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. 2020 Feb 12;10:2494. doi: 10.1038/s41598-020-59225-7

Figure 5.

Figure 5

Long-term pre-treatment for 48 h of normoxic HL1 cardiomyocytes with exosomes (100 μg) derived from hCPCs treated with low-dose ticagrelor (Tic 1 μM) prevents rising of cleaved caspase 3 levels (A) and apoptosis index (B) during severe hypoxia (1% O2), but not exosomes derived from hCPCs treated with high-dose ticagrelor (Tic 10 μM). Representative images of TUNEL staining of HL1 cells in each experimental condition are showed in panel C. As shown in panels D, exosomes released from hCPCs treated in the presence of adenosine (ADE, 10 μM) and EHNA (10 μM) do not prevents rising of cleaved caspase 3 levels in hypoxic cardiomyocytes. Representative images of full-length blots/gels of proteins cleaved caspase 3 and glyceraldehyde 3-phosphate dehydrogenase (GAPDH) are showed in panel A and D. Levels of cleaved caspase 3 are normalized on GAPDH levels and expressed as arbitrary units (a.u.) of cleaved caspase 3 (19 kDa, MW)/GAPDH (37 kDa, MW) ratio. All measurements are mean ± SD. *p < 0.05 vs. untreated condition (Vehicle: sterile phosphate buffer solution); #p < 0.05 vs. hypoxia; p < 0.05 vs. Exo-Vehicle; p < 0.05 vs. Exo-Tic 1 μM.