[Nifedipine attenuates vascular inflammation via inhibin NF-κB activity].

OBJECTIVE: To explore the effects and related mechanism of nifedipine on vascular inflammation induced by cuff placement. METHODS: Adult male C57BL/6J mice (10 to 12 weeks of age) were assigned to control (no cuff placement without nifedipine), cuff placement (cuff placement without nifedipine) and treatment (cuff placement with nifedipine 1 or 5 mg×kg(-1)×d(-1)) groups. Activity of NF-κB in injured artery was measured 5 days after operation. MCP-1 expression and nuclear translocation of NF-κB were examined in injured artery 7 days after operation. RESULTS: DNA-binding activity of NF-κB was significantly increased in the injured artery 5 days after cuff placement which could be downregulated by nifedipine 5 mg×kg(-1)×d(-1). MCP-1 mRNA expression in the injured arteries was increased 7 days after cuff placement and which could be significantly attenuated by nifedipine 5 mg×kg(-1)×d(-1). Cuff placement decreased the cytoplasmic level of p50, IκBα, IκBß, and increased the nuclear level of p50. Nifedipine 5 mg×kg(-1)×d(-1) significantly attenuated these changes. CONCLUSION: Our results suggest that high dose nifedipine could suppresses expression of MCP-1 induced by injured arteries via the inhibin NF-κB DNA binding activity, thereby attenuating vascular inflammation.

[Relation between apolipoprotein CIII gene polymorphism and coronary artery disease].

OBJECTIVE: To explore the relation between apolipoprotein CIII (ApoCIII) gene polymorphism and coronary artery disease (CAD). METHODS: Peripheral blood samples were collected from 400 healthy blood donors and 360 CAD patients. Total cholesterol (TC), triglycerides (TG), high-density lipoproteins cholesterol (HDL-C), low-density lipoproteins cholesterol (LDL-C), and ApoCIII were detected. Fluorescence quantitative PCR was used to detect the ApoCIII) gene polymorphisms. Genomic DNA was extracted from whole blood samples. We study the relation between variants of ApoCIII-625 and -455 and CAD by FQ-PCR. Then we explore the relation between variants of ApoCIII-625 and -455 and the concentration of lipid. All objects were measured about Total Cholesterol (TC), Triglycerides (TG), high-density lipoproteins cholesterol (HDL-C), low-density lipoproteins cholesterol (LDL-C) and ApoCIII. RESULTS: The ApoCIII-455C homozygote rate of the CAD patients was 70.1%, significantly higher than that of the healthy persons (53.1%). The ApoCIII-625del-455c phenotype rate of the CAD patients was 49.3%, significantly higher than that of the healthy persons. The ApoCIII-455C expression rates of the patients with hyperlipidemia and those with hyperlipidemia combined with CAD were high. There was no significant difference in the expression of ApoCIII-455c between the CAD patients and the normal persons. CONCLUSION: The gene polymorphisms of ApoCIII-455 increase the risk of CAD. ApoCIII-455C gene is positively related to the risk of CAD. The homozygotes of the ApoCIII-455C gene have high risk of CAD. ApoCIII-455C in cooperation with -625 (del) will increase the risk of CAD.