Nuclear factor κB and IKB expression and calcium deposition of atherosclerotic plaques in apolipoprotein E and low density lipoprotein receptor knockout mice.
- Author:
Feng-zhen YANG
1
;
Jun ZHOU
;
Wen-wen LI
;
Fang WANG
;
Pu-yuan WEN
;
Li ZHOU
;
Jian-gang WANG
;
Xing-xing ZHENG
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Apolipoproteins E; genetics; metabolism; Calcium; metabolism; Female; I-kappa B Proteins; metabolism; Male; Mice; Mice, Inbred C57BL; Mice, Knockout; NF-kappa B; metabolism; Plaque, Atherosclerotic; metabolism; pathology; Receptors, LDL; genetics; metabolism
- From: Chinese Journal of Cardiology 2012;40(8):684-689
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo observe the histopathological features, nuclear factor-κB (NFκB) and IKB expressions as well as calcium deposition of atherosclerosis plaques (AS) in apolipoprotein E (ApoE) and low density lipoprotein receptor (LDLR) knockout mice (ApoE(-/-), LDLR(-/-)fed high-fat diet.
METHODSEight C57BL/6J mice fed with normal diet were used as control, 32 ApoE(-/-) mice and LDLR(-/-) mice were divided into normal diet and high-fat diet groups (n = 8 each). After 4 months, aorta was collected for morphologic (HE, Oil Red O, Von Kossa) and immunohistochemistry (nuclear factor-κB, IKB, macrophage surface molecule-3, α-smooth action protein) analysis.
RESULTSDegree of AS in ApoE(-/-) and LDLR(-/-) mice fed with high-fat diet were significantly severer than those fed with normal diet and AS was more significant in ApoE(-/-) mice than in LDLR(-/-) mice. NFκB and IKB expressions in high-fat diet group were significantly higher than the normal diet group (P < 0.05). Double-labeling of NFκB revealed dominant expression in smooth muscle cells. Calcium deposition was significantly more in ApoE(-/-) mice fed with high-fat diet than mice fed with normal diet (P < 0.05) and was similar in LDLR(-/-) mice fed with high and normal diet (P > 0.05).
CONCLUSIONHigh-fat diet contributes to the formation of AS plagues in ApoE(-/-) and LDLR(-/-) mice joined by upregulated NFκB and IKB expressions and calcium deposition.