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. 2024 Apr 17;44:35. doi: 10.1007/s10571-024-01467-4

Fig. 2.

Fig. 2

The 3-MA inhibits autophagy and induces cell apoptosis and death and FoxG1 overexpression alleviates these effects. A Western blot showing the changes in Beclin1, LC3, SQSTM1/P62, and FoxG1 expression in the N2A cells after different concentrations of 3-MA treatment (2.5 mM, 5 mM, 10 mM, 15 mM, and 20 mM) for 24 h. (B [F5,30 = 25.91, P < 0.0001], D [F5,30 = 5.886, P = 0.0056], E [F5,30 = 11.90, P = 0.0003]). Bar chart indicates the relative expression of these proteins in (A). (C [F5,30 = 117.3, P < 0.0001]) Bar chart indicates the expression of LC3 II/LC3 I in (A). (F [F5,30 = 25.59, P < 0.0001]) Cell viability was evaluated by BioTeck. G Apoptosis analysis by flow cytometry after 3-MA treatments for different times (12 h, 24 h, 48 h, and 72 h). (H [F4,25 = 7.982, P = 0.0213], I [F4,25 = 32.06, P = 0.0009]) The proportions of apoptotic cells and dead cells in (G). J FoxG1/N2A cell lines and pCDH/N2A cell lines were treated with 10 mM 3-MA for 48 h, apoptosis analysis by flow cytometry after treatments. (K [F2,15 = 251.9, P < 0.0001], L [F2,15 = 104.1, P < 0.0001]) The proportions of apoptotic cells and dead cells in J. GAPDH was used as western blot loading control. Values are expressed as means ± SEM. *P < 0.05, **P < 0.01, ***P < 0.001. For each group, n = 6/group