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目的:探讨芍药苷(paeoniflorin,PF)对ApoE(apolipoprotein E,载脂蛋白E)基因缺失(ApoE-/-)小鼠动脉粥样硬化的作用。方法:采用紫外可见分光光度法测定体外芍药苷的抗氧化能力包括还原力、过氧化自由基清除能力以及DPPH自由基清除能力。18只雄性ApoE-/-小鼠随机分为芍药苷组和生理盐水组,ApoE-/-小鼠高脂喂养8周,于第6周开始灌胃给予60mg·kg-1芍药苷,qd,持续8周。小鼠眼眶取血,分离血浆,检测小鼠血浆中总胆固醇(TC),三酰甘油(TG)、游离胆固醇(FC)以及SOD水平。小鼠脱臼处死后分离胸腹主动脉,油红O染色检测胸腹主动脉的脂质沉积。结果:0.2 mg·ml-1维生素C甲醇溶液与32 mg·ml-1芍药苷甲醇溶液的还原力相当,随着剂量增加芍药苷还原力升高。DPPH自由基清除力也随着剂量增加而增加,其中,0.8 mg·ml-1芍药苷甲醇溶液具有约50%DPPH自由基清除力。同时,4 mg·ml-1芍药苷甲醇溶液具有约50%过氧化自由基清除力。动物实验研究结果表明:芍药苷组小鼠血浆SOD水平升高26.9%,与生理盐水组比较,差异显著(P<0.01)。60 mg·kg-1芍药苷显著降低小鼠血浆中TC和TG水平(P<0.05),但对血浆中FC水平作用不明显。与生理盐水组比较,芍药苷组腹主动脉脂质沉积显著减少(P<0.05)。结论:芍药苷可延缓ApoE-/-小鼠动脉粥样硬化的发展,其机制可能与其抗氧化及降低血脂水平有关。
Objective: To investigate the effect of paeoniflorin (PF) on atherosclerosis in Apolipoprotein E (Apolipoprotein E) deficient (ApoE-/-) mice. Methods: The anti-oxidation ability of paeoniflorin in vitro was determined by UV-Vis spectrophotometry, including reducing power, peroxide scavenging ability and DPPH free radical scavenging ability. Eighteen male ApoE-/- mice were randomly divided into paeoniflorin group and normal saline group. ApoE-/- mice were fed with high fat for 8 weeks, and 6 mg·kg-1 paeoniflorin was administered by gavage at the 6th week. Last 8 weeks. Blood was taken from the eyelids of the mice, plasma was separated, and plasma total cholesterol (TC), triglyceride (TG), free cholesterol (FC), and SOD levels were measured. The thoracoabdominal aorta was isolated after the mice were sacrificed and oil red O staining was used to detect lipid deposition in the thoracoabdominal aorta. RESULTS: The reducing power of 0.2 mg·ml-1 vitamin C methanol solution and 32 mg·ml-1 paeoniflorin methanol solution were equivalent. With the increase of dose, the reducing power of paeoniflorin increased. The DPPH radical scavenging power also increased with increasing doses, wherein the 0.8 mg·ml-1 paeoniflorin methanol solution had about 50% DPPH radical scavenging power. At the same time, 4 mg·ml-1 paeoniflorin methanol solution had a scavenging power of about 50% peroxidase. The results of animal experiments showed that the plasma SOD level in the paeoniflorin group was increased by 26.9%, which was significantly different from that of the saline group (P<0.01). Paeoniflorin at 60 mg·kg-1 significantly reduced plasma TC and TG levels (P<0.05), but had no significant effect on plasma FC levels. Compared with the saline group, the lipid deposition in the abdominal aorta of the paeoniflorin group was significantly reduced (P<0.05). CONCLUSION: Paeoniflorin can delay the development of atherosclerosis in ApoE-/- mice, and its mechanism may be related to its anti-oxidation and lowering of blood lipids.