Oxidative Medicine and Cellular Longevity / 2019 / Article / Fig 6

Research Article

CD28 Deficiency Ameliorates Blast Exposure-Induced Lung Inflammation, Oxidative Stress, Apoptosis, and T Cell Accumulation in the Lungs via the PI3K/Akt/FoxO1 Signaling Pathway

Figure 6

CD28 deficiency attenuates blast exposure-induced lung injury through the PI3K/Akt/FoxO1 signaling pathway. (a) Representative western blot images of t-PI3K, p-PI3K, t-Akt, p-Akt, t-FoxO1, p-FoxO1, and β-actin. (b–d) Quantitative analysis of each group was conducted. Fold changes of WT (green bar) and CD28-/- (red bar) expressions are shown. (e–g) Representative immunofluorescent staining images of p-PI3K, p-Akt, and p-FoxO1 in the lungs. (h–j) Quantitative analysis of each group was performed. Fold changes of WT (green bar) and CD28-/- (red bar) expressions are shown. All experiments were repeated at least three times. Results are expressed as the ( per group). versus the control group; versus the WT group (two-way ANOVA; Bonferroni post hoc test). WT: C57BL/6 wild-type mice; CD28-/-: CD28 knockout mice.
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