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ARS Home » Southeast Area » Little Rock, Arkansas » Microbiome and Metabolism Research Unit » Research » Publications at this Location » Publication #253359
Title: Blueberry diet protect against atherosclerosis in apoE-deficient mice by inhibiting scavenger receptor expression

Author
item XIE, CHENGHUI - Arkansas Children'S Nutrition Research Center (ACNC)
item WU, XIANLI - Arkansas Children'S Nutrition Research Center (ACNC)
item NAGARAJAN, SHANMUGAM - Arkansas Children'S Nutrition Research Center (ACNC)

Submitted to: Federation of American Societies for Experimental Biology Conference
Publication Type: Abstract Only
Publication Acceptance Date: 2/11/2010
Publication Date: 4/12/2010
Citation: Xie, C., Wu, X., Nagarajan, S. 2010. Blueberry diet protect against atherosclerosis in apoE-deficient mice by inhibiting scavenger receptor expression [abstract]. Federation of American Societies for Experimental Biology Journal 24:342.5.

Interpretive Summary:

Technical Abstract: Atherosclerosis is an inflammatory process that leads to the onset of cardiovascular disease. The scavenger receptor-mediated uptake of oxLDL by macrophages leads to foam cell formation, which is an initial event in the formation of atherosclerotic fatty streak lesions. In this report, the mechanism contributing to the atheroprotective effects of blueberry supplemented diet was addressed in apoE -/- mice. ApoE knockout (ApoE-/-) mice fed AIN-93G diet (CD) formulated to contain 1% freeze-dried whole wild blueberries (CD1 percent BB) were found to have significantly less atherosclerotic lesions in aorta. Reduced mRNA expression of scavenger receptors (CD36, CD68 and SRA) were found in BB feeding aorta. These results were further verified by protein level, in heart tissue and in vitro study on macrophage. In conclusion, these findings suggest that the atheroprotective effect of the blueberries supplemented diet is mediated in part by inhibiting scavenger receptor expression that could result in reduced OXLDL endocytosis in an early event of atherogenesis.