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. 2020 Jun 23;41(4):813–826. doi: 10.1007/s10571-020-00888-1

Fig. 2.

Fig. 2

ABA inducing autophagic flux in glioblastoma cells. ABA-induced autophagy were reduced by the autophagy inhibitor 3-MA and added by enhancing autophagosome formation with bafilomycin A1 both in U87 cells (a) and A172 cells (b). a, b Western blotting at up row indicates the endogenous conversion of LC3-I to LC3-II and the expression of beclin 1 in U87 (a) and A172 cells (b) treated with DMSO (control) or ABA (200 μM) for 24 h in the presence and absence of 3-MA (10 mM). The data quantified by a densitometric analysis relative to GAPDH are shown on the right. **P < 0.01 compared with untreated controls, n = 3; ##P < 0.01 compared with 3-MA treatment, n = 3. Western blotting at low row indicates the conversion of LC3-I to LC3-II in U87 (a) and A172 cells (b) treated with DMSO (control) or ABA (200 μM) for 24 h in the presence and absence of bafilomycin A1 (Baf A1, 400 nM). The data quantified by a densitometric analysis relative to GAPDH are shown on the right. **P < 0.01 compared with untreated controls, n = 3; ##P < 0.01 compared with Baf A1 treatment, n = 3