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Fig. 5 | Respiratory Research

Fig. 5

From: The role of Src & ERK1/2 kinases in inspiratory resistive breathing induced acute lung injury and inflammation

Fig. 5

Activation of ERK1/2 through phosphorylation in lung tissue following IRB. The effect of upstream Src kinase inhibition and efficacy of the ERK activation inhibitor, PD98059 (representative western blot analysis, upper, band intensity quantification, lower). a. Following 3 h of IRB, activation of ERK was noticed in lung tissue samples (increased p-ERK to actin ratio relative to control), an effect that was blocked by Src inhibition. b. In contrast, ERK activation at 6 h of IRB was independent of Src kinase activation during IRB. c Administration of the inhibitor of ERK activation, PD98059 (1 mg/kg ip) prior to IRB, sufficiently attenuated the increase of p-ERK to actin ratio in lung tissue samples at 6 h IRB. Data presented as mean ± SEM, n = 3–6 per group for A, n = 6–9 per group for B and n = 6–8 per group for C, *p < 0.05 to ctr, #p < 0.05 to IRB equal time point, black bars, 6 h IRB, grey bars, 6 h IRB + Src Inh. a and b or 6 h IRB + ERK Inh. c

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