PMID- 29509268
OWN - NLM
STAT- MEDLINE
DCOM- 20191106
LR  - 20220408
IS  - 2284-0729 (Electronic)
IS  - 1128-3602 (Linking)
VI  - 22
IP  - 4
DP  - 2018 Feb
TI  - Atorvastatin improves plaque stability in diabetic atherosclerosis through the 
      RAGE pathway.
PG  - 1142-1149
LID - 14403 [pii]
LID - 10.26355/eurrev_201802_14403 [doi]
AB  - OBJECTIVE: To study the improving effect of atorvastatin on plaque stability in 
      diabetes mellitus (DM) mice complicated with atherosclerosis. MATERIALS AND 
      METHODS: Apolipoprotein E (ApoE)-/- mice were used to establish the DM mouse 
      model. Half of the mice received atorvastatin after successful modeling. ApoE-/- 
      and C57BL/6J mice were used as controls. Oil red O staining and Masson staining 
      were performed to detect the lipid and collagen components in mice. 
      Immunohistochemical assay was used to observe the expressions of smooth muscle 
      cell (SMC) and Ly-6c. The expressions of receptor for advanced glycation end 
      products (RAGE), monocyte chemoattractant protein-1 (MCP-1) and nuclear factor-kappaB 
      (NF-kappaB) in tissues were detected by Western blotting. Finally, the levels of 
      serum soluble RAGE (sRAGE), advanced glycation end products (AGEs), 
      malondialdehyde (MDA) and reduced glutathione (GSH) in mice were also detected. 
      RESULTS: Atorvastatin reduced the area of atherosclerotic plaque and improved the 
      stability of arterial plaque through reducing lipid deposition, the number of 
      macrophages and SMC, increasing collagen fibers. In mice in atorvastatin group, 
      the levels of serum AGEs and sRAGE were decreased. Moreover, atorvastatin 
      inhibited the downstream pathway of RAGE as well as DM, thus inducing the 
      oxidative stress. CONCLUSIONS: Atorvastatin improves plaque stability in diabetic 
      atherosclerosis through the RAGE pathway.
FAU - Zhou, F
AU  - Zhou F
AD  - Department of Neurology, The Third Affiliated Hospital of Nanchang University, 
      Nanchang, China. wuxm79@163.com.
FAU - Tan, Y
AU  - Tan Y
FAU - Chen, X-H
AU  - Chen XH
FAU - Wu, F-L
AU  - Wu FL
FAU - Yang, D-J
AU  - Yang DJ
FAU - Zhang, X-W
AU  - Zhang XW
FAU - Wu, X-M
AU  - Wu XM
FAU - Deng, Y-Q
AU  - Deng YQ
LA  - eng
PT  - Journal Article
PL  - Italy
TA  - Eur Rev Med Pharmacol Sci
JT  - European review for medical and pharmacological sciences
JID - 9717360
RN  - 0 (Ager protein, mouse)
RN  - 0 (Hydroxymethylglutaryl-CoA Reductase Inhibitors)
RN  - 0 (Receptor for Advanced Glycation End Products)
RN  - A0JWA85V8F (Atorvastatin)
SB  - IM
MH  - Animals
MH  - Atherosclerosis/*blood/drug therapy/pathology
MH  - Atorvastatin/pharmacology/*therapeutic use
MH  - Diabetes Mellitus/*blood/drug therapy/pathology
MH  - Hydroxymethylglutaryl-CoA Reductase Inhibitors/pharmacology/therapeutic use
MH  - Male
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mice, Knockout
MH  - Oxidative Stress/drug effects/physiology
MH  - Plaque, Atherosclerotic/*blood/drug therapy/pathology
MH  - Receptor for Advanced Glycation End Products/*blood
EDAT- 2018/03/07 06:00
MHDA- 2019/11/07 06:00
CRDT- 2018/03/07 06:00
PHST- 2018/03/07 06:00 [entrez]
PHST- 2018/03/07 06:00 [pubmed]
PHST- 2019/11/07 06:00 [medline]
AID - 14403 [pii]
AID - 10.26355/eurrev_201802_14403 [doi]
PST - ppublish
SO  - Eur Rev Med Pharmacol Sci. 2018 Feb;22(4):1142-1149. doi: 
      10.26355/eurrev_201802_14403.