PMID- 30662666
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20200930
IS  - 1943-8141 (Print)
IS  - 1943-8141 (Electronic)
IS  - 1943-8141 (Linking)
VI  - 10
IP  - 12
DP  - 2018
TI  - Muscone improves cardiac function in mice after myocardial infarction by 
      alleviating cardiac macrophage-mediated chronic inflammation through inhibition 
      of NF-kappaB and NLRP3 inflammasome.
PG  - 4235-4246
AB  - Muscone is the main active monomer of traditional Chinese medicine musk. Previous 
      studies have reported a variety of beneficial effects of muscone. However, the 
      effects of muscone on chronic inflammation after myocardial infarction (MI) are 
      rarely reported. This study evaluated the anti-inflammatory effects of muscone on 
      myocardial infarction by establishing a MI model in mice. We found that muscone 
      remarkably decreased the levels of inflammatory cytokines (IL-1beta, TNF-alpha and 
      IL-6), and ultimately improved cardiac function and survival rate. Furthermore, 
      the main anti-inflammatory effect of muscone was alleviating cardiac 
      macrophage-mediated inflammatory response in heart tissues after MI. Bone 
      marrow-derived macrophages (BMDMs) induced with lipopolysaccharide (LPS) were 
      used as an in vitro inflammation model to further clarify anti-inflammatory 
      mechanisms of muscone. Muscone significantly downregulated the levels of 
      LPS-induced inflammatory cytokines and inhibited NF-kappaB and NLRP3 inflammasome 
      activation in BMDMs. Moreover, ROS and antioxidant indices in LPS-induced BMDMs 
      were also ameliorated after muscone treatment. To sum up, our study found that 
      muscone alleviated cardiac macrophage-mediated chronic inflammation by inhibiting 
      NF-kappaB and NLRP3 inflammasome activation, thereby improving cardiac function in MI 
      mice. Besides, the inhibitory effect of muscone on inflammation may be related to 
      the scavenging of ROS. It is suggested that muscone may serve as a promising and 
      effective drug for post-MI treatment.
FAU - Du, Yingqiang
AU  - Du Y
AD  - Department of Cardiology, The First Affiliated Hospital of Nanjing Medical 
      University Nanjing, China.
FAU - Gu, Xin
AU  - Gu X
AD  - Department of Cardiology, The First Affiliated Hospital of Nanjing Medical 
      University Nanjing, China.
FAU - Meng, Haoyu
AU  - Meng H
AD  - Department of Cardiology, The First Affiliated Hospital of Nanjing Medical 
      University Nanjing, China.
FAU - Aa, Nan
AU  - Aa N
AD  - Department of Cardiology, The First Affiliated Hospital of Nanjing Medical 
      University Nanjing, China.
FAU - Liu, Shuiyuan
AU  - Liu S
AD  - Department of Cardiology, The First Affiliated Hospital of Nanjing Medical 
      University Nanjing, China.
FAU - Peng, Chengyi
AU  - Peng C
AD  - Department of Cardiology, The First Affiliated Hospital of Nanjing Medical 
      University Nanjing, China.
FAU - Ge, Yingbin
AU  - Ge Y
AD  - Department of Physiology, Nanjing Medical University Nanjing, China.
FAU - Yang, Zhijian
AU  - Yang Z
AD  - Department of Cardiology, The First Affiliated Hospital of Nanjing Medical 
      University Nanjing, China.
LA  - eng
PT  - Journal Article
DEP - 20181215
PL  - United States
TA  - Am J Transl Res
JT  - American journal of translational research
JID - 101493030
PMC - PMC6325512
OTO - NOTNLM
OT  - Muscone
OT  - NF-kappaB
OT  - NLRP3 inflammasome
OT  - anti-inflammation
OT  - macrophage
OT  - myocardial infarction
COIS- None.
EDAT- 2019/01/22 06:00
MHDA- 2019/01/22 06:01
PMCR- 2018/12/15
CRDT- 2019/01/22 06:00
PHST- 2018/08/28 00:00 [received]
PHST- 2018/11/19 00:00 [accepted]
PHST- 2019/01/22 06:00 [entrez]
PHST- 2019/01/22 06:00 [pubmed]
PHST- 2019/01/22 06:01 [medline]
PHST- 2018/12/15 00:00 [pmc-release]
PST - epublish
SO  - Am J Transl Res. 2018 Dec 15;10(12):4235-4246. eCollection 2018.