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补肾活血方对鹌鹑动脉粥样硬化的防治作用及其量效相关性 被引量:3

BuShen HuoXue Prescription on the Prevention and Its Dose-effect Relationship to Atherosclerosis
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摘要 目的:通过单纯高脂血症喂养法诱导建立鹌鹑动脉粥样硬化模型(AS模型),观察补肾活血方对血脂水平、主动脉管壁组织形态学的改变,探讨补肾活血方对高脂血症所致AS的防治作用及对AS斑块稳定性的影响。方法:通过连续12周的特制高脂饲料喂养,诱发鹌鹑动脉粥样硬化(AS)病变。①经过对总胆固醇(CHOL)、甘油三酯(TG)、低密度脂蛋白胆固醇(LDL-C)及高密度脂蛋白胆固醇(HDL-C)不同时间点的检测,动态观察补肾活血方对模型动物血脂水平的影响;②通过肉眼与HE染色观察模型动物主动脉的形态学变化。结果:①AS动物模型建立。实验动物鹌鹑均成功复制了AS模型。动脉中可见明显的AS斑块,呈点状或片状乳白色隆起,多位于主动脉窦至主动脉弓段;对照组未见AS病变,内膜光滑且管壁弹性好。②补肾活血方对模型动物的影响。给药11周时,鹌鹑血清中补肾活血方大剂量组的CHOL、TG、LDL-C含量均较模型组低(P<0.05),且对TG作用更为明显;其抗动脉粥样硬化指数HDL-C/LDL-C值比模型组高(P<0.05),而AI值较模型组低(P<0.05);补肾活血方中、小剂量组降血脂作用不明显(P>0.05);补肾活血方组血清的CHOL、TG、LDL-C含量均低于同时间点的模型组,在给药6周、8周时与模型组比较有显著性差异(P<0.05);血清HDL-C、HDL-C/LDL-C值、AI值与模型组比较差异不明显(P>0.05)。③AS斑块的形态学改变。对照组鹌鹑主动脉内膜光滑、完整,无细胞浸润;模型组内膜增厚,泡沫细胞丰富,平滑肌排列紊乱,内弹力板断裂,可见明显斑块;补肾活血方组和阳性组AS病变较轻,斑块形成范围较小。结论:补肾活血方有一定的降血脂作用且呈剂量依赖性,表现为降低血清TG、CHOL、LDL-C,略升高HDL-C;有较好的稳定斑块的作用且在一定程度上抑制AS病变的进程。 Objective:To observe the effects of BuShen HuoXue prescription on the level of blood lipid and tube wall histomorphology of aorta, and discuss the prevention of the prescription to atherosclerosis (AS) and its in-fluence on the stability of AS plaque by establishing AS models induced with high cholesterol feeding method. Methods:The models with AS were built up by high cholesterol feeding method for 12 consecutive weeks.①The effects of BuShen HuoXue prescription on the levels of blood lipid in animal models were observed by detecting to-tal cholesterol (CHOL), triglyceride (TG), low density lipoprotein cholesterol (LDL-C) and high density lipoprotein cholesterol (HDL-C) at different times;②Morphological changes of the aorta were explored by naked eyes and HE staining. Results:①To establish AS animal models, quail with AS was successfully duplicated. There were obvious AS plaque in the arota, showing dotted or platelike milky ridge, mostly located at aortic sinus to aortic arch;there was no pathological changes of AS in the control group, the inner membrane was smooth and stretchable.②The ef-fects of BuShen HuoXue prescription on animal models. The contents of CHOL, TG and LDL-C in the high dosage group of BuShen HuoXue prescriptions were lower than those in the model group (P&lt;0.05), and the effects on TG were more notable after administering the drugs for 11 weeks;the ratio of HDL-C/LDL-C was higher than that of the model group(P&lt;0.05) while AI value was lower than that of the model group(P&lt;0.05);low dose of BuShen HuoX-ue prescription was insignificant(P&gt;0.05);the contents of CHOL, TG, LDL-C in the group of BuShen HuoXue pre-scription were lower that these indexes in the model group at the same time, it had significant difference compared with the model group after administering the drug for six weeks and eight weeks (P&lt;0.05);the difference was in-significant when HDL-C, HDL-C/LDL-C and AI were compared with those of the model group (P&gt;0.05).③Mor-phological changes of AS plaque. Inner membrane of the quail in the control group was smooth, complete and with-out cellular infiltration;the membrane of the model group was thickened and rich of foam cells, the cells of smooth muscle were arranged in disorder, internal elastic lamina was fractured, obvious plaque could be seen;pathological changes in BuShen HuoXue prescription group and positive group were more lighter, and formation range of plaque was smaller. Conclusion: BuShen HuoXue prescription could decrease blood lipid in the dose-dependent manner, which demonstrates that it could lower TG, CHOL, LDL-C but raise HDL-C slightly, it could stabilize plaque and in-hibit the development of AS pathological changes to a certain degree.
出处 《西部中医药》 2014年第1期22-25,共4页 Western Journal of Traditional Chinese Medicine
关键词 动脉粥样硬化模型 补肾活血方 斑块 鹌鹑 实验动物 AS models BuShen HuoXue prescription plaque quail experimental animal
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参考文献2

  • 1Gillian Murphy,Hideaki Nagase.Progress in matrix metalloproteinase research[J].Molecular Aspects of Medicine.2008(5)
  • 2Peter Liu,Mei Sun,Sawsan Sader.Matrix metalloproteinases in cardiovascular disease[J].Canadian Journal of Cardiology.2006

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