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. 2020 Dec 11;11:569251. doi: 10.3389/fphar.2020.569251

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Copyright © 2020 Wang, Pan, Liu, Li, Lin, He, Xiao, Li and Lin

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Inhibiting p38 MAPK protects rPMVECs from OGD/R injury. (A) Fluorescent and bright field micrographs of rPMVECs transfected with lentivirus-expressing control or p38 MAPK-targeting shRNA. Levels of (B) p38 MAPK mRNA, (C) p-p38 MAPK protein, (D) HIF-1α mRNA, and (E) HIF-1α protein were measured. (F) Viability of rPMVECs was measured using the CCK-8 assay. (G) Activity of caspase 3 in rPMVECs was measured as an index of apoptosis. (H) The permeability coefficient in rPMVECs was measured as an index of the pulmonary blood–air barrier based on flux of the fluorescent marker FITC-dextran. (G) The level of NO in cultured rPMVEC supernatant in different groups was detected. ns: no statistical significance, *p < 0.05, each experiment was performed at least three times independently. Blocking p38 MAPK mitigates OGD/R-induced endothelial dysfunction.