Data/hora: 05/06/2024 14:41:33

Provedor de dados: 	56	
País: 	Brazil	
Título: 	Polydatin protects H9c2 cells from hypoxia-induced injury via up-regulating long non-coding RNA DGCR5	
Autores: 	Dai,Jinhua; Ma,Jianbo; Liao,Yufeng; Luo,Xianhai; Chen,Guofang.	
Data: 	2019-01-01	
Ano: 	2019	
Palavras-chave: 	Myocardial infarction; Apoptosis; Autophagy; PI3K/AKT/mTOR pathway; MEK/ERK pathway.	
Resumo: 	Polydatin (PD), a monocrystalline polyphenolic drug mainly found in the roots of Polygonum cuspidatum, has various pharmacological activities. Long non-coding RNAs (lncRNA) DiGeorge syndrome critical region gene 5 (DGCR5) was found to participate in the suppression of multiple cancers. Here, we proposed to study the effect of PD on myocardial infarction (MI) by inducing DGCR5. CCK-8 assay was performed to detect the viability of H9c2 cells. Flow cytometry was utilized to test apoptosis of H9c2 cells. These results determined the optimal concentration and effect time of hypoxia as well as PD. Si-DGCR5 was transfected into cells and the expression level was determined by qRT-PCR. Western blot was utilized to evaluate the expression of apoptosis-related proteins, Bcl-2, Bax, and cleaved-caspase-3, as well as autophagy-associated proteins including Beclin-1, p62, and LC3-II/LC3-I. As a result, PD efficiently attenuated hypoxia-induced apoptosis and autophagy in H9c2 cells. The expression of DGCR5 was down-regulated by hypoxia and up-regulated by PD. Besides, knocking-down the expression of DGCR5 inhibited the protection of PD in H9c2 cells. In addition, PD up-regulated the accumulation of DGCR5, DGCR5 decreased the expression of Bcl-2 and p62, raised the expression of Bax and cleaved-caspase-3, and the proportion of LC3-II/LC3-I. PD stimulated the PI3K/AKT/mTOR and MEK/ERK signaling pathways via up-regulating the expression of DGCR5. Our data demonstrated that PD reduced cell apoptosis and autophagy induced by hypoxia in cardiomyocytes. Moreover, PD activated PI3K/AKT/mTOR and MEK/ERK signaling pathways by up-regulating the expression of DGCR5.	
Tipo: 	Info:eu-repo/semantics/article	
Idioma: 	Inglês	
Identificador: 	http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2019001200613	
Editor: 	Associação Brasileira de Divulgação Científica	
Relação: 	10.1590/1414-431x20198834	
Formato: 	text/html	
Fonte: 	Brazilian Journal of Medical and Biological Research  v.52 n.12 2019	
Fonte: 	info:eu-repo/semantics/openAccess