Corticosterone accelerates atherosclerosis in the apolipoprotein E-deficient mouse.

Area of Science:

• Cardiovascular Science
• Endocrinology
• Immunology

Background:

• Chronic stress is a significant risk factor for atherosclerosis and cardiovascular disease.
• Elevated corticosterone levels are observed in animal models of chronic stress.
• The direct role of corticosterone in exacerbating atherosclerosis requires further investigation.

Purpose of the Study:

• To determine if corticosterone is sufficient to exacerbate atherosclerosis in vivo.
• To investigate the physiological changes associated with corticosterone-induced atherosclerosis.

Main Methods:

• Apolipoprotein E (ApoE)-deficient mice were fed a high-fat diet for 13 weeks.
• Mice were exposed to corticosterone (CORT) or vehicle (Con) in their drinking water.
• Atherosclerotic plaque area, white blood cell counts, serum cytokine levels, and lipid profiles were analyzed.

Main Results:

• Corticosterone treatment significantly increased atherosclerotic plaque area at the aortic root.
• Corticosterone-induced atherosclerosis was associated with lower white blood cell counts and serum IL-1β.
• Elevated serum total cholesterol, LDL, VLDL, and sd-LDL were observed in corticosterone-treated mice.

Conclusions:

• Corticosterone is sufficient to exacerbate atherosclerosis in vivo, despite its anti-inflammatory properties.
• The pro-atherogenic effects of corticosterone are primarily linked to dyslipidemia.
• These findings highlight the critical role of corticosterone in the development of atherosclerosis.