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目的观察葛根素对载脂蛋白E基因敲除(Apo E-/-)小鼠主动脉粥样硬化(AS)病变、血脂水平、内脏脂肪素(visfatin)及炎症因子IL-6及TNF-α表达的影响。方法 50只SPF级8周龄雄性Apo E-/-小鼠予高脂饲料喂养随机分为5组:葛根素低、中、高剂量组分别给予葛根素300,600,1200 mg·kg-1·d-1灌胃;辛伐他汀组灌服辛伐他汀5 mg·kg-1·d-1;模型组灌服等剂量生理盐水。另设10只相同基因背景和周龄的雄性C57BL/6J小鼠为对照组予普通饲料喂养。16周后测小鼠体质量、血清脂质及visfatin、血浆IL-6及TNF-α含量;HE染色观察小鼠主动脉组织AS斑块面积;western blotting测小鼠主动脉visfatin蛋白的表达。结果各给药组小鼠体质量增加值、血清visfatin、TG、TC、LDL-C水平、血浆IL-6及TNF-α含量、主动脉visfatin蛋白表达均显著低于模型组(P<0.05),血清HDL-C高于模型组(P<0.05);辛伐他汀组、葛根素中、高剂量组小鼠主动脉AS斑块面积百分比显著低于模型组(P<0.05)。结论葛根素可通过降血脂、减小AS斑块面积、降低IL-6及TNF-α含量等发挥抗AS效应,其机制可能与降低visfatin表达有关。
Objective To observe the effects of puerarin on aortic atherosclerosis (AS), blood lipids, visfatin and inflammatory cytokines IL-6 and TNF-α in apolipoprotein E knockout mice (Apo E-/-) The effect of expression. Methods Fifty SPF 8-week-old male Apo E-/- mice were fed with high-fat diet and randomly divided into 5 groups: Puerarin low, middle and high dose groups were given puerarin 300, 600, 1200 mg·kg-1·d, respectively. -1 gavage; simvastatin group was given simvastatin 5 mg·kg-1·d-1; model group was given an equal dose of normal saline. In addition, 10 male C57BL/6J mice of the same genetic background and age were used as the control group to feed normal diets. After 16 weeks, the body weight, serum lipids, visfatin, plasma IL-6 and TNF-α levels were measured. The plaque area of aortic tissue was observed by HE staining. The expression of visfatin protein was measured by western blotting. Results The increase in body weight, serum visfatin, TG, TC, LDL-C levels, plasma IL-6 and TNF-α levels, and aortic visfatin protein expression were significantly lower in the treated groups than in the model group (P<0.05). Serum HDL-C levels were higher than those in the model group (P<0.05). The percentage of AS plaques in the aorta was significantly lower in the simvastatin, puerarin, and high-dose groups than in the model group (P<0.05). Conclusion Puerarin can exert anti-AS effect by reducing blood lipids, reducing AS plaque area and decreasing IL-6 and TNF-α content. The mechanism may be related to the decrease of visfatin expression.