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. 2020 Aug 26;9(1):1809064. doi: 10.1080/20013078.2020.1809064

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© 2020 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group on behalf of The International Society for Extracellular Vesicles.

This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial License (http://creativecommons.org/licenses/by-nc/4.0/), which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Figure 6. — Extracellular vesicles (EVs) derived from human neural stem cells (hNSCs) display anti-inflammatory properties, and pervasively permeate the brain following an intranasal administration. Figure A shows data from the macrophage assay. LPS, lipopolysaccharide; DEX, dexamethasone; EVs, extracellular vesicles. Note that the addition of hNSC-EVs to LPS stimulated macrophage cultures resulted in a dose-dependent suppression of interleukin-6 (IL-6) release by macrophages, implying an anti-inflammatory effect. The effect was significant when 4 × 10⁹ or more EVs were added to macrophage + LPS cultures (a). ****, p < 0.0001. Figures (b1–b6) show that an intranasal (IN) administration of hNSC-EVs after 2 hours of acute seizure activity (a mouse model of status epilepticus) is adequate for reducing the concentration of multiple cytokines in the hippocampus. The cytokines that showed significant reductions following hNSC-EV treatment include the tumour necrosis factor-alpha (TNF-α; B1), interleukin-1 beta (IL-1β; B2), interferon-gamma (IFN-γ; b3), monocyte chemoattractant protein −1 (MCP-1; b4), leptin (b5) and the platelet-derived growth factor (PDGF-BB; b6). hNSC-EV treatment also normalized the anti-inflammatory protein IL-10 after status epilepticus (b7). Figures c1 and c2 show that normalization of TNF-α and IL-1β found through cytokine array following EV treatment could also be confirmed with individual ELISA. *p < 0.05, **p < 0.01, ***p < 0.001. NS, not significant. Figures d1-d15 illustrate the incorporation of PKH-26 labelled hNSC-EVs (red dots) by different cells in various regions of the rat brain at 6 hours after an IN administration. The figures illustrate NeuN⁺ neurons (d1-d5), calbindin⁺ Purkinje neuron (d6), IBA-1⁺ microglia (d7-d12) and astrocytes positive for GFAP (d13), S-100β (d14) or both GFAP and S-100β (d15). Figures e1-e12 illustrate the incorporation of PKH-26 labelled hNSC-EVs (red dots) by NeuN⁺ neurons (e1-e6) and IBA-1⁺ microglia (e7-e12) in various regions of the mouse brain at 6 hours after an IN administration. mPFC, medial prefrontal cortex (d1, d7, e1, e7); SSC, somatosensory cortex (d2, d8, e2, e8); DG, dentate gyrus (d3, d9, e3, e9); CA1 subfield (d4, d10); CA3 subfield (d5, d11, e4, e10); CBM, cerebellum (d6, d12); thalamus (e5, e11); and amygdala (e6, e12). Scale bar: 25 μm.