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Non-coding RNAs in acute ischemic stroke:from brain to periphery
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作者 Shuo Li Zhaohan Xu +7 位作者 Shiyao Zhang Huiling Sun Xiaodan Qin Lin Zhu Teng Jiang Junshan Zhou fuling yan Qiwen Deng 《Neural Regeneration Research》 SCIE CAS 2025年第1期116-129,共14页
Acute ischemic stroke is a clinical emergency and a condition with high morbidity,mortality,and disability.Accurate predictive,diagnostic,and prognostic biomarkers and effective therapeutic targets for acute ischemic ... Acute ischemic stroke is a clinical emergency and a condition with high morbidity,mortality,and disability.Accurate predictive,diagnostic,and prognostic biomarkers and effective therapeutic targets for acute ischemic stroke remain undetermined.With innovations in high-throughput gene sequencing analysis,many aberrantly expressed non-coding RNAs(ncRNAs)in the brain and peripheral blood after acute ischemic stroke have been found in clinical samples and experimental models.Differentially expressed ncRNAs in the post-stroke brain were demonstrated to play vital roles in pathological processes,leading to neuroprotection or deterioration,thus ncRNAs can serve as therapeutic targets in acute ischemic stroke.Moreover,distinctly expressed ncRNAs in the peripheral blood can be used as biomarkers for acute ischemic stroke prediction,diagnosis,and prognosis.In particular,ncRNAs in peripheral immune cells were recently shown to be involved in the peripheral and brain immune response after acute ischemic stroke.In this review,we consolidate the latest progress of research into the roles of ncRNAs(microRNAs,long ncRNAs,and circular RNAs)in the pathological processes of acute ischemic stroke–induced brain damage,as well as the potential of these ncRNAs to act as biomarkers for acute ischemic stroke prediction,diagnosis,and prognosis.Findings from this review will provide novel ideas for the clinical application of ncRNAs in acute ischemic stroke. 展开更多
关键词 acute ischemic stroke apoptosis blood–brain barrier damage circular RNAs excitatory toxicity long non-coding RNAs MICRORNAS NEUROINFLAMMATION non-coding RNAs oxidative stress
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Waking Up Brain with Electrical Stimulation to Boost Memory in Sleep:A Neuroscience Exploration
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作者 Zhe Zhong fuling yan Chunming Xie 《Neuroscience Bulletin》 SCIE CAS CSCD 2024年第6期852-854,共3页
Imagine that,in the future,you could enhance your memory by applying a mild electric current to your brain during sleep.This might sound like science fiction,but it is based on cutting-edge neuroscience research.Sleep... Imagine that,in the future,you could enhance your memory by applying a mild electric current to your brain during sleep.This might sound like science fiction,but it is based on cutting-edge neuroscience research.Sleep is widely recognized as a crucial factor for long-term memory consolidation,but the exact mechanisms by which the brain coordinates neural activity across different regions during sleep to reorganize and integrate memories are unknown[1,2]. 展开更多
关键词 SLEEP INTEGRATE APPLYING
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Influence of Ginkgo Biloba extract on beta-secretase in rat hippocampal neuronal cultures following chronic hypoxic and hypoglycemic conditions 被引量:2
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作者 Xueneng Guan fuling yan 《Neural Regeneration Research》 SCIE CAS CSCD 2008年第10期1065-1069,共5页
BACKGROUND: Preparation of Ginkgo leaf has been widely used to improve cognitive deficits and dementia, in particular in Alzheirner's disease patients. However, the precise mechanism of action of Ginkgo leaf remains... BACKGROUND: Preparation of Ginkgo leaf has been widely used to improve cognitive deficits and dementia, in particular in Alzheirner's disease patients. However, the precise mechanism of action of Ginkgo leaf remains unclear. OBJECTIVE: To explore the effect of Ginkgo Biloba extract (Egb761), Ginaton, on β -secretase expression in rat hippocampal neuronal cultures following chronic hypoxic and hypoglycemic conditions. DESIGN, TIME AND SETTNG: Completely by randomized, grouping study. The experiment was performed at the Laboratory of Molecular Imaging, Southeast University between August 2006 and August 2007. MATERIALS: A total of 128 Wistar rats aged 24 hours were selected, and hippocampal neurons were harvested for primary cultures. METHODS: On day 7, primary hippocampal neuronal cultures were treated with Egb761 (0, 25, 50, 100, 150, and 200μg/mL) under hypoxic/hypoglycemic or hypoglycemic culture conditions for 12, 24, and 36 hours, respectively. Hippocampal neurons cultured in primary culture medium served as control. MAIN OUTCOME MEASURES: Cell viability was assayed using 3-(4,5-Dimethylthiazol-2-yl)- 2,5-diphenyltetrazolium bromide (MTT); fluorescence detection of β -secretase activity was performed; Western Blot was used to measure β -secretase expression. RESULTS: Cell viability under hypoxic/hypoglycemic or hypoglycemic culture conditions was significantly less than control cells (P 〈 0.05). Under hypoxic/hypoglycemic or hypoglycemic culture conditions, treatment with 25 μg/mL Egb761 did not alter cell viability. However, 〉 25 μg/mL Egb761 induced greater cell viability (P 〈 0.05). No differences were observed between hypoxic/hypoglycemic or hypoglycemic cells (P 〉 0.05). α -secretase activity was increased after 12 hours in hypoxic/hypoglycemic culture (P 〈 0.01). There were no significant differences between the 12-, 24-, or 36-hour Egb761 groups and the hypoxic/hypoglycemic groups (P 〉 0.05). β -secretase activity was greater after 12, 24, and 36 hours in hypoxic/hypoglycemic culture conditions, compared with control conditions (P 〈 0.05). β-secretase activity was significantly decreased in neurons treated with Egb761 for 12, 24, or 36 hours, compared with the hypoxichaypoglycemic group (P 〈 0.05). β -secretase protein expression was significantly up-regulated in neurons cultured in hypoxic/hypoglycemic conditions for 12, 24, or 36 hours, compared to control cells (P 〈 0.05), and was decreased compared to neurons treated with Egb761 (P 〈 0.05). CONCLUSION: β -secretase expression and activity in rat neonatal hippocampal neurons were influenced by hypoxic and hypoglycemic culture. Egb761 played a protective role in hippocampal neurons damaged by chronic hypoxic and hypoglycemic culture conditions, possibly through its effect on β -secretase expression and activity. 展开更多
关键词 α -secretase β -secretase Alzheirner's disease chronic hypoxia hippocampal neuron HYPOGLYCEMIA
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