PMID- 30628693
OWN - NLM
STAT- MEDLINE
DCOM- 20190524
LR  - 20211020
IS  - 1791-3004 (Electronic)
IS  - 1791-2997 (Print)
IS  - 1791-2997 (Linking)
VI  - 19
IP  - 3
DP  - 2019 Mar
TI  - Luteolin suppresses lipopolysaccharide‑induced cardiomyocyte hypertrophy and 
      autophagy in vitro.
PG  - 1551-1560
LID - 10.3892/mmr.2019.9803 [doi]
AB  - Luteolin (LTL) serves essential roles in a wide variety of biological processes. 
      Lipopolysaccharide (LPS) can lead to myocardial hypertrophy and autophagy. 
      However, the roles of LTL on LPS‑induced cardiomyocyte hypertrophy and autophagy 
      in rat cardiomyocytes have not yet been fully elucidated. In the present study, 
      the morphology of cultured rat cardiomyocytes was observed under an inverted 
      microscope. Cell viability was detected by MTT assay. alpha‑Actinin and 
      microtubule‑associated protein 1 light chain 3 (LC3) expression levels were 
      measured by immunofluorescence assay. In addition, the expression levels of 
      atrial natriuretic peptide/brain natriuretic peptide (ANP/BNP), LC3, and 
      autophagy‑ and Wnt signaling pathway‑associated genes were analyzed by reverse 
      transcription‑quantitative polymerase chain reaction or western blot assays. The 
      results indicated that LTL increased the cell viability of cardiomyocytes treated 
      with LPS. LTL decreased the expression of cardiac hypertrophy associated markers 
      (ANP and BNP). LTL decreased alpha‑actinin and LC3 expression levels in LPS‑treated 
      cardiomyocytes. It was also demonstrated that LTL suppressed the mRNA and protein 
      expression levels of LPS‑mediated autophagy and Wnt signaling pathway‑associated 
      genes. In addition, it was demonstrated that silencing of beta‑catenin inhibited 
      LPS‑induced cardiomyocyte hypertrophy and the formation of autophagosomes. Thus, 
      the present study suggested that LTL protected against LPS‑induced cardiomyocyte 
      hypertrophy and autophagy in rat cardiomyocytes.
FAU - Li, Xing
AU  - Li X
AD  - Teaching and Research Section of Traditional Chinese Medicine, Jiangsu Jiankang 
      Vocational College, Nanjing, Jiangsu 210018, P.R. China.
FAU - Liu, Jian
AU  - Liu J
AD  - Department of Cardiovascular Medicine, Affiliated Hospital of Nanjing University 
      of Traditional Chinese Medicine, Nanjing, Jiangsu 210029, P.R. China.
FAU - Wang, Jianfeng
AU  - Wang J
AD  - China Pharmaceutical University, Nanjing, Jiangsu 210009, P.R. China.
FAU - Zhang, Donghua
AU  - Zhang D
AD  - China Pharmaceutical University, Nanjing, Jiangsu 210009, P.R. China.
LA  - eng
PT  - Journal Article
DEP - 20190102
PL  - Greece
TA  - Mol Med Rep
JT  - Molecular medicine reports
JID - 101475259
RN  - 0 (LC3 protein, rat)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (Microtubule-Associated Proteins)
RN  - 0 (RNA, Messenger)
RN  - 114471-18-0 (Natriuretic Peptide, Brain)
RN  - 85637-73-6 (Atrial Natriuretic Factor)
RN  - KUX1ZNC9J2 (Luteolin)
SB  - IM
MH  - Animals
MH  - Atrial Natriuretic Factor/genetics
MH  - Autophagy/*drug effects
MH  - Disease Models, Animal
MH  - Gene Expression/drug effects
MH  - Humans
MH  - Hypertrophy/chemically induced/*drug therapy/pathology
MH  - Lipopolysaccharides/toxicity
MH  - Luteolin/*administration & dosage
MH  - Microtubule-Associated Proteins/genetics
MH  - Myocytes, Cardiac/*drug effects/pathology
MH  - Natriuretic Peptide, Brain/genetics
MH  - RNA, Messenger/genetics
MH  - Rats
MH  - Signal Transduction/drug effects
PMC - PMC6390050
OTO - NOTNLM
OT  - luteolin
OT  - lipopolysaccharide
OT  - cardiomyocyte hypertrophy
OT  - autophagy
OT  - cardiomyocytes
EDAT- 2019/01/11 06:00
MHDA- 2019/05/28 06:00
PMCR- 2019/01/02
CRDT- 2019/01/11 06:00
PHST- 2017/12/03 00:00 [received]
PHST- 2018/11/05 00:00 [accepted]
PHST- 2019/01/11 06:00 [pubmed]
PHST- 2019/05/28 06:00 [medline]
PHST- 2019/01/11 06:00 [entrez]
PHST- 2019/01/02 00:00 [pmc-release]
AID - mmr-19-03-1551 [pii]
AID - 10.3892/mmr.2019.9803 [doi]
PST - ppublish
SO  - Mol Med Rep. 2019 Mar;19(3):1551-1560. doi: 10.3892/mmr.2019.9803. Epub 2019 Jan 
      2.