Skip to main content
Figure 2 | Respiratory Research

Figure 2

From: Pharmacological inhibition of GSK-3 in a guinea pig model of LPS-induced pulmonary inflammation: II. Effects on skeletal muscle atrophy

Figure 2

Muscle protein turnover signaling is not affected following chronic LPS-treatment and GSK-3 inhibition. Protein synthesis and protein degradation-related signaling molecules were determined in whole muscle homogenates of the extensor digitorum longus (EDL) muscles by Western blot analysis of guinea pigs that were treated intranasally with LPS or SB216763 for 12 weeks. Representative immunoblots depict protein levels of (A) phospho-Akt (p-Akt), total Akt, phospho-GSK-3β (p-GSK-3β), total GSK-3β, phospho-eukaryotic initiation factor 2Bϵ (p-eIF2Bϵ), GAPDH, (B) phospho-mammalian target of rapamycin (p-mTOR), total mTOR, phospho-p70S6K (p-p70S6K), total p70S6K, phospho-S6 (p-S6), phospho-4E-BP1 (p-4E-BP1), total 4E-BP1, GAPDH, (C) phospho-FoXO1 (p-FoXO1), total FoXO1, phospho-FoXO3a (p-FoXO3a), total FoXO3a and GAPDH. The accompanying bar graphs show the densitometric analysis results (means ± SEM, n = 6), represented as a percentage of the vc control group corrected for GAPDH. All data is shown as a ratio of phospho- to total protein for each target (except p-eIF2Bϵ, p-S6 and (p-) 4E-BP1). *p < 0.05 compared with the vc control group. NS: not significant.

Back to article page