动脉粥样硬化的炎症机制及阿魏酸钠的干预作用

The inflammation mechanism of atherosclerotic and intervention effects of sodium ferulate

建立动脉粥样硬化(AS)大鼠模型,灌胃阿魏酸钠(SF),探讨其炎症以及干预炎症反应的机制。SD大鼠随机分为正常组、模型组、阳性组[辛伐他汀2mg.(kg.d)-1],SF 3个剂量组[80、40、20mg.(kg.d)-1]。建模第2周开始给药,连续8周。全自动生化仪测定血清TC、TG、LDL-C、HDL-C含量,酶联免疫吸附法检测血清ox-LDL、IL-10、TNF-α、CRP含量;取主动脉及肝脏制作切片,显微镜观察组织形态结构。结果表明:模型大鼠血清TC、TG、LDL-C均显著升高,HDL-C有所下降,分别与正常组比较均有显著差异(P<0.01);SF可以降低动脉粥样硬化大鼠血清TC、TG含量(P<0.01),提高HDL-C和IL-10含量(P<0.01),且可降低ox-LDL、TNF-α、CRP水平(P<0.01)。说明AS形成伴随炎症因子异常,SF通过抑制炎症因子、减少ox-LDL生成,调节血脂,减少泡沫细胞形成,进而减轻AS斑块形成,改善血管壁和肝脏脂肪变性的病理改变,从而预防AS。

atherosclerosis（AS） rat model was established to study the pathogenesis of inflammatory mechanism and sodium ferulate（sodium ferulate,SF） interfered with the inflammatory response.SD rats were randomly divided into six groups： normal control group,model group,positive control group [simvastatin 2 mg·（kg·d）-1],sodium ferulate（SF） group treat with 80,40,20 mg·（kg·d）-1,each group including 10 rats.Except normal group,established rats model of AS started drug intervention in the second week of model making,and last for 8 week.The automatic biochemical analyzer was used to measure the level of TC,TG,LDL-C,HDL-C in the serum and the level of ox-LDL,IL-10,TNF-α,CRP in the serum was measured by Elisa.Part of liver and aortic tissue was taken to make slices for observing liver＇s and aortic＇s morphological structure with microscope.Results showed that TC,TG,LDL-C of model group significantly increased,HDL-C significantly decreased,and compared with the normal group there was significant difference（P 0.01）.Giving sodium ferulate could low down the level of TC,TG（P0.01）,significantly reduce ox-LDL,TNF-α,CRP（P0.01） and elevate the level of HDL-C and IL-10（P0.01） in the serum of rats with atherosclerosis.AS formation was accompanied with inflammatory cytokines unusual.Sodium ferulate could inhibit the inflammatory reaction and reduce the generation of ox-LDL,so as to reduce the formation of foam cell,and then inhibit the formation of atherosclerotic plaque,and to improve the pathological changes of the vascular wall and liver steatosis,prevent or delay occurrence and development of atherosclerosis.