PMID- 23318172
OWN - NLM
STAT- MEDLINE
DCOM- 20130816
LR  - 20220321
IS  - 1090-2104 (Electronic)
IS  - 0006-291X (Linking)
VI  - 431
IP  - 2
DP  - 2013 Feb 8
TI  - Apocynin suppresses the progression of atherosclerosis in apoE-deficient mice by 
      inactivation of macrophages.
PG  - 124-30
LID - S0006-291X(13)00050-8 [pii]
LID - 10.1016/j.bbrc.2013.01.014 [doi]
AB  - Production of reactive oxygen species (ROS) and other proinflammatory substances 
      by macrophages plays an important role in atherogenesis. Apocynin 
      (4-hydroxy-3-methoxy-acetophenone), which is well known as a NADPH oxidase 
      inhibitor, has anti-inflammatory effects including suppression of the generation 
      of ROS. However, the suppressive effects of apocynin on the progression of 
      atherosclerosis are not clearly understood. Thus, we investigated 
      anti-atherosclerotic effects of apocynin using apolipoprotein E-deficient 
      (apoE(-/-)) mice in vivo and in mouse peritoneal macrophages in vitro. In 
      atherosclerosis-prone apoE(-/-) mice, apocynin suppressed the progression of 
      atherosclerosis, decreased 4-hydroxynonenal-positive area in atherosclerotic 
      lesions, and mRNA expression of monocyte chemoattractant protein-1 (MCP-1) and 
      interleukin-6 (IL-6) in aorta. In mouse peritoneal macrophages, apocynin 
      suppressed the Ox-LDL-induced ROS generation, mRNA expression of MCP-1, IL-6 and 
      granulocyte/macrophage colony-stimulating factor, and cell proliferation. 
      Moreover, immunohistochemical studies revealed that apocynin decreased the number 
      of proliferating cell nuclear antigen-positive macrophages in atherosclerotic 
      lesions of apoE(-/-) mice. These results suggested that apocynin suppressed the 
      formation of atherosclerotic lesions, at least in part, by inactivation of 
      macrophages. Therefore, apocynin may be a potential therapeutic material to 
      prevent the progression of atherosclerosis.
CI  - Copyright (c) 2013 Elsevier Inc. All rights reserved.
FAU - Kinoshita, Hiroyuki
AU  - Kinoshita H
AD  - Department of Metabolic Medicine, Faculty of Life Sciences, Kumamoto University, 
      Kumamoto 860-8556, Japan.
FAU - Matsumura, Takeshi
AU  - Matsumura T
FAU - Ishii, Norio
AU  - Ishii N
FAU - Fukuda, Kazuki
AU  - Fukuda K
FAU - Senokuchi, Takafumi
AU  - Senokuchi T
FAU - Motoshima, Hiroyuki
AU  - Motoshima H
FAU - Kondo, Tatsuya
AU  - Kondo T
FAU - Taketa, Kayo
AU  - Taketa K
FAU - Kawasaki, Shuji
AU  - Kawasaki S
FAU - Hanatani, Satoko
AU  - Hanatani S
FAU - Takeya, Motohiro
AU  - Takeya M
FAU - Nishikawa, Takeshi
AU  - Nishikawa T
FAU - Araki, Eiichi
AU  - Araki E
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20130111
PL  - United States
TA  - Biochem Biophys Res Commun
JT  - Biochemical and biophysical research communications
JID - 0372516
RN  - 0 (Acetophenones)
RN  - 0 (Anti-Inflammatory Agents, Non-Steroidal)
RN  - 0 (Apolipoproteins E)
RN  - 0 (Ccl2 protein, mouse)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Interleukin-6)
RN  - 0 (Lipoproteins, LDL)
RN  - 0 (RNA, Messenger)
RN  - 0 (Reactive Oxygen Species)
RN  - 0 (oxidized low density lipoprotein)
RN  - 143011-72-7 (Granulocyte Colony-Stimulating Factor)
RN  - B6J7B9UDTR (acetovanillone)
SB  - IM
MH  - Acetophenones/*therapeutic use
MH  - Animals
MH  - Anti-Inflammatory Agents, Non-Steroidal/*therapeutic use
MH  - Apolipoproteins E/genetics
MH  - Atherosclerosis/*drug therapy/pathology
MH  - Chemokine CCL2/biosynthesis
MH  - Granulocyte Colony-Stimulating Factor/biosynthesis
MH  - Interleukin-6/biosynthesis
MH  - Lipoproteins, LDL/metabolism
MH  - Macrophages/*drug effects
MH  - Mice
MH  - Mice, Mutant Strains
MH  - RNA, Messenger/biosynthesis
MH  - Reactive Oxygen Species/antagonists & inhibitors
EDAT- 2013/01/16 06:00
MHDA- 2013/08/21 06:00
CRDT- 2013/01/16 06:00
PHST- 2013/01/03 00:00 [received]
PHST- 2013/01/05 00:00 [accepted]
PHST- 2013/01/16 06:00 [entrez]
PHST- 2013/01/16 06:00 [pubmed]
PHST- 2013/08/21 06:00 [medline]
AID - S0006-291X(13)00050-8 [pii]
AID - 10.1016/j.bbrc.2013.01.014 [doi]
PST - ppublish
SO  - Biochem Biophys Res Commun. 2013 Feb 8;431(2):124-30. doi: 
      10.1016/j.bbrc.2013.01.014. Epub 2013 Jan 11.