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. 2025 Apr 18;56(7):1872–1882. doi: 10.1161/STROKEAHA.124.048964

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© 2025 The Authors.

Stroke is published on behalf of the American Heart Association, Inc., by Wolters Kluwer Health, Inc. This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution, and reproduction in any medium, provided that the original work is properly cited.

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Figure 3. — Effect of hypoxic-preconditioned mesenchymal stem cells (HP-MSCs) on microglia activation after hypoxic-ischemic (HI) injury in vivo and lipopolysaccharide (LPS) exposure in vitro. A, Perilesional locations of images taken in ionized calcium-binding adapter molecule 1 (IBA1)-stained brain sections at P28. B, Quantification of perimeter of IBA1⁺ cells. C, Quantification of Feret diameter of IBA1⁺ cells. D, Representative fluorescent images of perilesional IBA1⁺ cells (40×) in SHAM controls, HI-vehicle (VEH), HI–normoxic-preconditioned MSC (NP-MSC), and HI–HP-MSC mice. E, left, schematic overview of non-contact co-culture of primary-isolated mouse microglia exposed to 50 ng/mL LPS with NP-MSCs or HP-MSC (purple cells) in the hanging insert, green dots represent MSC secretome that can reach the medium of the microglia; right, TNF-α (tumor necrosis factor-α) secretion by microglia after 24-hour exposure to LPS. Data represent mean±SD. B and C, SHAM: n=17, HI-VEH: n=19, HI–NP-MSC: n=22, and HI–HP-MSC: n=21. E, n=5 per condition. DAPI indicates 4',6-diamidino-2-phenylindole. *P<0.05, **P<0.01, ***P<0.001 between indicated groups, ####P<0.0001 compared with non-LPS condition.