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. 2024 Nov 13;19:157. doi: 10.1186/s13020-024-01029-2

Fig. 5.

Fig. 5

Attenuation of ROS overproduction and ER stress contributes to the neuroprotective effects of PAE. A ROS inducer trimethylamine N-Oxide (TMAO) or ER stress activator tunicaymycin (Tu) blocked the effect of PAE (1.6 mg/mL) on cell viability determined by MTT assay, while the antioxidant N-Acetyl-L-cysteine (NAC) or the ER stress inhibitor sodium 4-phenylbutyrate (4-PBA) mimicked the effect of PAE (1.6 mg/mL) on cell viability. Hoechst (B and C) and Calcein-PI staining (D and E) was performed to assess the cell loss in each group (bar = 100 μm). PAE inhibited the cell loss caused by MPP+, whereas TMAO or tunicaymycin attenuated the effects of PAE. NAC or 4-PBA mimicked the effects of PAE (B-E). Results are expressed as mean ± SD, n = 3, *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001, vs. control group, ##p < 0.01, ###p < 0.001, ####p < 0.0001, vs. MPP+ treated group, ^p < 0.05, ^^p < 0.01, ^^^^p < 0.0001, vs. MPP+ + PAE group