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作 者:王敏[1] 李先平[1] 赵立玲[2] 曹虹[1] 梁好[1] 唐爱国[1] 罗湘杭[2]
机构地区:[1]中南大学湘雅二医院检验科,湖南省长沙市410011 [2]中南大学代谢内分泌研究所,湖南省长沙市410011
出 处:《中国全科医学》2010年第24期2700-2703,共4页Chinese General Practice
基 金:国家自然科学基金(30700891)
摘 要:目的探讨载脂蛋白E(ApoE)基因缺陷小鼠血液生化指标的变化。方法选取28周龄雄性ApoE基因缺陷小鼠6只和同性别、同周龄的野生型C57BL/6 J(WT)雄鼠10只,采用全自动生化分析仪分别测定其血清中三酰甘油(TG)、总胆固醇(TC)、低密度脂蛋白(LDL-C),高密度脂蛋白(HDL-C)、载脂蛋白B(Apo-B)、超敏C反应蛋白(hs-CRP)、游离脂肪酸(NEFA)、肌酸激酶(CK)、肌酸激酶同工酶(CK-MB)、乳酸脱氢酶(LDH)、缺血修饰白蛋白(IMA)、骨保护素(OPG)、碱性磷酸酶(ALP)、γ谷氨酰转移酶(γGT)、钙(Ca)和磷(P)的含量。结果与WT小鼠相比,ApoE基因缺陷小鼠血清中血脂指标TG、TC、LDL-C、ApoB、hs-CRP和NE-FA明显升高,而HDL-C明显降低,差异有统计学意义(P<0.05);心肌酶学指标CK、LDH和IMA与WT小鼠比较,差异有统计学意义(P<0.05),两组间CK-MB比较,差异无统计学意义(P=0.08)。ApoE基因缺陷小鼠血清中骨代谢相关指标OPG水平明显增高,ALP水平明显降低,与WT小鼠比较,差异有统计学意义(P<0.05),而Ca、P和γGT水平间差异无统计学意义(P>0.05)。结论 ApoE基因缺陷小鼠血液生化指标的变化与动脉粥样硬化密切相关,且伴随心肌功能的损伤以及骨代谢异常。Objective To investigate the changes of blood biochemical markers in 28-week-old male mice with apolipoprotein E(ApoE)gene deficiency.Methods Six 28-week-old male mice with ApoE deficiency(ApoE-/-) and 10 sex-and age-matched C57BL/6J mice(WT) were enrolled in this study.Automatic biochemistry analyzer was used to determine the concentrations of triglycerides(TG),total cholesterol(TC),low density lipoprotein cholesterol(LDL-C),high density lipoprotein cholesterol(HDL-C),apolipoprotein B(ApoB),high sensitivity C-reactive protein(hs-CRP),non-esterifed fatty acid(NEFA),creatine kinase(CK),creatine kinase-isozymesisoenzymes(CK-MB),lactate dehydrogenase(LDH),albumin ischemia-modified(IMA),osteoprotegerin(OPG),alkaline phosphatase(ALP),gamma-glutamytransferase(γGT),calcium(Ca) and phosphorus(P).Results The lelves of serum TG,TC,LDL-C,ApoB,hs-CRP and NEFA were significantly higher,HDL-C lower in ApoE-/-group than in WT group(P0.05).There was significant difference in CK,LDH and IMA between 2 groups(P0.05),but not in CK-MB(P= 0.08).OPG levels were significantly higher,ALP levels lower in ApoE-/-group than in WT group(P0.05),but no significant difference was noted in Ca,P,γGT(P0.05).Conclusion The blood biochemical changes are closely related to atherosclerosis in mice with ApoE gene deficiency,accompanied by myocardial function and bone metabolism.
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