PMID- 31707400
OWN - NLM
STAT- MEDLINE
DCOM- 20200323
LR  - 20200323
IS  - 1643-3750 (Electronic)
IS  - 1234-1010 (Print)
IS  - 1234-1010 (Linking)
VI  - 25
DP  - 2019 Nov 10
TI  - Alisol B 23-Acetate Ameliorates Lipopolysaccharide-Induced Cardiac Dysfunction by 
      Suppressing Toll-Like Receptor 4 (TLR4)/NADPH Oxidase 2 (NOX2) Signaling Pathway.
PG  - 8472-8481
LID - 10.12659/MSM.918252 [doi]
AB  - BACKGROUND Cardiac dysfunction during endotoxemia is a major cause of 
      cardiovascular disease with high morbidity and mortality. Alisol B 23-acetate 
      (AB23A) is a triterpenoid extracted from the Rhizoma Alismatis, a kind of 
      traditional Chinese medicine, exhibits anti-inflammatory activity on endotoxemia. 
      This investigation aimed to uncover the protective e ff ects of AB23A against 
      sepsis-induced cardiac dysfunction. MATERIAL AND METHODS Adult male C57BL/6 mice 
      received lipopolysaccharide (LPS) (20 mg/kg intravenous) stimulation, with or 
      without pre-treatment of AB23A (10 mg/kg, 20 mg/kg, or 40 mg/kg). 
      Histopathological staining and cardiac function were performed 4 hours after LPS 
      stimulation. Then the levels of interleukin (IL)-6, IL-1ss, and tumor necrosis 
      factor (TNF)-alpha were monitored with enzyme-linked immunosorbent assay (ELISA). 
      In addition, H9C2 cells were treated with LPS (5 mug/mL) with or without 
      pre-treated with AB23A (0.1 muM, 1 muM, or 10 muM), and the production of reactive 
      oxygen species (ROS) was detected by DCFH-DA combined with flow cytometry. The 
      expression of Toll-like receptor 4 (TLR4), NADPH oxidase 2 (NOX2), NOX4, P38, 
      p-P38, extracellular-signal-regulated kinase (ERK), and p-ERK were assessed by 
      western blotting. RESULTS AB23A improved the survival rate and ameliorated 
      myocardial injury, decreased inflammatory infiltration and the level of IL-6, 
      IL-1ss, and TNF-alpha in the LPS-stimulated mouse model. Moreover, AB23A inhibited 
      the ROS production in LPS-treated H9C2 cells. In addition, AB23A suppressed the 
      levels of TLR4 and NOX2 as well as the activation levels of P38 and ERK both in 
      vivo and in vitro. CONCLUSIONS AB23A reduced LPS-induced myocardial dysfunction 
      by inhibiting inflammation and ROS production through the TLR4/NOX2 pathway.
FAU - Wang, BinYan
AU  - Wang B
AD  - College of Pharmacy, Zhejiang Chinese Medical University, Hangzhou, Zhejiang, 
      China (mainland).
FAU - Chen, Liang
AU  - Chen L
AD  - Laboratory Animal Research Center, Zhejiang Chinese Medical University, Hangzhou, 
      Zhejiang, China (mainland).
FAU - Dai, LingHao
AU  - Dai L
AD  - Academy of Traditional Chinese Medicine, Zhejiang Chinese Medical University, 
      Hangzhou, Zhejiang, China (mainland).
FAU - Fang, WenMing
AU  - Fang W
AD  - College of Pharmacy, Zhejiang Chinese Medical University, Hangzhou, Zhejiang, 
      China (mainland).
FAU - Wang, Hui
AU  - Wang H
AD  - College of Pharmacy, Zhejiang Chinese Medical University, Hangzhou, Zhejiang, 
      China (mainland).
LA  - eng
PT  - Journal Article
DEP - 20191110
PL  - United States
TA  - Med Sci Monit
JT  - Medical science monitor : international medical journal of experimental and 
      clinical research
JID - 9609063
RN  - 0 (Cholestenones)
RN  - 0 (Drugs, Chinese Herbal)
RN  - 0 (Interleukin-6)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (Reactive Oxygen Species)
RN  - 0 (Tlr4 protein, mouse)
RN  - 0 (Toll-Like Receptor 4)
RN  - 0 (Triterpenes)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 0 (alisol B 23-acetate)
RN  - 0 (triterpenoid TP-222)
RN  - EC 1.6.3.- (NADPH Oxidase 2)
RN  - EC 1.6.3.- (NADPH Oxidases)
RN  - EC 2.7.11.24 (Mitogen-Activated Protein Kinases)
RN  - EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases)
SB  - IM
MH  - Animals
MH  - China
MH  - Cholestenones/*pharmacology
MH  - Drugs, Chinese Herbal/pharmacology
MH  - Endotoxemia/*drug therapy
MH  - Heart Diseases/chemically induced/*drug therapy/physiopathology
MH  - Inflammation
MH  - Interleukin-6/metabolism
MH  - Lipopolysaccharides/pharmacology
MH  - Male
MH  - Medicine, Chinese Traditional/methods
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mitogen-Activated Protein Kinases/metabolism
MH  - NADPH Oxidase 2/metabolism
MH  - NADPH Oxidases/metabolism
MH  - Phosphorylation
MH  - Reactive Oxygen Species/metabolism
MH  - Sepsis
MH  - Signal Transduction/drug effects
MH  - Toll-Like Receptor 4/metabolism
MH  - Triterpenes/pharmacology
MH  - Tumor Necrosis Factor-alpha/metabolism
MH  - p38 Mitogen-Activated Protein Kinases/metabolism
PMC - PMC6863037
EDAT- 2019/11/11 06:00
MHDA- 2020/03/24 06:00
PMCR- 2019/11/10
CRDT- 2019/11/11 06:00
PHST- 2019/11/11 06:00 [entrez]
PHST- 2019/11/11 06:00 [pubmed]
PHST- 2020/03/24 06:00 [medline]
PHST- 2019/11/10 00:00 [pmc-release]
AID - 918252 [pii]
AID - 10.12659/MSM.918252 [doi]
PST - epublish
SO  - Med Sci Monit. 2019 Nov 10;25:8472-8481. doi: 10.12659/MSM.918252.