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. 2014 Nov;148(5):2335–2344. doi: 10.1016/j.jtcvs.2014.04.037

Figure 3.

Figure 3

Effect of p38-mitogen-activated protein kinase (MAPK) inhibition on lung physiology and signaling. The lungs were subjected to deflation and reinflation in the absence of SB203580 (D/R) or in the presence of 50 μM of SB203580 (D/R +SB203580). A, Dynamic compliance and vascular resistance were measured throughout the experiment. Data are expressed as the mean ± standard error of the mean of 6 lungs per group. B, Tissue samples were collected at the end of equilibration (baseline), deflation, or reperfusion. Whole cell extracts were immunoblotted for phosphorylated (p)-p38-MAPK, p-hsp27, p-ERK, or p-Akt. Equal protein loading was verified by immunoblotting for total p38-MAPK or total ERK1/2. The blots were quantified using scanning densitometry. The results were normalized to total p38-MAPK or total ERK1/2 and are expressed as the mean ± standard error of the mean of 4 lungs per group. ∞P < .05 compared with deflation without SB203580; *P < .05 compared with reinflation without SB203580 (unpaired t test). ERK1/2, Extracellular signal-regulated kinase 1 and 2; Bas, baseline.