Fig. 1.

Neural precursor cells (NPCs) induce cerebroprotection and reduce blood–brain barrier (BBB) permeability in the acute stroke phase in normolipidemic and hyperlipidemic mice. A Infarct volume and B brain edema evaluated by cresyl violet staining, C extravasated serum IgG abundance and D collagen-IV⁺ ischemic microvessels exhibiting glycoprotein-Ibα (GP-Ibα)⁺ microthrombosis, assessed by immunohistochemistry, E brain hemorrhage formation, determined by diaminobenzidine staining, as well as F laser Doppler flow during ischemia and after reperfusion above the core of the middle cerebral artery territory of normolipidemic mice on normal diet and hyperlipidemic mice on Western diet, which were exposed to 30 min intraluminal middle cerebral artery occlusion (MCAO). Mice were intravenously treated with vehicle (200 µl of 0.1 M phosphate-buffered saline [PBS]) or adult NPCs (10⁶ cells in 200 µl of 0.1 M PBS) immediately after reperfusion, followed by animal sacrifice at 48 h post-MCAO. Representative brain sections and microphotographs are shown. Note that hyperlipidemia exacerbates infarct volume, BBB permeability, and brain hemorrhage formation, but does not abolish the neuroprotective effects of NPCs in the acute stroke phase. Furthermore, note that GP-Ibα⁺ microthrombosis is not influenced by NPCs in either group, whereas brain hemorrhage formation is increased in NPC-treated hyperlipidemic mice compared with NPC-treated normolipidemic mice. Data are medians (lines inside boxes)/means (crosses inside boxes) ± interquartile ranges with minimum/maximum values as whiskers [in (A–E)] or means ± S.D. values [in (F)]. *P < 0.05/**P < 0.01/***P < 0.001 (n = 12 mice for normal diet/vehicle, n = 12 for normal diet/NPC, n = 10 for Western diet/vehicle, n = 11 for Western diet/NPC). Scale bar, 1 mm [in (A–C)], 20 µm [in (D)] and 200 µm [in (E)]