Conclusion
These results suggested that SFN had a protective effect on cardiomyocytes undergoing IRI, and its mechanism may be realized via activating the Nrf2/HO-1 pathway, thereby inhibiting apoptosis. This might provide a new approach for the treatment of ischaemic heart disease.
Methods
Cardiomyocytes were divided into four groups as follows: control group (normoxic condition), SFN group (5 μmol/L), hypoxia/reoxygenation (H/R) group (1 h, 3 h) and SFN + H/R group. Cell viability was determined by MTT method. Levels of creatine kinase (CK), nitric oxide (NO), superoxide dismutase (SOD) and maleic dialdehyde (MDA) were determined by colorimetric method. Cell apoptosis, levels of reactive oxygen species (ROS) and mitochondrial membrane potential (MMP) were determined by flow cytometry. Levels of Bax, Bcl-2, C caspase-3, NF-E2-related factor 2 (Nrf2) and haem oxygenase-1 (HO-1) were detected by Western blot.
Objective
This study explores the mechanisms of SFN preconditioning on ischaemia/reperfusion injury (IRI).Materials and
Results
H/R model inhibited cell viability, increased the levels of LDH, CK, Bax and C caspase-3, and decreased the levels of NO, Bcl-2, while the effect of H/R was partially reversed by SFN. SFN treatment reduced ROS, MDA (from 4.9 nM to 2.8 nM) production, elevated SOD level (from 39.5 U/mL to 61.7 U/mL) and improved MMP damage. Under the effect of SFN, up-regulation of nuclear Nrf2 expression and down-regulation of cytosolic Nrf2 expression were observed, which led to Nrf2 nuclear translocation and enhanced the expression of HO-1.