酒精对大鼠血清NOS活性及ADMA含量的影响  

Effect of Alcohol on Serum NOS Activity and ADMA Concentration in Rat Models

作　　者：李友[1] 贺彬琪[1] 李瑛[1] 邹丽君[1] 李程[1] 让蔚清[1] 

机构地区：[1]南华大学公共卫生学院,湖南衡阳421001

出　　处：《实用预防医学》2007年第2期315-318,共4页Practical Preventive Medicine

基　　金：湖南省卫生厅科研课题资助(B200508)

摘　　要：目的研究不同浓度的酒精对大鼠血清中NOS活性及其内源性抑制物ADMA含量的影响。方法动物实验选用SD大鼠(雄性、56只、体重约250 g)灌胃给予不同剂量饮用酒处理组(红星二锅头,1 ml/100 g),每天一次,连续2个月,建立酒精摄入的动物实验模型。实验分为7组(n=8)。(1)对照组,(2)低、中、高三个剂量的饮用酒组(红星二锅头,14 V/V2、8 V/V5、6 V/V),(3)高脂饮食组,(4)高脂饮食联合中剂量饮用酒组(28 V/V):灌胃给予红星二锅头的同时,给予高脂饲料,(5)维生素E保护组,在(4)组基础上,每天给予维生素E(100 mg/kg,灌酒前1 h灌胃给予)。2个月后,按常规取动物血清,测定MDA、NO的含量与NOS(包括iNOS、eNOS、总NOS)的活性及ADMA含量。结果与对照组相比,酒精、高脂饮食、酒精联合高脂饮食能显著升高MDA、NO、ADMA含量,降低eNOS活性,升高iNOS活性;维生素E能扭转上述生物学效应。结论酒精能增加脂质过氧化产物,影响NOS活性,干扰NO代谢。其机制可能与内源性一氧化氮合酶抑制物ADMA水平有关。维生素E对其损伤有一定的保护作用。Objective To study the effect of alcohol on serum ADMA level and NOS activities in rat models. Methods Sprague Dawley male rats weighing about 250g were actively given with three doses of alcohol （14V/V, 28V/V, and 56V/V） by intragastric feeding .at a rate of 1mL/100g, one time per day for two months. On the 60th day, blood samples were collected from femoral arteries, centrifuged （3500rpm, 10min） and separated immediately. Serum levels of MDA （thiobarbituricacid method）, NO （Griess method） and ADMA （HPLO） were determined. Serum activity of NOS （biochemical approach） was determined. The experimental rats were randomly divided into 7 groups： （1） negative control group, rats were given with equal volume of distilled water; （2） the alcohol groups, rats were given with different concentrations of alcohol （Hongxing Erguotou, 14V/V, 28V/V, and 55V/V） ; （3） high fat diet group, rats were given with high fat diet; （4） high fat diet ＆ alcohol at intermediate concentration group （28V/V） ; （5） VitE （100mg/kg） protected group, rats were given with Vitamin E at 1 hour before intragastric alcohol administration, while high fat diet was fed. Results Alcohol and/or high fat diet increased the serum levels of MDA, NO and ADMA, inhibited the activity of eNOS and increased the activity of iNOS. Vitamin E ameliorated the injurious effects induced by alcohol and high fat diet. Conclusion Alcohol is an important risk factor of hyperlipoidemia and endothelial damage. It induces the production of the blood lipid and lipid peroxidation, interferes with the metabolism of NO. The injurious mechanism induced by alcohol is related to the lipid peroxidation and the serum level of ADMA. Vitamin E can protect against the injurious effect induced by alcohol and high fat diet.

关 键 词：酒精 脂质过氧化 一氧化氮合酶 不对称性二甲基精氨酸 心脑血管疾病 

分 类 号：R54[医药卫生—心血管疾病]