Animal model for cigarette-smoke-induced atherosclerosis and related methods
View Patent ↗Provided herein are non-human animal models and related methods useful for the identification, characterization, and analysis of the effects of environmental stimuli on the development and progression of pathological conditions. The environmental stimuli can include, but are not limited to, exposure to tobacco (e.g., cigarette, etc.) smoke. Exemplary pathological conditions include, but are not limited to, atherosclerosis, other cardiovascular disease (CVD), and the like. Also provided herein are non-human animal models and related methods useful for the identification, characterization, and analysis of pharmaceutical compounds, compositions, and/or formulations that can be used to prevent or treat a given pathological condition brought on by exposure to a given environmental condition.
1. A method of producing a rodent model of atherosclerosis comprising the steps of:
exposing the rodent model to an inhaled environmental stimulus for from about 14 days to up to 28 days; and
analyzing the extent of atherosclerosis in the rodent model,
wherein the environmental stimulus is cigarette smoke,
wherein the rodent is a guinea pig, and
wherein atherosclerosis is determined by aortic plaque formation, thickening of the aortic wall, and/or narrowing of the aortic lumen in rodents exposed to cigarette smoke as compared to rodents not exposed to cigarette smoke.
2. The method of claim 1 wherein antioxidant levels in the rodent model are regulated.
3. The method of claim 2 wherein the antioxidant levels are regulated by manipulating diet of the rodent model.
4. The method of claim 2 wherein the antioxidant is vitamin C.
5. A method of evaluating one or more test compounds useful for the prevention or treatment of atherosclerosis comprising the steps of:
exposing a rodent model to an inhaled environmental-stimulus for from about 14 days to up to 28 days, wherein the rodent has further been exposed to one or more test compounds either before or after atherosclerosis has developed in the rodent; and
analyzing whether the one or more test compounds have prevented the development of atherosclerosis in the rodent model when the rodent model was exposed to the one or more test compounds before exposure to the environmental stimulus or whether the one or more test compounds have ameliorated the symptoms of atherosclerosis in the rodent model when the rodent model was exposed to the one or more test compounds after or concurrent with exposure to the environmental stimulus and after or concurrent with development of atherosclerosis,
wherein the environmental stimulus is cigarette smoke,
wherein the rodent is a guinea pig, and
wherein atherosclerosis is determined by aortic plaque formation, thickening of the aortic wall, and/or narrowing of the aortic lumen in rodents exposed to cigarette smoke as compared to rodents not exposed to cigarette smoke.
6. The method of claim 5 wherein antioxidant levels in the rodent model are regulated.
7. The method of claim 6 wherein the antioxidant levels are regulated by manipulating diet of the rodent model.
8. The method of claim 6 wherein the antioxidant is vitamin C.
9. A rodent model for the identification and characterization of test compounds useful for the prevention and treatment of atherosclerosis, wherein the atherosclerosis is induced by exposure of the rodent to cigarette smoke for from about 14 days to up to 28 days, wherein the rodent is a guinea pig, wherein atherosclerosis is determined by aortic plaque formation, thickening of the aortic wall, and/or narrowing of the aortic lumen in rodents exposed to cigarette smoke as compared to rodents not exposed to cigarette smoke.
10. The rodent model of claim 9 , wherein antioxidant levels in the rodent are regulated by diet.
11. The rodent model of claim 10 , wherein the antioxidant is vitamin C.
12. The rodent model of claim 9 , wherein the rodent is not fed with high lipid or high cholesterol diet.
13. The method of claim 1 , wherein the rodent model is not fed with high lipid or high cholesterol diet.
14. The method of claim 5 , wherein the rodent model is not fed with high lipid or high cholesterol diet.