Registro completo |
Provedor de dados: |
BJMBR
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País: |
Brazil
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Título: |
Emodin protects H9c2 cells from hypoxia-induced injury by up-regulating miR-138 expression
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Autores: |
Zhang,Xuezhi
Qin,Qiaoji
Dai,Hongyan
Cai,Shanglang
Zhou,Changyong
Guan,Jun
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Data: |
2019-01-01
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Ano: |
2019
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Palavras-chave: |
Emodin
Myocardial infarction
Hypoxia injury
MiR-138
Sirt1/AKT pathway
Wnt/β-catenin pathway
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Resumo: |
Myocardial infarction (MI) is a common presentation for ischemic heart disease, which is a leading cause of death. Emodin is a Chinese herbal anthraquinone used in several diseases. However, the effect of emodin in hypoxia-induced injury in cardiomyocytes has not been clearly elucidated. Our study aimed to clarify the functions of emodin in hypoxia-induced injury in rat cardiomyocytes H9c2 and explore the underlying mechanism. The effects of emodin on cell viability and apoptosis were analyzed by the Cell counting kit-8 assay and flow cytometry assay, respectively. The cell proliferation- and cell apoptosis-related proteins were detected by western blot. qRT-PCR was used to determine the relative expression of miR-138. Cell transfection was performed to alter miR-138 and MLK3 expression. miR-138 target was performed by dual luciferase activity assay. Sirt1/AKT and Wnt/β-catenin pathways-related factors phosphorylation were analyzed by western blot. Emodin inhibited hypoxia-induced injury in H9c2 cells by promoting cell viability and reducing cell apoptosis. miR-138 was down-regulated by hypoxia treatment but up-regulated by emodin. Up-regulation of miR-138 alleviated hypoxia-induced cell injury. Down-regulation of miR-138 attenuated the growth-promoting effect of emodin on hypoxia-induced injury, whereas up-regulation of miR-138 enhanced the growth-promoting effects of emodin. The underlying mechanism might be by inactivating Sirt1/AKT and Wnt/β-catenin pathways. MLK3 was negatively regulated by miR-138 expression and inactivated Sirt1/AKT and Wnt/β-catenin pathways. Emodin alleviated hypoxia-induced injury in H9c2 cells via up-regulation of miR-138 modulated by MLK3, as well as by activating Sirt1/AKT and Wnt/β-catenin pathways.
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Tipo: |
Info:eu-repo/semantics/article
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Idioma: |
Inglês
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Identificador: |
http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2019000300603
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Editor: |
Associação Brasileira de Divulgação Científica
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Relação: |
10.1590/1414-431x20187994
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Formato: |
text/html
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Fonte: |
Brazilian Journal of Medical and Biological Research v.52 n.3 2019
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Direitos: |
info:eu-repo/semantics/openAccess
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