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. 2020 Jul 2;27(1):938–952. doi: 10.1080/10717544.2020.1785052

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© 2020 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group.

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

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Figure 6. — Effects of NM-aFGF-PEG-lips combine with UTMD on the protein expression levels of FGF1 and AKT-related signaling pathways of oxidative stress in cardiac tissues. (A) Expression of FGF1, p-AKT, AKT, p-GSK-3βand GSK-3α/βin cardiac tissues as measured by western blot analyses. (B–D) The quantification data of western blot for FGF1, p-AKT/AKT and p-GSK-3β/GSK-3α/β. (E) Expression of Nrf2, SOD2 and NQO1 in cardiac tissues as detected by western blot analyses. (F) The quantification data of western blot for Nrf2, SOD2 and NQO1. N = 10 per group. Data are presented as Mean ± SD. ^ap < .05 vs control group; ^bp < .05 vs DM group; ^cp < .05 vs NM-aFGF-PEG-lips + UTMD. NM-aFGF-PEG-lips: non-mitogenic acidic fibroblast growth factor- PEGylated -liposomes; DM: diabetes mellitus; UTMD: ultrasound-targeted MB destruction; GAPDH: glyceraldehyde 3-phosphate dehydrogenase.