| 摘要: | In this study the effects of low-dose aspirin (5 mg/kg) on adhesion molecule and chemokineexpression in a hyperlipidemic rat model. Six-week-old Sprague-Dawley (SD) rats were assigned to twocontrol groups receiving either a regular diet or high-fat diet (HFD) and a treatment group fed HFD with5 mg/kg aspirin for a 10-week period. Compared with the regular diet control group, the HFD control grouphad higher body weight, lower levels of high-density lipoprotein, higher concentrations of insulin,triglyceride, total cholesterol, and low-density lipoprotein, but no differences in blood glucose and glycatedhemoglobin. The prothrombin time (PT) and activated partial thromboplastin time (aPTT) were clearlyshortened in the HFD group.That group also had increased expression of intercellular adhesion molecule-1(ICAM-1), ICAM-2, ICAM-3, vascular cell adhesion molecule (VCAM), platelet endothelial cell adhesionmolecule (PECAM) and P-selectin in platelets and vascular adhesion protein-1 in lymphocyte and in aortaincreased expressions of ICAM-1, ICAM-2, ICAM-3, VCAM, PECAM, E-selectin, monocyte chemoattractantprotein-1 (MCP-1) and CCR2. The HFD rats also had increased PKCα, IκB kinase α (IKKα), p65, mitogenactivatedprotein kinases (MAPKs) (p38, c-Jun N-terminal kinases 1, extracellular signal-regulated kinase1/2), and their phosphorylated forms. Low-dose aspirin improved HFD-induced hyperinsulinemia andhyperlipidemia, recovered PT and aPTT, inhibited upregulation of adhesion molecules and chemokines andreduced expression of PKCα, IKKα, p65, and MAPKs. Low-dose aspirin ameliorates HFD-inducedhyperlipidemia and hyperinsulinemia, and prevents HFD-induced expression of adhesion molecules and chemokine formation. |
