Protective functions of myricetin in LPS-induced cardiomyocytes H9c2 cells injury by regulation of MALAT1.
Eur J Med Res
; 24(1): 20, 2019 Apr 26.
Article
em En
| MEDLINE
| ID: mdl-31027517
ABSTRACT
BACKGROUND:
Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is a crucial mediator in response to inflammation. Myricetin protects cardiomyocytes against inflammatory injury. However, it's still unexplored whether myricetin exerted anti-inflammatory properties via MALAT1. The purpose of our study was to validate the cardio-protective function of myricetin against myocarditis and its underlying mechanism in vitro.METHODS:
H9c2 cells were pre-incubated with myricetin before stimulation with lipopolysaccharide (LPS). Enforced silence of MALAT1 was achieved by transducing short hairpin (sh)-MALAT1 into H9c2 cells. Next, cell viability and apoptotic cells were detected with cell counting kit-8 (CCK-8) and Annexin V-fluorescein isothiocyanate/propidium iodide (Annexin V-FITC/PI) apoptosis detection kit, respectively. Western blot assay was conducted to examine apoptosis-relative proteins, pro-inflammatory factors, and signaling regulators. Quantitative real-time PCR (qRT-PCR) was performed to quantify pro-inflammatory factors and MALAT1 at mRNA levels. Enzyme-linked immune sorbent assay (ELISA) was employed to determine protein concentration of pro-inflammatory factors.RESULTS:
Myricetin ameliorated LPS-elicited reduction of cell viability, augment of apoptosis, and overexpression of monocyte chemo-attractant protein-1 (MCP-1) and interleukin-6 (IL-6) in H9c2 cells. Meanwhile, phosphorylation of p65 and inhibitor of nuclear factor kappa B alpha (IκBα) were suppressed. Besides, myricetin enhanced the expression of MALAT1 which was originally down-regulated by LPS. However, the protective effects of myricetin against LPS-caused inflammatory lesions were abrogated in MALAT1-deficiency cells, with the restored phosphorylation of p65 and IκBα.CONCLUSION:
Myricetin possessed an anti-inflammatory function against LPS-induced lesions in cardiomyocytes. Mechanically, myricetin up-regulated MALAT1, blocked LPS-evoked activation of nuclear factor-κB (NF-κB) inflammatory pathway, and, finally, exerted cardio-protective effects.Palavras-chave
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Base de dados:
MEDLINE
Assunto principal:
Flavonoides
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Cardiotônicos
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Miócitos Cardíacos
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RNA Longo não Codificante
Idioma:
En
Ano de publicação:
2019
Tipo de documento:
Article