PMID- 27062545
OWN - NLM
STAT- MEDLINE
DCOM- 20170621
LR  - 20220317
IS  - 1742-4658 (Electronic)
IS  - 1742-464X (Linking)
VI  - 283
IP  - 12
DP  - 2016 Jun
TI  - Pioglitazone alleviates inflammation in diabetic mice fed a high-fat diet via 
      inhibiting advanced glycation end-product-induced classical macrophage 
      activation.
PG  - 2295-308
LID - 10.1111/febs.13735 [doi]
AB  - Classically activated macrophages (M1) are associated with inflammation in 
      diabetic patients. Inflammation is a known risk factor in diabetes. The present 
      study tested the hypothesis that pioglitazone (PIO) alleviates inflammation in 
      diabetic mice fed a high-fat diet by inhibiting advanced glycation end-product 
      (AGE)-induced classical macrophage activation. It was found that AGE treatment 
      promoted the transcription of pro-inflammatory molecules and M1 surface markers, 
      whereas PIO increased the expression of anti-inflammatory genes and decreased the 
      expression of pro-inflammatory mediators in bone marrow-derived macrophages 
      (BMDMs) in a dose-dependent manner. Furthermore, pretreatment with PIO abrogated 
      the effects of AGE on pro-inflammatory markers and partly inhibited AGE-induced 
      nuclear factor-kappaB (NF-kappaB) activation. PIO treatment partly reduced the 
      inflammatory phenotype in diabetic ApoE(-/-) mice, and significantly reduced 
      NF-kappaB activation in plaques. Therefore, we conclude that PIO blocks classical 
      activation of macrophages and attenuates inflammation in mouse models of 
      diabetes.
CI  - (c) 2016 Federation of European Biochemical Societies.
FAU - Jin, Xian
AU  - Jin X
AD  - Department of Cardiology, Central Hospital of Minhang District, Shanghai, China.
AD  - Department of Cardiology, Xinhua Hospital, Shanghai Jiao Tong University School 
      of Medicine, China.
FAU - Liu, Liang
AU  - Liu L
AD  - Department of Cardiology, Xinhua Hospital, Shanghai Jiao Tong University School 
      of Medicine, China.
FAU - Zhou, Zhong'e
AU  - Zhou Z
AD  - Department of Cardiology, Central Hospital of Minhang District, Shanghai, China.
AD  - Department of Cardiology, Xinhua Hospital, Shanghai Jiao Tong University School 
      of Medicine, China.
FAU - Ge, Junhua
AU  - Ge J
AD  - Department of Cardiology, The Affiliated Hospital of Qingdao University, China.
FAU - Yao, Tongqing
AU  - Yao T
AD  - Department of Cardiology, Tongling People's Hospital, China.
FAU - Shen, Chengxing
AU  - Shen C
AD  - Department of Cardiology, Xinhua Hospital, Shanghai Jiao Tong University School 
      of Medicine, China.
LA  - eng
PT  - Journal Article
DEP - 20160509
PL  - England
TA  - FEBS J
JT  - The FEBS journal
JID - 101229646
RN  - 0 (Anti-Inflammatory Agents)
RN  - 0 (Glycation End Products, Advanced)
RN  - 0 (NF-kappa B)
RN  - 0 (Thiazolidinediones)
RN  - X4OV71U42S (Pioglitazone)
SB  - IM
MH  - Animals
MH  - Anti-Inflammatory Agents/administration & dosage
MH  - Bone Marrow/drug effects
MH  - Diabetes Mellitus, Experimental/complications/*drug therapy/genetics/pathology
MH  - Diet, High-Fat
MH  - Glycation End Products, Advanced/genetics
MH  - Humans
MH  - Inflammation/complications/*drug therapy/genetics/pathology
MH  - Macrophage Activation/*drug effects
MH  - Macrophages/drug effects
MH  - Mice
MH  - Mice, Inbred NOD
MH  - NF-kappa B/genetics
MH  - Pioglitazone
MH  - Thiazolidinediones/*administration & dosage
OTO - NOTNLM
OT  - NF-kappaB
OT  - advanced glycation end-product
OT  - inflammation
OT  - macrophage polarization
OT  - pioglitazone
EDAT- 2016/04/12 06:00
MHDA- 2017/06/22 06:00
CRDT- 2016/04/11 06:00
PHST- 2015/10/06 00:00 [received]
PHST- 2016/02/22 00:00 [revised]
PHST- 2016/04/06 00:00 [accepted]
PHST- 2016/04/11 06:00 [entrez]
PHST- 2016/04/12 06:00 [pubmed]
PHST- 2017/06/22 06:00 [medline]
AID - 10.1111/febs.13735 [doi]
PST - ppublish
SO  - FEBS J. 2016 Jun;283(12):2295-308. doi: 10.1111/febs.13735. Epub 2016 May 9.