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目的研究补肾和脉方(HMF)对载脂蛋白E基因敲除(Apo E~(-/-))小鼠动脉粥样硬化(AS)的治疗效果及可能机制。方法将24只Apo E~(-/-)小鼠随机分为高脂组、HMF组和阿托伐他汀组,每组8只。高脂组给予高脂饲料(0.25%胆固醇和15%可可脂)喂养,HMF组给予高脂饲料+HMF[1.37 g/(kg·d)]喂养,阿托伐他汀组给予高脂饲料+阿托伐他汀[5 mg/(kg·d)]喂养。8周后,戊巴比妥钠(0.8%,0.05 m L/10 g)腹腔注射麻醉,取小鼠胸主动脉切片,行常规HE染色观察胸主动脉斑块大小;行免疫组化染色检测巨噬细胞CD68、肿瘤坏死因子(TNF)-α、白细胞介素(IL)-1β和IL-8的表达水平。并采用日本全自动生化分析仪测量小鼠总胆固醇(TC)和总三酰甘油(TG)水平。结果 HMF组胸主动脉斑块大小,胸主动脉斑块内CD68、TNF-α、IL-1β和IL-8的表达水平,TC、TG水平均明显低于高脂组,高于阿托伐他汀组(均P<0.05)。结论 HMF具有抗动脉硬化作用,可抑制AS进展,其机制可能与降低血脂,减轻斑块炎症细胞浸润,减少炎症因子分泌有关。
Objective To investigate the therapeutic effect and its possible mechanism of Bushen Hemai recipe (HMF) on atherosclerosis (AS) in apolipoprotein E knockout (Apo E ~ (-) -) mice. Methods 24 Apo E ~ (- / -) mice were randomly divided into high fat group, HMF group and atorvastatin group, with 8 mice in each group. High fat diet group fed with high fat diet (0.25% cholesterol and 15% cocoa butter), HMF group fed high fat diet + HMF [1.37 g / (kg · d)], Atovavastatin group fed high fat diet + Atorvastatin [5 mg / (kg · d)] was fed. Eight weeks later, pentobarbital sodium (0.8%, 0.05 m L / 10 g) was injected intraperitoneally into the thoracic aorta and the thoracic aortic plaque size was observed by routine HE staining. Immunohistochemical staining Macrophage CD68, tumor necrosis factor (TNF) -α, interleukin (IL) -1β and IL-8. The total cholesterol (TC) and total triglyceride (TG) in mice were measured by automatic biochemical analyzer in Japan. Results The plaque size of thoracic aorta, the levels of CD68, TNF-α, IL-1β and IL-8, the levels of TC and TG in the thoracic aortic plaques in HMF group were significantly lower than those in the hyperlipidemia group Statin group (all P <0.05). Conclusion HMF has anti-atherosclerosis effect and inhibits the progression of AS. Its mechanism may be related to the reduction of blood lipid, the infiltration of inflammatory cells in plaque and the decrease of the secretion of inflammatory cytokines.