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Eur J Med Res. 2019 Apr 26;24(1):20. doi: 10.1186/s40001-019-0378-5.

Protective functions of myricetin in LPS-induced cardiomyocytes H9c2 cells injury by regulation of MALAT1.

Author information

1
Department of Cardiology, The First People's Hospital of Changzhou, No. 185 Juqian Street, Changzhou, 213000, China. sunjinliang0055@sina.com.
2
Department of Cardiology, The First People's Hospital of Changzhou, No. 185 Juqian Street, Changzhou, 213000, China.

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.

KEYWORDS:

Anti-inflammation; MALAT1; Myricetin; NF-κB

PMID:
31027517
PMCID:
PMC6485133
DOI:
10.1186/s40001-019-0378-5
[Indexed for MEDLINE]
Free PMC Article

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