BACKGROUND/AIM: Congenital heart disease (CHD) is a catastrophic disease. Emodin possesses biological properties in protecting against some diseases. Our study investigated to explore the effects of emodin on hypoxia-stimulated cardiomyocytes, which mimicked CHD in vitro. METHODS: H9c2 cells were stimulated with hypoxia and then the cells were treated with or without emodin, and/or transfected with miR-26a mimic, pcDNA-survivin and their corresponding negative control (NC). Cell viability and cell apoptosis were detected by Cell Counting kit-8 assay and flow cytometry, respectively. In addition, the expression of apoptotic proteins, Janus kinase 1 (JNK)/signal transducer and activator of transcription 3 (STAT3) pathway factors, and survivin were evaluated by using Western blot analysis. The expression of miR-26a was analyzed by quantitative real time polymerase chain reaction (qRT-PCR). Moreover, the target of miR-26a was verified by using a luciferase report assay. RESULTS: Hypoxia significantly decreased cell viability and increased cell apoptosis, and the accumulated levels of cleaved caspase-3 and cleaved-caspase-9 were upregulated by hypoxia compared with the control. However, emodin administration led to the opposite result. A further result showed that emodin increased the phosphorylation of JNK/STAT3 pathway-related proteins and the pathway inhibitor AG490 impaired the protective effects of emodin on hypoxia-induced injury. In addition, emodin negatively regulated the miR-26a expression, and overexpression of miR-26a enhanced cell apoptosis and upregulated the expression of cleaved-caspase-3 and cleaved-caspase-9 compared with the NC. Moreover, emodin statistically upregulated the expression of survivin, and overexpression of miR-26a decreased the expression of survivin. The luciferase of miR-26a overexpression was decreased in the wild type of the survivin group. CONCLUSION: Emodin protects hypoxia-induced cell injury as evidenced by increasing cell viability and decreasing apoptosis through downregulation of miR-26a as well as activation of the JNK/STAT3 pathway.
BACKGROUND/AIM: Congenital heart disease (CHD) is a catastrophic disease. Emodin possesses biological properties in protecting against some diseases. Our study investigated to explore the effects of emodin on hypoxia-stimulated cardiomyocytes, which mimicked CHD in vitro. METHODS: H9c2 cells were stimulated with hypoxia and then the cells were treated with or without emodin, and/or transfected with miR-26a mimic, pcDNA-survivin and their corresponding negative control (NC). Cell viability and cell apoptosis were detected by Cell Counting kit-8 assay and flow cytometry, respectively. In addition, the expression of apoptotic proteins, Janus kinase 1 (JNK)/signal transducer and activator of transcription 3 (STAT3) pathway factors, and survivin were evaluated by using Western blot analysis. The expression of miR-26a was analyzed by quantitative real time polymerase chain reaction (qRT-PCR). Moreover, the target of miR-26a was verified by using a luciferase report assay. RESULTS:Hypoxia significantly decreased cell viability and increased cell apoptosis, and the accumulated levels of cleaved caspase-3 and cleaved-caspase-9 were upregulated by hypoxia compared with the control. However, emodin administration led to the opposite result. A further result showed that emodin increased the phosphorylation of JNK/STAT3 pathway-related proteins and the pathway inhibitor AG490 impaired the protective effects of emodin on hypoxia-induced injury. In addition, emodin negatively regulated the miR-26a expression, and overexpression of miR-26a enhanced cell apoptosis and upregulated the expression of cleaved-caspase-3 and cleaved-caspase-9 compared with the NC. Moreover, emodin statistically upregulated the expression of survivin, and overexpression of miR-26a decreased the expression of survivin. The luciferase of miR-26a overexpression was decreased in the wild type of the survivin group. CONCLUSION: Emodin protects hypoxia-induced cell injury as evidenced by increasing cell viability and decreasing apoptosis through downregulation of miR-26a as well as activation of the JNK/STAT3 pathway.