Key result
Low-dose atorvastatin (10 mg/kg/day) significantly increased regional blood flow, neovascularization, and the expression of angiogenic factors in ischemic hindlimbs, while also increasing endothelial progenitor cell numbers in hypertensive rats.
Why the study?
Does atorvastatin improve angiogenesis and endothelial progenitor cell formation in rat models of hindlimb ischemia and hypertension?
Does atorvastatin improve angiogenesis and endothelial progenitor cell formation in rat models of hindlimb ischemia and hypertension?
p-value: p=<0.05
Low-dose atorvastatin promotes angiogenesis in ischemic hindlimbs and increases endothelial progenitor cell formation, suggesting potential therapeutic utility for severe limb ischemia.
Hypothesis-generating for angiogenesis in hypertensive ischemia models; leaves open translation to human peripheral artery disease.
AIM: To investigate the mechanisms underlying the pro-angiogenic effects of statin, the effects of atorvastatin were investigated on the expression of angiogenic factors in ischemic hindlimbs of rats. The function and number of endothelial progenitor cells (EPCs) were investigated in hypertensive rats. METHODS: Hindlimb ischemia rats were administered 10 or 30 mg/kg/day atorvastatin orally for 2 weeks. Angiogenesis was evaluated by a laser Doppler and by Isolectin-B4 immunostaining. The expressions of VEGF, IL-8, angiopoietin (Ang)-1, Ang-2, eNOS, and hemoxidase (HO)-1 were evaluated by Western blotting and immunohistochemistry. Spontaneously hypertensive rats (SHR) were administered 10 mg/kg/day atorvastatin. EPC function was evaluated by colony formation and migration. The EPC number was evaluated by CD34-positive cells. RESULTS: A lowdose of atorvastatin, but not a highdose, significantly increased regional blood flow. Atorvastatin significantly increased the expressions of VEGF, IL-8, Ang-1, Ang-2, eNOS, and HO-1 proteins in ischemic hindlimbs. Atorvastatin significantly increased the number and colony formation of EPCs and decreased oxidation in mononuclear cells from SHR. CONCLUSION: Atorvastatin strongly induced angiogenesis with increases in angiogenic cytokines, HO-1 and EPC numbers. Statins are thus considered potertial agents for therapeutic angiogenesis.
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Matsumura et al. (2009) studied Hindlimb ischemia and hypertension. Atorvastatin vs. 0.5% methylcellulose (vehicle control) was evaluated on Regional blood flow and neovascularization in ischemic hindlimb (p=<0.05). Low-dose atorvastatin (10 mg/kg/day) significantly increased regional blood flow, neovascularization, and the expression of angiogenic factors in ischemic hindlimbs, while also increasing endothelial progenitor cell numbers in hypertensive rats.
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