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作 者:贾乙[1] 李晓辉[1] 张海港[1] 刘雅[1] 张翼冠[1]
机构地区:[1]第三军医大学药学院新药研究中心,重庆400038
出 处:《现代生物医学进展》2008年第7期1245-1247,共3页Progress in Modern Biomedicine
基 金:国家自然科学基金资助(30470465;30371768)
摘 要:目的:观察持续性炎症对动脉粥样硬化大鼠肝素后脂蛋白脂酶活性及相关代谢物的影响。方法:试验动物分为4组:对照组、单纯高脂饮食组、炎症组和抗炎组。单纯高脂饮食组给予高脂饮食;炎症组除高脂饮食外,用酵母多糖腹腔注射(20 mg/kg,1次/3天)进行炎症刺激;抗炎组动物除按炎症组处理外,用阿司匹林进行抗炎治疗;对照组为正常饮食。动物饲养8周。第4、8周时测血清肝素后脂蛋白脂酶的活性,并用ELISA法检测TNF-α和CRP水平以及酶法测定TG、LDL和HDL含量。结果:与单纯高脂动脉粥样硬化大鼠相比,叠加的炎症刺激能明显升高血清中TNF-α和CRP水平,并显著降低肝素后脂蛋白脂酶活性,TNF-α和CRP水平的变化与肝素后脂蛋白脂酶活性的变化均呈显著负相关:同时,血清TG、LDL含量显著升高,而HDL含量显著降低;阿司匹林(12 mg/kg,1次/日)能明显降低大鼠血清中TNF-α和CRP的水平,升高肝素后脂蛋白脂酶活性,降低TG和LDL的含量,并升高HDL含量。结论:持续性全身炎症刺激可以明显降低动脉粥样硬化大鼠模型血清肝素后脂蛋白脂酶活性,从而加重TG、LDL和HDL的代谢紊乱。Objective: To determine the role of durative systemic inflammation on the activity of post-heparin lipoprotein lipase (LPL) in atherosclerotic rats. Methods: Rats were randomly divided into four groups: control group, simple high-fat diet group, inflammation group and anti-inflammation group. All of these animals except the rats in control group were fed with high-fat diet for 8 weeks. Besides high-lipid diet, zymosan was injected intraperitoneally (20 mg/kg, once every three days ) as additional inflammatory stimulation in inflammation group. Aspirin was given ( 12 mg/kg, once daily) in anti-inflammation group. The samples of serum were obtained at the 4th and 8th week. TNF-α and CRP levels were determined with ELISA kits, and the activity of post-heparin lipoprotein lipase, serum TG, LDL and HDL levels were measured with commercial kits, respectively. Results: Compared with simple high-fat diet group, post-heparin LPL activity was decreased significantly in inflammation group. At the same time, the levels of TNF-α, CRP, LDL and TG in serum increased significantly while HDL decreased. And the changes of serum lipid levels presented negative correlation with that of activity of post-heparin LPL. Anti-inflammation treatment could decrease serum TNF-α, CRP, LDL and TG levels, and increase post-heparin LPL activity HDL markedly. Conclusions: Inflammation could decrease the activity of post-heparin LPL and aggravate the disorder of the metabolism of TG, LDL and HDL in atherosclerotic rats.
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