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[Nuclear factor κB and IKB expression and calcium deposition of atherosclerotic plaques in apolipoprotein E and low density lipoprotein receptor knockout mice].

Fengzhen Yang, Jun Zhou, Wenwen Li, Fang Wang, Pu-yuan Wen, Li Zhou, Jiangang Wang, Xingxing Zheng

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Abstract

OBJECTIVE: To 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. METHODS: Eight 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. RESULTS: Degree 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). CONCLUSION: High-fat diet contributes to the formation of AS plagues in ApoE(-/-) and LDLR(-/-) mice joined by upregulated NFκB and IKB expressions and calcium deposition.

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What this paper is about

OBJECTIVE: To 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. METHODS: Eight 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. RESULTS: Degree 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). CONCLUSION: High-fat diet contributes to the formation of AS plagues in ApoE(-/-) and LDLR(-/-) mice joined by upregulated NFκB and IKB expressions and calcium deposition.

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Available abstract

OBJECTIVE: To 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. METHODS: Eight 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. RESULTS: Degree 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). CONCLUSION: High-fat diet contributes to the formation of AS plagues in ApoE(-/-) and LDLR(-/-) mice joined by upregulated NFκB and IKB expressions and calcium deposition.

Key concepts: Apolipoprotein E, LDL receptor, Endocrinology, Internal medicine, Apolipoprotein B, Knockout mouse, Lipoprotein, Receptor

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[Nuclear factor κB and IKB expression and calcium deposition of atherosclerotic plaques in apolipoprotein E and low density lipoprotein receptor knockout mice]. — Research Paper | ScholarLens