Pravastatin improves atherosclerosis in mice with hyperlipidemia by inhibiting TREM-1/DAP12

To study the protective effect of pravastatin on blood vessels in mice with hyperlipemia.

Apolipoprotein E (ApoE)-/- and triggering receptor expressed on myeloid (TREM)-/ApoE-/- mice were selected and fed with high-fat food, which were then subdivided into the control group and the pravastatin intervention group. C57BL/6J mice were used as controls. Oil Red O staining was used to stain aortas and sections so as to observe the level and basic composition of plaques. Immunohistochemistry was applied to detect inflammatory cells expression in aortic plaques. Real-time polymerase chain reaction (PCR) was employed to detect the expressions of TREM-1, tumor necrosis factor-alpha (TNF-α), and interleukin-1 (IL-1) messenger ribonucleic acids (mRNAs) in vascular tissues of mice in different groups, and the expressions of TREM-1, DNAX-activating protein of molecular mass 12 (DAP12), TNF-α, and IL-1 were detected via Western blotting technique.

Pravastatin reduced the area of atherosclerotic plaques and improved the plaque formation by reducing lipid deposits and alleviating plaque inflammatory responses. In the pravastatin group, the expression of TREM-1 in the aorta atherosclerotic plaque of mice was decreased, the expressions of TREM-1 and DAP12 genes and proteins in vascular tissue cells declined, and the expressions of the downstream inflammatory factors, TNF-α, IL-1 were reduced.

Pravastatin improves atherosclerosis (AS) in mice by inhibiting TREM-1/DAP12.