PMID- 31027517 OWN - NLM STAT- MEDLINE DCOM- 20190814 LR - 20240402 IS - 2047-783X (Electronic) IS - 0949-2321 (Print) IS - 0949-2321 (Linking) VI - 24 IP - 1 DP - 2019 Apr 26 TI - Protective functions of myricetin in LPS-induced cardiomyocytes H9c2 cells injury by regulation of MALAT1. PG - 20 LID - 10.1186/s40001-019-0378-5 [doi] LID - 20 AB - 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 (IkappaBalpha) 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 IkappaBalpha. 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-kappaB (NF-kappaB) inflammatory pathway, and, finally, exerted cardio-protective effects. FAU - Sun, Jinliang AU - Sun J AD - Department of Cardiology, The First People's Hospital of Changzhou, No. 185 Juqian Street, Changzhou, 213000, China. sunjinliang0055@sina.com. FAU - Sun, Jianhui AU - Sun J AD - Department of Cardiology, The First People's Hospital of Changzhou, No. 185 Juqian Street, Changzhou, 213000, China. FAU - Zhou, Xuezhong AU - Zhou X AD - Department of Cardiology, The First People's Hospital of Changzhou, No. 185 Juqian Street, Changzhou, 213000, China. LA - eng PT - Journal Article PT - Retracted Publication DEP - 20190426 PL - England TA - Eur J Med Res JT - European journal of medical research JID - 9517857 RN - 0 (Cardiotonic Agents) RN - 0 (Flavonoids) RN - 0 (Inflammation Mediators) RN - 0 (Lipopolysaccharides) RN - 0 (MALAT1 long noncoding RNA, rat) RN - 0 (NF-kappa B) RN - 0 (RNA, Long Noncoding) RN - 76XC01FTOJ (myricetin) RIN - Eur J Med Res. 2024 Apr 1;29(1):212. PMID: 38561857 MH - Animals MH - Cardiotonic Agents/*pharmacology MH - Cell Line MH - Flavonoids/chemistry/*pharmacology MH - Inflammation/pathology MH - Inflammation Mediators/metabolism MH - Lipopolysaccharides MH - Myocytes, Cardiac/drug effects/*metabolism/*pathology MH - NF-kappa B/metabolism MH - RNA, Long Noncoding/genetics/*metabolism MH - Rats MH - Signal Transduction/drug effects MH - Up-Regulation/drug effects/genetics PMC - PMC6485133 OTO - NOTNLM OT - Anti-inflammation OT - MALAT1 OT - Myricetin OT - NF-kappaB COIS- The authors declare that they have no competing interests. EDAT- 2019/04/28 06:00 MHDA- 2019/08/15 06:00 PMCR- 2019/04/26 CRDT- 2019/04/28 06:00 PHST- 2019/01/02 00:00 [received] PHST- 2019/04/10 00:00 [accepted] PHST- 2019/04/28 06:00 [entrez] PHST- 2019/04/28 06:00 [pubmed] PHST- 2019/08/15 06:00 [medline] PHST- 2019/04/26 00:00 [pmc-release] AID - 10.1186/s40001-019-0378-5 [pii] AID - 378 [pii] AID - 10.1186/s40001-019-0378-5 [doi] PST - epublish SO - Eur J Med Res. 2019 Apr 26;24(1):20. doi: 10.1186/s40001-019-0378-5.