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. 2021 Nov 17;8:788655. doi: 10.3389/fcvm.2021.788655

Figure 2.

Figure 2

Mdivi-1 treatment retarded excessive mitochondrial fission, ROS production, mitochondrial dysfunction and cellular senescence, which were induced by ox-LDL. (A) Representative images and quantitative analysis of Mito-tracker Red in ox-LDL-treated cells with mdivi-1 or the control vehicle. Scale bar = 10 μm. *P < 0.05 vs. ox-LDL with the control (n = 3 per group). (B) Electron microscopic images and quantitative analysis of mitochondria and average mitochondrial areas in ox-LDL-treated cells with mdivi-1 or the control. Scale bar = 1 μm. *P < 0.05 vs. ox-LDL with the control (n = 4 per group). (C) Immunoblots and quantitative analysis for Mfn1, Mfn2, Opa1, and β-actin in ox-LDL-treated cells with mdivi-1 or the control (n = 3 per group). (D) Representative images and quantitative analysis of SA-β gal staining of ox-LDL-treated cells with mdivi-1 or the control. **P < 0.01 vs. ox-LDL with the control (n = 9 per group). (E) Immunoblots and quantitative analysis for p53, p21, and β-actin in ox-LDL-treated cells with mdivi-1 or the control. *P < 0.05 vs. ox-LDL with the control (n = 3 per group). (F) Representative images of MitoSox Red in ox-LDL-treated cells with mdivi-1 or the control. Scale bar = 100 μm. (G) Representative images and quantitative analysis of JC-1 staining in ox-LDL-treated cells with mdivi-1 or the control. Scale bar = 100 μm. *P < 0.05 vs. ox-LDL with the control (n = 3 per group). All data are presented as the mean ± SEM. Statistical analysis were conducted by Wilcoxon rank sum test (A-C,E,G) and Student's t-test (D).