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. Author manuscript; available in PMC: 2022 May 28.
Published in final edited form as: Eur Respir J. 2021 Dec 23;58(6):2003694. doi: 10.1183/13993003.03694-2020

FIGURE 1.

FIGURE 1

Phosphorylated AMP-activated protein kinase (pAMPK) is depleted in Br2-injured mice lung and rat alveolar type II epithelial (L2) cells. a–d) Representative Western blot images of pAMPK and total AMPK (tAMPK) levels and quantitative pAMPK to tAMPK ratio in lung tissue of mice exposed to Br2 (600 ppm for 45 min) and returned to room air for the indicated periods of time (a, b) and of rat L2 cells (100 ppm, 10 min). pAMPK level was significantly reduced in mice lung tissue and in L2 cells by 24 h post Br2 exposure (c, d). e, f) In the groups receiving AICAR 6 h post injury, pAMPK levels were significantly elevated compared to their untreated groups and approached normal (air control) values. Administration of AICAR in the absence of injury in animals and cells produced no significant difference to the air control group. Data are presented as mean±sem, n=5–7 animals per group. Significance was determined by one-way ANOVA followed by Tukey’s post hoc test. Fold air in b, d, f indicates the change relative to the air control.