PMID- 26376109
OWN - NLM
STAT- MEDLINE
DCOM- 20160801
LR  - 20161125
IS  - 1532-2513 (Electronic)
IS  - 0892-3973 (Linking)
VI  - 37
IP  - 5
DP  - 2015
TI  - Protective effect of astragaloside IV on lipopolysaccharide-induced cardiac 
      dysfunction via downregulation of inflammatory signaling in mice.
PG  - 428-33
LID - 10.3109/08923973.2015.1080266 [doi]
AB  - CONTEXT: Astragaloside IV (ASI) is a major and active saponin derivative of 
      Astragalus membranaceus (Fisch) Bge. The anti-inflammatory properties of ASI are 
      important for its cardioprotective effects. However, the molecular mechanisms of 
      the protective effect of ASI on lipopolysaccharide (LPS)-induced cardiac 
      dysfunction is yet to be elucidated. OBJECTIVE: This study was designed to 
      investigate the therapeutic effects and possible mechanisms of ASI against 
      LPS-induced septic cardiac dysfunction and inflammation in mice. MATERIALS AND 
      METHODS: Mice were intraperitoneally injected with ASI (20 mg/kg) for 1 week 
      before LPS challenge (10 mg/kg, i.p.). Left ventricular performance and 
      morphology were analyzed using echocardiography 6 h after LPS induction. 
      Activities of lactate dehydrogenase (LDH) in serum were measured and serum levels 
      of cardiac troponin I (cTnI) were quantified by ELISA. Serum levels of tumor 
      necrosis factor-alpha (TNF-alpha), monocyte chemotactic protein 1 (MCP-1), interleukin-6 
      (IL-6) and IL-1beta were also quantified by ELISA. The protein expressions of NF-small ka, CyrillicB 
      p65 and p-AKT in heart tissues were detected using Western blot analysis. 
      RESULTS: LPS administration deteriorated cardiac function and was attenuated by 
      ASI pretreatment. ASI attenuated LPS-induced the increase of LDH and cTnI 
      activities in mice. ASI also prevented NF-small ka, CyrillicB activation and subsequent myocardial 
      inflammatory responses in endotoxemic mice. The effects of ASI were closely 
      associated with the phosphatidylinositol-3-kinase (PI3K/AKT) signaling pathway, 
      as characterized by ASI-induced activation in phospho-Akt. ASI also extended the 
      lifespan of toxemic mice. CONCLUSION: ASI significantly attenuated LPS-induced 
      cardiac dysfunction and inflammatory mediator production by inhibiting NF-small ka, CyrillicB and 
      activating PI3K/AKT signaling pathway.
FAU - Zhao, Peng
AU  - Zhao P
AD  - a Graduate School of Medicine, Tianjin Medical University , Tianjin , China and.
AD  - b Tianjin Key Laboratory of Cardiovascular Remodeling and Target Organ Injury, 
      Institute of Cardiovascular Disease and Heart Center, Pingjin Hospital, Logistics 
      University of the Chinese People's Armed Police Forces , Tianjin , China.
FAU - Wang, Ying
AU  - Wang Y
AD  - b Tianjin Key Laboratory of Cardiovascular Remodeling and Target Organ Injury, 
      Institute of Cardiovascular Disease and Heart Center, Pingjin Hospital, Logistics 
      University of the Chinese People's Armed Police Forces , Tianjin , China.
FAU - Zeng, Shan
AU  - Zeng S
AD  - b Tianjin Key Laboratory of Cardiovascular Remodeling and Target Organ Injury, 
      Institute of Cardiovascular Disease and Heart Center, Pingjin Hospital, Logistics 
      University of the Chinese People's Armed Police Forces , Tianjin , China.
FAU - Lu, Jie
AU  - Lu J
AD  - b Tianjin Key Laboratory of Cardiovascular Remodeling and Target Organ Injury, 
      Institute of Cardiovascular Disease and Heart Center, Pingjin Hospital, Logistics 
      University of the Chinese People's Armed Police Forces , Tianjin , China.
FAU - Jiang, Tie-Min
AU  - Jiang TM
AD  - b Tianjin Key Laboratory of Cardiovascular Remodeling and Target Organ Injury, 
      Institute of Cardiovascular Disease and Heart Center, Pingjin Hospital, Logistics 
      University of the Chinese People's Armed Police Forces , Tianjin , China.
FAU - Li, Yu-Ming
AU  - Li YM
AD  - b Tianjin Key Laboratory of Cardiovascular Remodeling and Target Organ Injury, 
      Institute of Cardiovascular Disease and Heart Center, Pingjin Hospital, Logistics 
      University of the Chinese People's Armed Police Forces , Tianjin , China.
LA  - eng
PT  - Journal Article
DEP - 20150916
PL  - England
TA  - Immunopharmacol Immunotoxicol
JT  - Immunopharmacology and immunotoxicology
JID - 8800150
RN  - 0 (Cytokines)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (Rela protein, mouse)
RN  - 0 (Saponins)
RN  - 0 (Transcription Factor RelA)
RN  - 0 (Triterpenes)
RN  - 3A592W8XKE (astragaloside A)
RN  - EC 2.7.11.1 (Oncogene Protein v-akt)
SB  - IM
MH  - Animals
MH  - Cytokines/blood
MH  - Heart Diseases/blood/*chemically induced/*prevention & control
MH  - Inflammation/chemically induced/metabolism
MH  - Lipopolysaccharides/*toxicity
MH  - Mice
MH  - Myocardium/*metabolism
MH  - Oncogene Protein v-akt/metabolism
MH  - Saponins/*pharmacology
MH  - Signal Transduction/*drug effects
MH  - Transcription Factor RelA/metabolism
MH  - Triterpenes/*pharmacology
OTO - NOTNLM
OT  - Astragaloside IV
OT  - NF-small ka, CyrillicB
OT  - PI3K/Akt signaling
OT  - cardiac dysfunction
OT  - sepsis/septic shock
EDAT- 2015/09/17 06:00
MHDA- 2016/08/02 06:00
CRDT- 2015/09/17 06:00
PHST- 2015/09/17 06:00 [entrez]
PHST- 2015/09/17 06:00 [pubmed]
PHST- 2016/08/02 06:00 [medline]
AID - 10.3109/08923973.2015.1080266 [doi]
PST - ppublish
SO  - Immunopharmacol Immunotoxicol. 2015;37(5):428-33. doi: 
      10.3109/08923973.2015.1080266. Epub 2015 Sep 16.