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. 2020 Oct 19;22(6):5378–5384. doi: 10.3892/mmr.2020.11612

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Copyright: © Zhu et al.

This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

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Figure 5. — Dex may inhibit alveolar epithelial cell apoptosis and decrease the Bak/Bcl-2 ratio through ERK1/2 activation. (A) Representative western blotting images of pro- and cl-caspase-3, p-ERK1/2, t-ERK1/2, Bak and Bcl-2 in the lung. The semi-quantified protein expression level of (B) cl-caspase-3, (C) p-ERK/t-ERK and (D) Bak/Bcl-2. Data are presented as the mean ± SD (n=6). *P<0.05, **P<0.01 vs. Sham; ^#P<0.05, ^##P<0.01 vs. VILI; ^&P<0.05, ^&&P<0.01 VILI+L-Dex+PD vs. VILI+L-Dex group; ^$$P<0.01 VILI+H-Dex+PD vs VILI+H-Dex. Cl, cleaved; Dex, dexmedetomidine; H-Dex, high dose Dex at 10 µg/kg; L-Dex, low dose Dex at 1 µg/kg; p-, phosphorylated; PD, PD98059; t-, total; VILI, ventilator-induced lung injury.