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Assessing Therapeutic Angiogenesis in a Murine Model of Hindlimb Ischemia
Published on: June 8, 2019
Fenofibrate enhances neovascularization in a murine ischemic hindlimb model
Akira Katayama1, Yasutaka Yamamoto, Kohei Tanaka
1Department of Genetic Medicine and Regenerative Therapeutics, Tottori University Graduate School of Medical Science, Yonago, Japan.
Journal of Cardiovascular Pharmacology
|August 25, 2009
Summary
Fenofibrate enhances neovascularization by stimulating the nitric oxide (NO) pathway. This study shows fenofibrate improves blood flow and capillary density in ischemic limbs, an effect blocked by inhibiting NO.
Area of Science:
- Cardiovascular Research
- Pharmacology
- Molecular Biology
Background:
- Nitric oxide (NO) pathway is crucial for neovascularization.
- Fenofibrate's potential to influence NO-mediated processes is under investigation.
Purpose of the Study:
- To evaluate the effect of fenofibrate on neovascularization in a murine ischemic hindlimb model.
- To elucidate the role of the nitric oxide pathway in fenofibrate-induced neovascularization.
Main Methods:
- Murine ischemic hindlimb model treated with fenofibrate and/or NG-nitro-l-arginine methyl ester hydrochloride (L-NAME).
- Assessment of limb blood perfusion, capillary density, serum NO levels, and aortic NOS activity.
- In vitro studies using human umbilical vein endothelial cells to assess NOS activity and angiogenesis.
Main Results:
- Fenofibrate significantly increased limb blood perfusion, capillary density, serum NO levels, and aortic NOS activity.
- These fenofibrate-induced effects were abolished by L-NAME, indicating NO pathway involvement.
- Fenofibrate reduced serum triglyceride levels, but this was independent of neovascularization improvement.
- In vitro, fenofibrate stimulated NOS activity and angiogenesis, which was blocked by L-NAME.
Conclusions:
- Fenofibrate enhances neovascularization in a murine hindlimb ischemia model.
- The mechanism involves the activation of the NO pathway in endothelial cells.
- Triglyceride-lowering effects are not responsible for the observed neovascularization benefits.
