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. 2021 Oct 22;22(21):11422. doi: 10.3390/ijms222111422

Figure 5.

Figure 5

PSPAs ameliorate mitochondrial dysfunction through mitophagy to inhibit KP-induced pyroptosis. (A) Immunoblotting of LC3 in PSPAs-treated and controlled AMs after treating with or without KP at an MOI of 20:1 for 6 h. (B) Autophagosome images of cells treated as in (A) under a transmission electron microscope. Red arrows indicate autophagosomes. (C) Cells were transfected with RFP-LC3 plasmids for 24 h, followed by treatment with or without KP at an MOI of 20:1 for 6 h and staining with MitoTracker Green for 30 min. The number of co-localized RFP-LC3 puncta (red) and MitoTracker Green (green) was quantified. Yellow arrows indicate colocalization. (D) Immunoblotting of Parkin, PINK1, and LC3 in the mitochondrion of cells treated as in (A). (E) Immunoblotting of NLRP3, Caspase1, GSDMD, and IL-1β in PSPAs-treated and controlled AMs treated with or without KP at an MOI of 20:1 for 6 h, in combination with or without 2 μM Mdivi-1. (F) Flow cytometric analysis of the Annexin V/PI positive rate, (G) MtROS, and (H) JC-1 detected by fluorescence assay in cells treated as in (E). (I) MTT assay of PSPAs-treated and controlled AMs with or without KP at an MOI of 20:1 for 6 h, in combination with or without 1 μM Mdivi-1. Data (mean ± SEM) are representative of three independent experiments. One-way ANOVA (Tukey’s post-hoc); * p < 0.05, ** p < 0.01, *** p < 0.001.