Mucin 1 Inhibits Ferroptosis and Sensitizes Vitamin E to Alleviate Sepsis-Induced Acute Lung Injury through GSK3β/Keap1-Nrf2-GPX4 Pathway

Figure 6

Vitamin E inhibited the occurrence of ferroptosis and alleviated lung injury in lung tissues and alveolar epithelial cells of sepsis. (a, b) Western blot assay was performed to evaluate the effect of vitamin E on the expression level of GPX4 in lung tissues of sepsis mice. (c–f) The expression levels of redox products in lung tissues of sepsis mice. (g, h) Flow cytometry was used to detect the levels of lipid peroxides in MLE-12 cells. (i) The effects of vitamin E on the morphology of ferroptosis-related organelles were assessed by TEM. (j) HE staining results in each group. (k) Lung injury scores and lung wet-dry weight ratio in each group. (l–o) Levels of TNF-α, IL-1β, IL-6, and IL-10 in sera of each group. (p–s) Levels of TNF-α, IL-1β, IL-6, and IL-10 in BALF of each group. (t–z) Western blot assay was used to evaluate the effects of vitamin E on the expression levels of related genes. All data were expressed in the form of ; , , and .

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