Fig. 6From: Combined exposure to fine particulate matter and high glucose aggravates endothelial damage by increasing inflammation and mitophagy: the involvement of vitamin DMitophagy and inflammation induced by high glucose and PM in HUVECs were regulated by the JNK and p38 signaling pathways. HUVECs were pretreated with high glucose (30 mM) for 24 h and then treated with PM (50 μg/ml) for 8 h or a specified period. A, B The levels of p-ERK, p-p38, and p-JNK were detected at different time points (0, 0.5, 1, 2, 4, and 8 h) using Western blotting. C HUVECs were pretreated with PD98059 (10 μM), SP600125 (5 μM) or SB203580 (15 μM) for 1 h before PM stimulation. AO was used to detect the formation of autolysosomes. Bar = 50 μm. D, E HUVECs were pretreated with PD98059 (10 μM), SP600125 (5 μM) or SB203580 (15 μM) for 1 h before PM stimulation. The expression levels of ICAM-1, VCAM-1 p62, LC3B and Bnip3 were detected using Western blotting. F HUVECs were pretreated with PD98059 (10 μM), SP600125 (5 μM) or SB203580 (15 μM) for 1 h before PM stimulation. Representative fluorescence images showing the adhesion of fluorescein-labeled THP-1 cells to HUVECs. *P < 0.05 compared with the HG + PM 0.5 h group; †P < 0.05 compared with the HG + PM groupBack to article page