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. Author manuscript; available in PMC: 2018 Dec 1.
Published in final edited form as: J Cell Physiol. 2017 May 3;232(12):3775–3785. doi: 10.1002/jcp.25857

Figure 7. Effects of irisin on mitochondrial membrane depolarization and mitochondrial permeability transition pore (mPTP) opening in cardiomyoblasts exposed to hypoxia/reoxygenation.

Figure 7

Figure 7

Figure 7

A: Irisin attenuated the mitochondrial damages in H9c2 cardiomyoblasts exposed to hypoxia/reoxygenation. Cardiomyoblast mitochondrial damage was assessed by examining mitochondrial membrane depolarization. The MitoCapture dye accumulates in the mitochondria under the condition of normoxia, emitting a red signal. In apoptotic cells, the MitoCapture diffuses into the cytoplasm and emits a green signal. B: Onset of mPTP is demonstrated by loss of green fluorescence signal from mitochondria. Detailed methods for measurement of mPTP was described in materials and methods. Scale bar: 100 μm. C: Quantitation analysis of mPTP in H9c2 cardiomyoblasts exposed to hypoxia/reoxygenation. The results represent 3–4 independent experiments counting 150–200 cells/condition. Values represent means±SE (n=3–4/group). *P<0.05, ***P<0.001. D: Quantitative analysis of mitochondrial swelling in different treatments. Values represent means±SE (n=3/group). N: Normoxia; H; hypoxia; R: reoxygenation; ***P<0.001.