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Published on: February 20, 2019
A study on the expression of FGF-21 and NF-κB pathway in the tissues of atherosclerotic mice
1Shanghai Chest Hospital, Shanghai Jiaotong University, Shanghai, China. zhangminxk@126.com.
Objective:
To study the relationship between the expressions of fibroblast growth factor (FGF)-21 and NF-κB signal transduction pathway in the tissues of atherosclerotic mice.
Materials And Methods:
A total of 40 apoE-/- male mice at 8 weeks were selected and randomly divided into 4 groups. 10 mice in group A were normally fed with diet. 10 mice in group B were fed with high-fat diet. 10 mice in group C were fed with high-fat diet + pravastatin. 10 mice in group D were fed with high-fat diet + subcutaneous injection of exogenous recombinant FGF-21 protein. Another 10 C57BL/6J mice at 8 weeks were normally fed with diet (group E). They were killed after 12 weeks to collect retinal venous blood. ELISA method was applied to detect the levels of serum FGF-21, NF-κB, monocyte chemo attractant protein (MCP-1), matrix metalloproteinase (MMP)-9 and TNF-α. Immunohistochemical staining and RT-PCR method were applied to detect the expression of FGF-21 in aortic arch and liver tissues. RT-PCR method and Western blot method were applied to detect the expression of NF-κB, MCP-1, MMP-9 and TNF-α in aortic arch and liver tissues.
Results:
The levels of serum FGF-21, NF-κB, MCP-1, MMP-9 and TNF-α in group B were higher than those of group A and group E, and those of group C and group D were lower than those of group B (except FGF-21 in group D). The differences had statistical significance (p<0.05). The positive staining rates of FGF-21 in endothelial cells of aortic arch and liver tissues in group B were higher than those group A and group E, and those of group C and group D were lower than those of group B. The differences had statistical significance (p<0.05). The expression levels of FGF-21mRNA, NF-κB, MCP-1, MMP-9, TNF-αmRNA and protein in endothelial cells of aortic arch and liver tissues in group B were higher than those group A and group E, and those of group C and group D were lower than those of group B. The differences had statistical significance (p<0.05).
Conclusions:
FGF-21 may participate in the occurrence of atherosclerosis (AS), which is related to the activation of the NF-κB pathway. Lipid-lowering therapy can inhibit the activation of FGF-21 and NF-κB. Exogenous FGF-21 can also lower the activation of NF-κB and interpose in atherosclerosis process.
Insights
Fibroblast growth factor (FGF)-21 is involved in atherosclerosis development through the NF-κB pathway. Both lipid-lowering therapy and exogenous FGF-21 can reduce NF-κB activation, suggesting therapeutic potential.
Area of Science:
- Cardiovascular Research
- Molecular Biology
- Endocrinology
Background:
- Atherosclerosis (AS) involves complex inflammatory processes.
- The role of fibroblast growth factor (FGF)-21 in AS pathogenesis is under investigation.
- The nuclear factor kappa B (NF-κB) pathway is a key regulator of inflammation in AS.
Purpose of the Study:
- To investigate the relationship between FGF-21 expression and NF-κB pathway activation in atherosclerotic mice.
- To evaluate the effects of lipid-lowering therapy and exogenous FGF-21 on these markers.
Main Methods:
- ApoE-/- mice were fed high-fat diets, with some receiving pravastatin or FGF-21.
- Serum and tissue levels of FGF-21, NF-κB, MCP-1, MMP-9, and TNF-α were measured.
- Techniques included ELISA, immunohistochemistry, RT-PCR, and Western blot.
Main Results:
- High-fat diet increased FGF-21, NF-κB, MCP-1, MMP-9, and TNF-α levels.
- Pravastatin and FGF-21 treatments reduced these markers compared to the high-fat diet group.
- FGF-21 expression in tissues correlated with NF-κB pathway activation.
Conclusions:
- FGF-21 appears to play a role in atherosclerosis development, linked to NF-κB pathway activation.
- Lipid-lowering therapy and exogenous FGF-21 can modulate FGF-21 and NF-κB activity.
- These findings suggest potential therapeutic strategies targeting the FGF-21/NF-κB axis in AS.
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