PMID- 28357449
OWN - NLM
STAT- MEDLINE
DCOM- 20190726
LR  - 20220408
IS  - 1615-6692 (Electronic)
IS  - 0340-9937 (Linking)
VI  - 43
IP  - 3
DP  - 2018 May
TI  - Myricetin protects cardiomyocytes from LPS-induced injury.
PG  - 265-274
LID - 10.1007/s00059-017-4556-3 [doi]
AB  - BACKGROUND: Sepsis-induced cardiomyopathy is a well-known cause of mortality. 
      Recent evidence has highlighted the important role of myricetin in 
      anti-inflammation and anti-oxidative stress. However, little is known about its 
      effect on endotoxin-induced cardiomyopathy. We examined the effect of myricetin 
      on lipopolysaccharide (LPS)-induced cardiomyocyte injury and the underlying 
      mechanisms in vitro. METHODS: mRNA expression of interleukin (IL)-1beta, IL-6, 
      and tumor necrosis factor (TNF)-alpha was examined via reverse 
      transcription-quantitative polymerase chain reaction (RT-qPCR). Protein 
      expression levels of NF-kappaB/p65, IkappaB, IL-1beta, IL-6, and TNF-alpha were assesses 
      via Western blotting. Immunofluorescence (IF) was used to determine the nuclear 
      translocation of p65. Commercial kits were employed to detect the level of 
      oxidative markers and to quantify NF-kappaB/p65 both in the cytoplasm and the 
      nucleus. Finally, terminal deoxy-nucleotidyl transferase-mediated dUTP nick end 
      labeling (TUNEL) was performed to evaluate the apoptosis of H9c2 cardiomyocytes. 
      RESULTS: The results showed that myricetin blunted the overexpression of 
      IL-1beta, IL-6, and TNF-alpha markedly by inhibiting the NF-kappaB/P65 signaling 
      pathway. Furthermore, myricetin treatment led to the downregulation of reactive 
      oxygen species (ROS) accompanied by increased expression of superoxide dismutase 
      and glutathione peroxidase. TUNEL-positive nuclei were rarely detected following 
      myricetin treatment. CONCLUSION: Our findings suggest that myricetin is 
      a valuable protective agent against endotoxin-induced early inflammatory 
      responses in H9c2 cardiomyocytes, which involves regulation of ROS and the 
      IkappaB/NF-kappab signaling pathway.
FAU - Chen, S
AU  - Chen S
AD  - School of Pharmacy, Hubei University of Science and Technology, 437100, Hubei 
      Xianning, China.
FAU - Fan, B
AU  - Fan B
AD  - School of Pharmacy, Hubei University of Science and Technology, 437100, Hubei 
      Xianning, China. baoleifan_xn@126.com.
LA  - eng
PT  - Journal Article
TT  - Myricetin schutzt Kardiomyozyten vor LPS-induzierten Verletzungen.
DEP - 20170329
PL  - Germany
TA  - Herz
JT  - Herz
JID - 7801231
RN  - 0 (Flavonoids)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (NF-kappa B)
RN  - 76XC01FTOJ (myricetin)
MH  - Animals
MH  - Cardiomyopathies
MH  - *Flavonoids/pharmacology
MH  - Lipopolysaccharides
MH  - *Myocytes, Cardiac/drug effects
MH  - NF-kappa B
MH  - Rabbits
OTO - NOTNLM
OT  - Cardiomyocytes
OT  - Inflammation
OT  - Lipoglycans
OT  - Oxidative stress
OT  - Sepsis
EDAT- 2017/03/31 06:00
MHDA- 2019/07/28 06:00
CRDT- 2017/03/31 06:00
PHST- 2016/10/26 00:00 [received]
PHST- 2017/02/22 00:00 [accepted]
PHST- 2017/01/24 00:00 [revised]
PHST- 2017/03/31 06:00 [pubmed]
PHST- 2019/07/28 06:00 [medline]
PHST- 2017/03/31 06:00 [entrez]
AID - 10.1007/s00059-017-4556-3 [pii]
AID - 10.1007/s00059-017-4556-3 [doi]
PST - ppublish
SO  - Herz. 2018 May;43(3):265-274. doi: 10.1007/s00059-017-4556-3. Epub 2017 Mar 29.