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. 2022 Jun 30;12:11086. doi: 10.1038/s41598-022-14832-4

Figure 2.

Figure 2

Abrogation of aberrant autophagy by CSP7 in mice with silica-induced PF. (A) Representative Western blot images showing the expression of p53, p53 phosphorylation at serine 15 residue (p53S15P), lipidated LC3B (LC3BII), p62 and ATG12-ATG5 complex in lung homogenates of naïve WT mice, and WT mice (n = 5–7) with silica-induced PF left untreated or treated with CSP7 as described in Fig. 1A. β-actin serves as loading control. MW: Molecular weight. kDa: Kilodalton. (B) Bar graph showing decreased LC3B, p62 and ATG5 mRNA in the lung homogenates of silica-exposed WT mice treated with CSP7. Representative immunohistochemistry images showing inhibition of (C) LC3B and (D) p62 expression by CSP7 in lungs of WT mice exposed to silica. Scale bar: 20 μm. (E) Representative immunoblot images showing inhibition of p53, p53S15P, LC3BII, p62 and ATG12-ATG5 expression in AECs isolated from silica exposed WT mice treated with CSP7 in vivo. β-actin serves as loading control. MW: Molecular weight. kDa: Kilodalton. Each experiment was repeated at least 2–3 times and data is presented as mean + SD and p values were obtained by one-way Anova with Turkey’s multiple comparison test and log-rank tests, respectively.