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Fig. 3 | BMC Cardiovascular Disorders

Fig. 3

From: The role of Asprosin in patients with dilated cardiomyopathy

Fig. 3

a Asprosin prevents hypoxia-induced cell death. Cardiomyoblast H9c2 cells were treated with different doses of asprosin for 24 h and exposed to hypoxia and normoxia conditions for 6 h. Cell viability was examined with a trypan blue exclusion test (n = 4 in each group). One-way analysis of variance with Greisser-Greenhouse correction and Holm-Sidak’s multiple comparisons were used to calculate the changes in cell viability. **P < 0.01, normoxia vs hypoxia without asprosin. †P < 0.05, asprosin 2.5 or 10 μg/ml vs 0 μg/ml. b Asprosin increases mitochondrial respiration and proton leak. Cardiomyoblasts H9c2 cells were treated with asprosin 2.5 μg/ml for 24 h and exposed to 3% H2O2 for 4 h (n = 4). Mitochondrial respiratory analysis of oxygen consumption rate. c Quantification of maximal respiration and proton leak. *P < 0.05, H2O2 vs H2O2 with Asprosin group by Mann-Whitney test

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