Effect of Descurainia sophia on H2O2-induced myocardial injury via suppressing oxidative stress and autophagy pathway / 中草药

ABSTRACT

Objective To study the protective effect of aqueous extract from Descurainia Sophia (DS) on H2O2-induced H9c2 cardiomyocyte injury and to initially explore the potential mechanism. Methods The peaks of main components in DS were analyzed and identified by HPLC-MS. H9c2 cell injury model was established by H2O2. H9c2 cells were cultured in vitro and divided into control group, model group, probucol group, and DS at 100, 200, 400 μg/mL groups. In order to reveal the possible molecular mechanisms, the viability of H9c2 cells was measured by MTT assay; The apoptosis rate, autophagy rate, mitochondrial membrane potential, and reactive oxygen species (ROS) level were detected by flow cytometry; The relative indicators of cell oxidative stress were determined by biochemical kit; The expression levels of apoptosis-related protein and the autophagy-related protein were evaluated by Incell-western method. Results Seven components with the highest content were identified in DS through the results of mass spectrometry. Compared with the model group, DS can improve the cell viability (P < 0.05, 0.01) and survival rate of H9c2 cells (P < 0.01); At the same time, apoptosis was attenuated (P < 0.01), mitochondrial membrane potential was upregulated (P < 0.01), apoptosis related proteins Caspase-3, Bax/Bcl-2 were obviously downregulated (P < 0.01), autophagy phenomenon was attenuated (P < 0.01), autophagy related proteins LC3B and p62 were upregulated (P < 0.01). In addition, ROS level was decreased (P < 0.01), T-SOD and GSH-PX were upregulated and the levels of LDH and MDA were significantly decreased (P < 0.01). Conclusion This study suggests that DS can effectively protect H2O2-induced H9c2 cells injury, and the mechanism may be associated with improving oxidative stress in cells, inhibiting cell apoptosis and autophagy, which may be related to flavonoid glycosides.