PMID- 21040784
OWN - NLM
STAT- MEDLINE
DCOM- 20110406
LR  - 20131121
IS  - 1879-0720 (Electronic)
IS  - 0928-0987 (Linking)
VI  - 42
IP  - 1-2
DP  - 2011 Jan 18
TI  - Escin attenuates acute lung injury induced by endotoxin in mice.
PG  - 73-80
LID - 10.1016/j.ejps.2010.10.008 [doi]
AB  - Endotoxin causes multiple organ dysfunctions, including acute lung injury (ALI). 
      The current therapeutic strategies for endotoxemia are designed to neutralize one 
      or more of the inflammatory mediators. Accumulating experimental evidence 
      suggests that escin exerts anti-inflammatory and anti-edematous effects. The aim 
      of this study was to evaluate the effect of escin on ALI induced by endotoxin in 
      mice. ALI was induced by injection of lipopolysaccharide (LPS) intravenously. The 
      mice were given dexamethasone or escin before injection of LPS. The mortality 
      rate was recorded. Tumor necrosis factor-alpha (TNF-alpha), interleukin 1beta (IL-1beta) and 
      nitric oxide (NO) were measured. Pulmonary superoxide dismutase (SOD), 
      glutathione peroxidase (GPx) activity, glutathione (GSH), malondialdehyde (MDA) 
      contents, and myeloperoxidase (MPO) activity were also determined. The expression 
      of glucocorticoid receptor (GR) level was detected by Western blotting. 
      Pretreatment with escin could decrease the mortality rate, attenuate lung injury 
      resulted from LPS, down-regulate the level of the inflammation mediators, 
      including NO, TNF-alpha, and IL-1beta, enhance the endogenous antioxidant capacity, and 
      up-regulating the GR expression in lung. The results suggest that escin may have 
      potent protective effect on the LPS-induced ALI by inhibiting of the inflammatory 
      response, and its mechanism involves in up-regulating the GR and enhancing the 
      endogenous antioxidant capacity.
CI  - Copyright (c) 2010 Elsevier B.V. All rights reserved.
FAU - Xin, Wenyu
AU  - Xin W
AD  - Department of Pharmacology, School of Pharmacy, Yantai University, Yantai, 
      Shandong, PR China.
FAU - Zhang, Leiming
AU  - Zhang L
FAU - Fan, Huaying
AU  - Fan H
FAU - Jiang, Na
AU  - Jiang N
FAU - Wang, Tian
AU  - Wang T
FAU - Fu, Fenghua
AU  - Fu F
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20101030
PL  - Netherlands
TA  - Eur J Pharm Sci
JT  - European journal of pharmaceutical sciences : official journal of the European 
      Federation for Pharmaceutical Sciences
JID - 9317982
RN  - 0 (Anti-Inflammatory Agents, Non-Steroidal)
RN  - 0 (Antioxidants)
RN  - 0 (Interleukin-1beta)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 0 (lipopolysaccharide, E coli O55-B5)
RN  - 31C4KY9ESH (Nitric Oxide)
RN  - 6805-41-0 (Escin)
RN  - EC 1.11.1.7 (Peroxidase)
RN  - EC 1.11.1.9 (Glutathione Peroxidase)
RN  - EC 1.15.1.1 (Superoxide Dismutase)
SB  - IM
MH  - Acute Lung Injury/chemically induced/enzymology/immunology/pathology/*prevention 
      & control
MH  - Animals
MH  - Anti-Inflammatory Agents, Non-Steroidal/administration & dosage/*therapeutic use
MH  - Antioxidants/metabolism
MH  - Blotting, Western
MH  - Escin/administration & dosage/*therapeutic use
MH  - Glutathione Peroxidase/metabolism
MH  - Interleukin-1beta/immunology
MH  - Lipopolysaccharides/*toxicity
MH  - Lung/*drug effects/enzymology/immunology/pathology
MH  - Male
MH  - Mice
MH  - Nitric Oxide/biosynthesis
MH  - Peroxidase/metabolism
MH  - Superoxide Dismutase/metabolism
MH  - Survival Analysis
MH  - Tumor Necrosis Factor-alpha/immunology
EDAT- 2010/11/03 06:00
MHDA- 2011/04/07 06:00
CRDT- 2010/11/03 06:00
PHST- 2010/08/17 00:00 [received]
PHST- 2010/10/21 00:00 [accepted]
PHST- 2010/11/03 06:00 [entrez]
PHST- 2010/11/03 06:00 [pubmed]
PHST- 2011/04/07 06:00 [medline]
AID - S0928-0987(10)00353-2 [pii]
AID - 10.1016/j.ejps.2010.10.008 [doi]
PST - ppublish
SO  - Eur J Pharm Sci. 2011 Jan 18;42(1-2):73-80. doi: 10.1016/j.ejps.2010.10.008. Epub 
      2010 Oct 30.