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. 2012 May 28;3:161. doi: 10.3389/fphys.2012.00161

Figure 3.

Figure 3

GSH supplementation prevents the LPS-mediated translocation of Bax and caspase 3 activation. Bax protein levels were measured in the mitochondria isolated from lung homogenates of vehicle, LPS, LPS + GSH-EE, and GSH-EE treated mice using Western blot analysis (A). Mitochondrial Bax protein levels from LPS-treated mouse lungs were significantly higher and GSH-EE prevented this translocation (A). Activated caspase 3 and 7 protein levels and activity were also determined in lung homogenates from all four groups. LPS-treated mice had significantly increased activated caspase 3 protein levels that was reduced by GSH-EE pre-treatment (B). The activated caspase 7 protein levels were also upregulated in LPS-treated mice, but did not change after GSH-EE pre-treatment (C). The increase in activated caspase 3 protein levels correlated with an increase in caspase 3/7 activity in lungs of mice exposed to LPS, which was significantly decreased in presence of GSH-EE (D). Values are mean ± SEM; n = 3–6/group. *P < 0.05 vs. vehicle; †P < 0.05 vs. LPS.