High fatty acid induced H9c2 cardiomyocytes injury through mitochondrial pathways / 中国药理学通报

ABSTRACT

Aim: To explore the role of mitochondrial apoptosis pathway in high fatty acid induced injury in H9c2 cardiomyocytes. Methods: Cardiomyocytes were exposed to different concentrations of palmitic acid (PA) at 0 ∼0. 4 mmol · L-1 for 24 h and different time points (0 ∼48 h) of PA 0.2 mmol · L-1. Cell viability was measured by MTT; the intracellular reactive oxygen species (ROS) was detected by ROS kit; the cells were detected by apoptosis kit; the cell mitochondrial membrane potential changes were detected by mitochondrial membrane potential kit, and the protein expressions of mitochondrial apoptosis pathway such as Cyt-C, Cleaved caspase-3, Bax, and Bcl-2 were detected by Western blot. Results: When the cells were stimulated with PA for 24 h, the cell proliferation rates of 0. 2 and 0. 4 mmol · L-1 PA groups significantly decreased. The level of ROS increased gradually, the cell mitochondrial membrane potential decreased and the cell apoptosis increased. When the cells were stimulated with PA (0. 2 mmol · L-1) for 24 h, 36 h and 48 h, and all of the cell proliferation rates showed significant decline. Cardiomyocytes exposed to PA (0. 4 mmol · L-1) for 24 h showed an increase in the expression of mitochondrial related proteins (Cyt-C, Cleaved caspase-3 and Bax) (P < 0. 05), while Bcl-2 expression was significantly reduced (P < 0. 05). Conclusion: Mitochondrial apoptosis signaling pathway might play an important role in high fatty acid induced H9c2 myocardial injury.