in vitro to exert neuroprotective effects against ischemia injury. Moreover, our results for the first time demonstrated curcumin inhibited ischemia‐induced mitochondrial apoptosis via restricting Bax activation, w...
Source: Brain and Behavior - December 1, 2017 Category: Neurology Authors: Cai ‐Jun Xie, Ai‐Ping Gu, Jun Cai, Yi Wu, Rui‐Cong Chen Tags: ORIGINAL RESEARCH Source Type: research

Neurotrophic and neuroprotective effects of oxyntomodulin in neuronal cells and a rat model of stroke.
In this study, the neuroprotective effect of OXM was first examined in human neuroblastoma (SH-SY5Y) cells and rat primary cortical neurons. GLP-1R and GCGR antagonists, and inhibitors of various signaling pathways were used in cell culture to characterize the mechanisms of action of OXM. To evaluate translation in vivo, OXM-mediated neuroprotection was assessed in a 60-min, transient middle cerebral artery occlusion (MCAo) rat model of stroke. We found that OXM dose- and time-dependently increased cell viability and protected cells from glutamate toxicity and oxidative stress. These neuroprotective actions of OXM were mai...
Source: Experimental Neurology - November 13, 2016 Category: Neurology Authors: Li Y, Wu KJ, Yu SJ, Tamargo IA, Wang Y, Greig NH Tags: Exp Neurol Source Type: research

Silencing of Id2 attenuates hypoxia/ischemia-induced neuronal injury via inhibition of neuronal apoptosis.
This study was aimed to investigate whether knockdown of Id2 in neuronal cells could protect them from hypoxic and ischemic injury both in vitro and in vivo. Flow cytometric analysis was employed to assess neuronal apoptosis in CoCl2-treated neuroblastoma B35 cells engineered to overexpress or knockdown Id2 expression. In vivo knockdown of Id2 was performed in Sprague-Dawley rats by a single intracerebroventricular injection of Cy3-labeled and cholesterol-modified Id2-siRNA. We found that knockdown of Id2 attenuated H/I-induced neuronal apoptosis in vitro while overexpression of Id2 produced an opposite effect. In a rat mo...
Source: Behavioural Brain Research - July 14, 2015 Category: Neurology Authors: Guo L, Yang X, Lin X, Lin Y, Shen L, Nie Q, Ren L, Guo Q, Que S, Qiu Y Tags: Behav Brain Res Source Type: research

Type-1 interferons contribute to oxygen glucose deprivation induced neuro-inflammation in BE(2)M17 human neuroblastoma cells
Conclusions: This study confirms a role for type-1 IFN signalling in the neuro-inflammatory response following OGD in vitro and suggests its modulation through therapeutic blockade of IFNAR1 may be beneficial in reducing hypoxia-induced neuro-inflammation.
Source: Journal of Neuroinflammation - March 6, 2014 Category: Neurology Authors: Myles MinterMoses ZhangRobert AtesJuliet TaylorPeter Crack Source Type: research