虎杖苷通过降血脂抗ApoE-/-小鼠动脉粥样硬化的作用
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摘要
目的研究虎杖苷在ApoE-/-小鼠动脉粥样硬化治疗中的作用及其可能的机制。方法采用高脂饲料连续喂养12周ApoE-/-小鼠,建立动脉粥样硬化动物模型,将已经形成动脉粥样硬化ApoE-/-小鼠分为模型组,虎杖苷组,阳性药(辛伐他汀)组,每组8只,阳性药(辛伐他汀)以0.05 g·kg~(-1)·d~(-1)灌胃,虎杖苷0.2 g·kg~(-1)·d~(-1)灌胃,正常对照及模型组分别给予同体积的蒸馏水,连续灌胃28 d后,取血和冠状动脉,采用HE染色对冠状动脉的形态学改变进行观察;检测血清中高密度脂蛋白,氧化型的低密度脂蛋白,总胆固醇的含量。结果病理切片HE染色显示,虎杖苷组小鼠的血管组织形态较模型组有较明显的改善,和阳性药组结果类似,显示出虎杖苷对动脉粥样硬化具有较好的的治疗效果;模型组血液中氧化型低密度脂蛋白的含量约为正常对照的5.3倍,虎杖苷组血液中的氧化型低密度脂蛋白的含量约为正常对照的3倍,是模型组含量的56.6%,与模型组比较,虎杖苷可以显著的降低血清中氧化型低密度脂蛋白的水平(q=7.884,P<0.05)。结论虎杖苷可降低血脂,减少脂质的沉积,改善动脉粥样硬化血管组织的形态,具备治疗动脉粥样硬化的潜力。
Objective To determine whether polydatin could protect against atherosclerosis in ApoE deficient mice and to further reveal the potential mechanism.Methods Male ApoE-/-deficient mice(8 weeks old)were obtained and were given high-fat diet,while the normal control group was given normal diet.These high-fat diet mice were assigned into three groups: model group,polydatin group 0.2g·kg~(-1)·d~(-1),and positive drug group(Simvastatin,0.05 g·kg~(-1)·d~(-1)).The normal control group and model group were given the same volume of distilled water.All mice were administered orally,which continued for 28 days.Then,all mice were killed; serum and coronary arteries were saved.HE staining of coronary arteries was established.Serum high density lipoprotein,oxidized low density lipoprotein,and total cholesterol were measured.Results By HE staining,the results showed that polydatin had an obvious improvement in vascular tissue morphology in comparison with the model group,and positive drug group showed similar results,i.e,polydatin on atherosclerosis had good therapeutic effect.Oxidized low density lipoprotein in the blood of model group was about 5.3 times that of normal controls.Oxidized low density lipoprotein in the blood of polydatin group was about three times that of the normal controls,and 56.6%of the content of model group.Compared with the model group,polydatin significantly(q = 7.884,P < 0.05)reduced the levels of serum oxidized low density lipoprotein.Conclusions Polydatin can reduce blood fat,decrease lipid deposition,and improve the morphology of atherosclerotic vascular tissue in the treatment of atherosclerosis.
Objective To determine whether polydatin could protect against atherosclerosis in ApoE deficient mice and to further reveal the potential mechanism.Methods Male ApoE-/-deficient mice(8 weeks old)were obtained and were given high-fat diet,while the normal control group was given normal diet.These high-fat diet mice were assigned into three groups: model group,polydatin group 0.2g·kg~(-1)·d~(-1),and positive drug group(Simvastatin,0.05 g·kg~(-1)·d~(-1)).The normal control group and model group were given the same volume of distilled water.All mice were administered orally,which continued for 28 days.Then,all mice were killed; serum and coronary arteries were saved.HE staining of coronary arteries was established.Serum high density lipoprotein,oxidized low density lipoprotein,and total cholesterol were measured.Results By HE staining,the results showed that polydatin had an obvious improvement in vascular tissue morphology in comparison with the model group,and positive drug group showed similar results,i.e,polydatin on atherosclerosis had good therapeutic effect.Oxidized low density lipoprotein in the blood of model group was about 5.3 times that of normal controls.Oxidized low density lipoprotein in the blood of polydatin group was about three times that of the normal controls,and 56.6%of the content of model group.Compared with the model group,polydatin significantly(q = 7.884,P < 0.05)reduced the levels of serum oxidized low density lipoprotein.Conclusions Polydatin can reduce blood fat,decrease lipid deposition,and improve the morphology of atherosclerotic vascular tissue in the treatment of atherosclerosis.
引文
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[12]孟秋宏,刘宏宝,王剑波.虎杖苷通过PI3K/Akt信号通路调控Shh信号分子对氧糖剥夺/复氧肾小管上皮细胞的保护作用[J].细胞与分子免疫学杂志,2015,31(11):1452-1457.
[13]吴占庆,马强,冶国栋.虎杖苷对重症失血性休克患者心功能及外周血血小板线粒体的影响[J].中国生化药物杂志,2015,35(9):146-148.
[14]卞徽宁,孙传伟,陈华德,等.虎杖苷对成纤维细胞生物学特性的影响[J].中国组织工程研究与临床康复,2012,16(33):6111-6115.
[15]Liu LT,Guo G,Wu M,et al.The progress of the research on cardio-vascular effects and acting mechanism of polydatin[J].Chin J Integr Med,2012,18(9):714-719.
[2]谭宇卫,郑玉姣,王雅君,等.血脂异常及动脉粥样硬化中医研究进展[J].现代生物医学进展,2013,13(16):3197-3200.
[3]成利娟,葛朝亮,杨翠,等.小麦胚芽油抗动脉粥样硬化的药效学研究[J].安徽医药,2015,19(10):1849-1852.
[4]宋磊,钱之玉,陈真,等.动脉粥样硬化与炎症的关系及相关治疗药物[J].药学进展,2013,37(2):49-57.
[5]赵愉快,刘仲华,莫卓群.大孔吸附树脂对虎杖中虎杖苷的吸附分离效果的研究[J].湖南农业科学,2011(9):123-126.
[6]吴占庆,马强,冶国栋.虎杖苷对重症失血性休克患者心功能及外周血血小板线粒体的影响[J].中国生化药物杂志,2015,35(9):146-148.
[7]陈云燕,王兴民,宋瑞,等.重症失血性休克大鼠的外周血血小板线粒体的变化及虎杖苷的干预作用[J].南方医科大学学报,2013,29(9):882-888.
[8]夏婷婷,杨珺超,刘清源,等.虎杖药理作用研究进展[J].浙江中西医结合杂志,2016,26(3):294-297.
[9]Kullo IJ,Rooke TW.Clinical Practice.Peripheral artery disease[J].N Engl J Med,2016,374(9):861-871.
[10]Aronow HD,Beckman JA.Parsing atherosclerosis:The unnatural history of peripheral artery disease[J].Circulation,2016,134(6):438-440.
[11]黄波,江芬,薛莱,等.PPARβ在虎杖苷抗高糖高胰岛素诱导心肌肥大中的作用[J].中国药理学通报,2015,31(9):1264-1269.
[12]孟秋宏,刘宏宝,王剑波.虎杖苷通过PI3K/Akt信号通路调控Shh信号分子对氧糖剥夺/复氧肾小管上皮细胞的保护作用[J].细胞与分子免疫学杂志,2015,31(11):1452-1457.
[13]吴占庆,马强,冶国栋.虎杖苷对重症失血性休克患者心功能及外周血血小板线粒体的影响[J].中国生化药物杂志,2015,35(9):146-148.
[14]卞徽宁,孙传伟,陈华德,等.虎杖苷对成纤维细胞生物学特性的影响[J].中国组织工程研究与临床康复,2012,16(33):6111-6115.
[15]Liu LT,Guo G,Wu M,et al.The progress of the research on cardio-vascular effects and acting mechanism of polydatin[J].Chin J Integr Med,2012,18(9):714-719.