Protection of Luteolin-7-O-glucoside against apoptosis induced by hypoxia/reoxygenation through the MAPK pathways in H9c2 cells.

Myocardial hypertrophy is often associated with myocardial infarction. Luteolin-7-O-glucoside (LUTG) has the prosperity of preventing cardiomyocyte injury. The current study aimed to explore the potential protective effect of LUTG and its relevant mechanisms in the heart. To establish the cardiac hypertrophy model in vitro, Angiotensin II (Ang II) was used to stimuli H9c2 cells in this study. The CCK-8 assay showed that LUTG pretreatment improved cell viability of cardiomyocytes co-treated with Ang II and ischemia/reperfusion. LUTG decreased the reactive oxygen species levels. Furthermore, it was demonstrated LUTG could reduce the release amount of lactate dehydrogenase and recover the catalase activity according to the flow cytometry analysis, and activity detection, respectively in Ang II-H/R-treated H9c2 cells. In addition, the flow cytometry analysis showed that the pretreatment of LUTG mitigated cell apoptosis induced by hypoxia/reoxygenation in the cardiac hypertrophy model. Meanwhile, reverse transcription-quantitative polymerase chain reaction and western blot assays showed that the apoptosis-related genes, including poly (ADP-ribose) polymerase, Fas, Fasl and Caspase-3 were downregulated at the transcriptional and translational levels. Notably, the protien expression of phosphorylated (p)-extracellular signal-regulated kinas (ERK) 1/2, p-janus kinase and p-P38 were reduced, while the expression of p-ERK5 was elevated in the LUTG pretreatment groups compared with the hypoxia/reoxygenation treatment group. Based on these results, it was suggested that the anti-apoptosis effect of LUTG may be associated with regulating the activation of mitogen-activated protein kinases signaling pathways.