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440 results for “Neuroprotection”
Data from: Neuroprotection provided by hypothermia initiated with high transnasal flow with ambient air in a model of pediatric cardiac arrest
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Restoration of striatal neuroprotective pathways by kinase inhibitor treatment of Parkinson’s linked-LRRK2 mutant mice
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Code for: Multi-modal screening for synergistic neuroprotection of mild extremely preterm brain injury: Cell counting code repository
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Data from: A short peptide exerts neuroprotective effects on cerebral ischemia-reperfusion injury by reducing inflammation via the miR-6328/IKKβ/NF-κB axis
<p><strong><span>Background</span></strong></p> <p><span>Despite considerable efforts, ischemic stroke (IS) remains a challenging clinical problem. Therefore, the discovery of effective therapeutic and targeted drugs based on the underlying molecular mechanism is crucial for effective IS treatment.</span></p> <p><strong><span>Methods</span></strong></p> <p><span>A cDNA-encoding peptide was extracted and identified from RNA extracted from <em>Rana limnocharis</em> skin, and its neuroprotective properties were evaluated using a middle cerebral artery occlusion/reperfusion (MCAO/R) model in rats and an oxygen-glucose deprivation/reperfusion (OGD/R) model in neuron-like PC12 cells. The underlying molecular mechanisms were explored using microRNA (miRNA) sequencing, quantitative real-time polymerase chain reaction</span><span>, dual-luciferase reporter gene assay, and western blotting.</span></p> <p><strong><span>Results</span></strong></p> <p><span>A new peptide (NP1) with an amino acid sequence of '</span><span>FLPAAICLVIKTC</span><span>' was identified. NP1 showed no obvious toxicities <em>in vivo</em> and <em>in vitro</em>. I</span><span>ntraperitoneal administration of NP1 (10 nmol/kg) effectively reduced the volume of cerebral infarction and relieved neurological dysfunction in MCAO/R model rats. Moreover, NP1 significantly alleviated the decrease in viability of PC12 cells induced by OGD/R. NP1 effectively suppressed inflammation by reducing interleukin-1β (</span><span>IL-1β) and </span><span>tumor necrosis factor-</span><span>α (</span><span>TNF-α) levels </span><em><span>in vitro</span></em><span> and <em>in vivo</em>. Furthermore, NP1 up-regulated the expression of miRNA-6328, which targeted down-regulation of the inflammation-related factor inhibitor kappa B kinase β (</span><span>IKKβ),</span><span> thereby reducing nuclear factor-kappa B p65</span><span> (NF-κB</span><span> p65) and inhibitor of </span><span>NF-κB</span><span> (I-</span><span>κ</span><span>B) phosphorylation and inhibiting the </span><span>NF-κB</span><span> pathway.</span></p> <p><strong><span>Conclusions</span></strong></p> <p><span>NP1 exerted neuroprotective effects by reducing inflammation via the miRNA-6328/IKKβ/NF-κB axis. This study highlights the importance of peptides in the development of new drugs, elucidation of </span><span>pathological mechanisms, and discovery of new drug targets.</span></p>
Fig. 6 in Insight into tetrahydrofuran lignans from Isatis indigotica fortune with neuroprotective and acetylcholinesterase inhibitor activity
Fig. 6. The neuroprotective effects of compounds 1a/1b-7 against H2O2-induced injury in SH-SY5Y cells. After H2O2 (200 μM) treatment, cell viabilities were determined by MTT assay in the presence or absence of the tested compounds at different concentrations (12.5, 25, 50 μM).
Fig. 5 in Phenolic compounds from the flowers of Rosa hugonis Hemsl. and their neuroprotective effects
Fig. 5. Effects of compound 5 on PI3K/Akt/GSK-3β signaling pathway in 6- OHDA induced PC12 cells. The levels of total or phosphorylated PDK1, Akt and GSK-3β were identified by Western blot. β-Actin was used as a control.
Fig. 4 in Phenolic compounds from the flowers of Rosa hugonis Hemsl. and their neuroprotective effects
Fig. 4. Effects of compound 5 on 6-OHDA-induced ROS generation. (A) PC12 cell were treated with different concentration of compound 5 before exposure to 6- OHDA for 24 h. Cells were then stained with DCFH-DA. (a) Control; (b) 6-OHDA group; (c) 6-OHDA and 5 μM compound 5 treatment; (d) 6-OHDA and 10 μM compound 5 treatment. (B–C) PC12 cell were treated with different concentration of compound 5 before exposure to 6-OHDA for 24 h. The relative mRNA expression levels of SOD and CAT were determined by RT-qPCR. The values are presented as the mean ± SD (n = 3). *p <0.05 versus 6-OHDA group; #p <0.05 versus control group.
Fig. 3 in Phenolic compounds from the flowers of Rosa hugonis Hemsl. and their neuroprotective effects
Fig. 3. Effects of compound 5 on 6-OHDA-induced PC12 cell injury. (A) PC12 cells were preincubated with different concentration of compound 5 for 30 min and then exposed to 6-OHDA for 24 h. The values are presented as the mean ±SD (n =3). *p <0.05 versus 6-OHDA group; #p <0.05 versus control group. (B) PC12 cells were treated with different concentration of compound 5 for 24 h. The values are presented as the mean ± SD (n = 3). *p <0.05 versus control group. (C) The changes of morphology of PC12 cells in present of compound 5. (a) Control; (b) 6-OHDA group; (c) 6-OHDA and 5 μM compound 5 treatment; (d) 6-OHDA and 10 μM compound 5 treatment.
Fig. 6 in Diversity of sesquiterpenoids from Stellera chamaejasme with neuroprotective effects
Fig. 6. Neuroprotective effects of compounds on SNP-induced neurotoxicity in PC-12 cells. (A) Effects of compounds 1–20 on SNP-induced injury in PC12 cells at a concentration of 10 μM. Cells were pretreated with or without samples (1–20 and the positive control Eda) at for 2 h and then incubated with or without SNP (600 μM) for another 24 h. Cell viability was evaluated by the MTT method (n = 3). *p <0.05, **p <0.01, and ***p <0.001 compared with SNP alone group. (B) Effects of active compounds 5, 10, 11, 15, 16, and 18 on SNP-induced injury in PC12 cells at the concentrations of 2.5, 5, and 10 μM. The treatment and result analysis of the experiment were described as above. (C) Effects of the most active compound 11 on ROS production in PC-12 cells. After the pretreatment of the cells with or without 11 (10 μM) for 2 h, the cells were then exposed to SNP (600 μM) for another 24 h and followed by incubation with DCFH-DA (20 μM) for 30 min. Photography was taken with a fluorescence microscope. (D) Compound 11 could restore the MMP of PC-12 cells induced by SNP. Cells were pretreated with or without 11 (10 μM) for 2 h and then exposed to SNP (600 μM) for another 24 h. The MMP was measured by the JC-1 dye method. (E) Effects of 11 on level of Ho-1 mRNA in PC-12 cells. Cells were pretreated with or without indicated concentrations of 11 for 2 h and then incubated with or without SNP (600 μM) for another 24 h. After that, the targeted mRNA (Ho-1) was detected by quantitative realtime RT-PCR. The mRNA level was normalized to Gapdh and expressed as fold changes of the control (n = 3). *p <0.05 and ***p <0.001 versus the control (CT) group.
Fig. 3 in Diversity of sesquiterpenoids from Stellera chamaejasme with neuroprotective effects
Fig. 3, the observed NOE correlations of H-5/7-OH, H-5/H-9α, 7-OH/H-6α, and H-6α/H3-13 demonstrated those protons or groups should be in the same α-orientation, indicating the peroxide bridge to be β-oriented. Consequently, the large coupling constants of H-6β (J5,6b =
Fig. 6 in Astragalus species: Phytochemistry, biological actions and molecular mechanisms underlying their potential neuroprotective effects on neurological diseases
Fig. 6. The antiapoptotic effect of saponins in neurological diseases. They activate the PI3K/Akt survival pathway, promote the phosphorylationdependent inactivation of Bad, which leads to a decrease in caspasedependent neuronal apoptosis. Also, they maintain mitochondria integrity through modulation of p38 and mitogen-activated protein kinase (MEK) signalling pathways, which reduces the cytochrome c release and inhibits caspasedependent apoptosis (Wu et al., 2015).
Fig. 1 in Astragalus species: Phytochemistry, biological actions and molecular mechanisms underlying their potential neuroprotective effects on neurological diseases
Fig. 1. Chemical structures of the major constituents of triterpenoid saponins identified in Astragalus radix extract (Chu et al., 2010).
Fig. 5 in Astragalus species: Phytochemistry, biological actions and molecular mechanisms underlying their potential neuroprotective effects on neurological diseases
Fig. 5. Pathways through which Astragalus polysaccharides (APS) mediates anti-inflammatory effect (Zheng et al., 2020).
Fig. 3 in Astragalus species: Phytochemistry, biological actions and molecular mechanisms underlying their potential neuroprotective effects on neurological diseases
Fig. 3. Astragalus membranaceus: (A) Aerial parts, (B) Roots, (C) Root extract (Cited at https://www.cambridge.org).
Fig. 5 in Chemical constituents from the fruits of Illicium simonsii and their antiviral activity and neuroprotective effect
Fig. 5. The experimental ECD spectra of 3 and 4 and calculated ECD spectra of a pair of enantiomers of the corresponding simplified structures of 12a and 12b, and Δδ (δδ) 1H NMR values (blue and red data) for the MTPA esters of compounds 3a, 3b, 4a, and 4b. (For interpretation of the references to colour in this figure S R legend, the reader is referred to the Web version of this article.)
Fig. 9. Compound 4 in Four undescribed ergostane-type steroids from Lasiodiplodia pseudotheobromae and their neuroprotective activity
Fig. 9. Compound 4 preserves mitochondrial function in glutamate-treated SH-SY5Y cell lines. Cell lines were measured using JC-1 staining by flow cytometry. Cell lines were assessed using H2DCF-DA staining and flow cytometry. Data are presented as the means ± S.D. (n = 3). ###p <0.001 vs. the control group (the no glutamate or compound 4-treated group); *p <0.05 and **p <0.001 vs. the glutamate-treated group.
Fig. 7 in Four undescribed ergostane-type steroids from Lasiodiplodia pseudotheobromae and their neuroprotective activity
Fig. 7. Effects of compounds 1–4 on the viability of Glu-treated SH-SY5Y cell lines. Compound 4 exerted a concentration dependent protective effect on SHSY5Y cell lines. Control represents the no glutamate or compounds-treated group. Data are presented as the means ± S.D. (n = 3). Data are presented as the means ± S.D. (n = 3). *p <0.05, **p <0.01 and ***p <0.001 vs. the glutamate-treated group.
Fig. 8. Compound 4 in Four undescribed ergostane-type steroids from Lasiodiplodia pseudotheobromae and their neuroprotective activity
Fig. 8. Compound 4 decreased glutamate-induced cellular apoptosis in SH-SY5Y cell lines. (A) Cellular morphological changes were observed by phase contrast microscopy. (B) Flow cytometry was applied to determine the apoptotic ratio after Annexin V-FITC/PI staining. The percentage of apoptotic cells was calculated in the bar chart. Data are presented as the means S.D. (n 3). ###p <0.001 vs. the control group (the no glutamate or compound 4-treated group); *p <0.05 and ± = ***p <0.001 vs. the glutamate-treated group.
Fig. 5 in Structures and neuroprotective activities of triterpenoids from Cynomorium coccineum subsp. songaricum (Rupr.) J. Leonard
Fig. 5. Neuroprotective compounds against SK-N-SH cell death from C. coccineum subsp. songaricum (A: active compounds in Glu-induced neuronal death assay. B: active compounds in OGD-induced neuronal death assay. C: inactive compounds with nonpolar group at C-3. D: inactive compounds with different E-ring).
Fig. 1 in Structures and neuroprotective activities of triterpenoids from Cynomorium coccineum subsp. songaricum (Rupr.) J. Leonard
Fig. 1. Structures of four previously undescribed triterpenes isolated from C. coccineum subsp. songaricum.
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These curated guides explain access requirements, typical timelines, costs, and reuse considerations for widely used research datasets.
Allen Brain Atlas
Allen Brain Atlas is an Allen Institute collection of brain map atlases, datasets, APIs, and analysis tools covering mouse, human, and non-human primate brain resources.
Annotated Behaviour and Observability Dataset (ABODe)
ABODe is a University of Edinburgh DataShare dataset for behavior classification in group-housed mice using home-cage video, identities, bounding boxes, ground-plate positions, and annotator labels.
DANDI Archive for NWB datasets
DANDI is a BRAIN Initiative archive for publishing and sharing neurophysiology data, including electrophysiology, optophysiology, and behavioral data packaged as NWB and related standards.
International Brain Laboratory public data
The International Brain Laboratory public data releases expose standardized mouse decision-making experiments, including Neuropixels recordings, widefield calcium imaging, behavior, and session metadata accessed through the ONE API.
OpenNeuro
OpenNeuro is a free, open platform for sharing neuroimaging datasets, with public search, dataset pages, and download paths for web, S3, DataLad, and the OpenNeuro CLI.