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Published on: February 25, 2016
Nifedipine ameliorates ischemia-induced revascularization in diet-induced obese mice
Tetsutaro Kito1, Rei Shibata, Megumi Kondo
1Department of Cardiology, Nagoya University Graduate School of Medicine, Japan.
Background:
Obesity is a risk factor for the development of cardiovascular diseases that are associated with impaired angiogenesis. Nifedipine, a calcium-channel blocker, has a number of blood pressure (BP)-independent effects as well, such as improving endothelial function and decreasing oxidative stress. Here, we investigated whether nifedipine could improve the angiogenic responses in a diet-induced obese (DIO) model.
Methods:
DIO was induced by allowing 8-week-old C57BL/6J mice ad libitum access to a high-fat/high-sucrose (HF/HS) diet. Mice were randomly divided into two groups that were fed either the HF/HS or normal chow. At the age of 12 weeks, the animals were treated/not treated with nifedipine admixed with food at a concentration of 0.001%. Then, 1 week later, the mice were subjected to unilateral hind limb surgery.
Results:
Angiogenic repair of the ischemic hind limb was impaired in the DIO mice as compared with that in the control mice as evaluated by laser Doppler blood flowmetry (LDBF) and capillary density analysis. Treatment with nifedipine accelerated angiogenic repair in the DIO mice to a level equal to that seen in the control mice. DIO mice showed increased reactive oxygen species (ROS) production after hind limb ischemia. The number of endothelial progenitor cells (EPCs), which contribute to blood vessel formation, was also significantly lower in these mice. Nifedipine treatment ameliorated the oxidative status and increased the number of EPCs in the DIO mice.
Conclusions:
Our observations demonstrated that DIO impaired revascularization in response to tissue ischemia. Nifedipine ameliorated obesity-impaired revascularization through suppressing oxidative stress and enhancing the number of EPCs.
Insights
Nifedipine improves blood vessel formation in diet-induced obese mice. This calcium-channel blocker reduces oxidative stress and increases endothelial progenitor cells, aiding recovery from tissue ischemia.
Area of Science:
- Cardiovascular Research
- Obesity and Metabolism
- Angiogenesis and Vascular Biology
Background:
- Obesity is a significant risk factor for cardiovascular diseases, often linked to impaired angiogenesis.
- Nifedipine, a calcium-channel blocker, offers blood pressure-independent benefits including improved endothelial function and reduced oxidative stress.
- This study explores nifedipine's potential to enhance angiogenic responses in a diet-induced obese (DIO) mouse model.
Purpose of the Study:
- To investigate the effects of nifedipine on angiogenic repair in diet-induced obese mice.
- To determine if nifedipine can counteract obesity-related impairments in revascularization.
- To elucidate the mechanisms underlying nifedipine's action, focusing on oxidative stress and endothelial progenitor cells.
Main Methods:
- Diet-induced obesity (DIO) was established in C57BL/6J mice using a high-fat/high-sucrose diet.
- Mice were divided into DIO and control groups, with nifedipine treatment administered to a subset of DIO mice.
- Unilateral hind limb ischemia surgery was performed to assess angiogenic repair capacity.
Main Results:
- Angiogenic repair and blood flow recovery were significantly impaired in DIO mice compared to controls.
- Nifedipine treatment restored angiogenic repair in DIO mice to levels comparable to controls.
- DIO mice exhibited increased reactive oxygen species (ROS) and reduced endothelial progenitor cells (EPCs); nifedipine ameliorated these conditions.
Conclusions:
- Diet-induced obesity impairs revascularization following ischemic events.
- Nifedipine effectively counteracts obesity-induced deficits in revascularization.
- Nifedipine's beneficial effects are mediated by the suppression of oxidative stress and enhancement of endothelial progenitor cell counts.
