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. 2024 Apr 30;11:18. doi: 10.1186/s40580-024-00423-8

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© The Author(s) 2024

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 2 — Exosome-based therapy for cerebral IRI. A Tail vein injection of M2 microglia-derived exosomes (M2-EXO) attenuated cerebral IRI by downregulating of protease 14 (USP14) expression. (i) Cresyl violet-staining of brain sections, (ii) normalized infarct volume %, (iii) modified neurological severity score (mNSS), and (iv) number of apoptotic neurons in the brain of the mice treated with PBS, M2-EXO, miR-124 k/d EXO, miR-124 k/d EXO + IU1 and miR-cn EXO (exosomes from M2 microglia treated with a control lentivirus vector) [73]. B Intravenous injection of RvD2-loaded artificial exosomes, synthesized from the membranes of differentiated human promyelocytic leukemia cells (HL-60), reduced neurological damage following tMCAO. (i) Confocal images showed Dil-labeled nanovesicles (red), from differentiated HL-60 (HVs), adhering to the inflamed brain vasculature post tMCAO while nanovesicles from non-differentiated HL-60 (NVs) showing minimal binding. Blood vessels visualized by BSA-Cy5 (pink). Scale bar = 20 μm. (ii) TTC-stained brain sections revealed (iii) Infarct sizes and (iv) neurological deficit scores at 22 h after injection Reprinted with permission from [79]. Copyright 2019 American Chemical Society. C Intravenous injection of mAb GAP43-conjugated exosomes targeted specifically to damage neurons post cerebral IRI. (i) Scheme of conjugating mAb GAP43 to quercetin (Que)-loaded exosome surface to assemble Que/mAb GAP43-Exo. (ii) Fluorescence images of brains from tMCAO rats treated with PBS, Que, Que-Exo, and Que/mAb [81]. D Neural progenitor cell-derived exosomes modified with RGD peptides enhanced lesion targeting through intravenous injection. (i) Design of RGD-C1C2 and RGD-C1C2-decorated EV. (ii) Near Infrared Fluorescence images of mice brains the intravenous administration of PBS, Cy5.5-labeled EV, Scr-EV or RGD-EV. Quantitation of fluorescence intensity in the lesion region and ratios of fluorescence intensity in ipsilateral versus contralateral region [76]. E Intranasal administration of exosomes derived from adipose-derived MSC (ADSC-Exo) improved neurobehavior function and inhibited ferroptosis by downregulating CHAC1 expression via miR-760-3p. (i) Neurological deficits were evaluated using mNSS before and after tMCAO. (ii) Motor function was assessed. (iii) RT-qPCR results of CHAC1 mRNA expression. (iv) Western blot showing CHAC1 protein expression [82]