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出 处:《世界中医药》2016年第10期2098-2100,共3页World Chinese Medicine
基 金:中国博士后科学基金(编号:20080440498);国家自然科学基金青年项目(编号:81302964/H2708)
摘 要:目的:观察新活络效灵丹对ApoE基因敲除小鼠AS早期斑块的病理形态学改变及转化生长因子-β(TGF-β)表达的影响,探讨新活络效灵丹抗AS早期斑块的可能机制。方法:采用高脂饲料喂养ApoE基因敲除小鼠建立AS模型,将45只小鼠随机分为模型组、西药组、中药组,另将C57BL/6J小鼠10只设为空白对照组。在造模的同时即给予药物干预,空白对照组不予处理,模型组予以生理盐水0.3 m L/d,中药组给予新活络效灵丹9.67 g/(kg·d),西药组给予阿托伐他汀钙片3.33 mg/(kg·d),均每日灌胃1次,连续给药13周。取主动脉根部,HE染色进行病理观察,采用RT-PCR技术检测各组TGF-βmRNA的表达水平。结果:模型组主动脉内形成明显的AS斑块,并出现脂质核心,泡沫细胞增多,大量的巨噬细胞的浸润;西药组管壁可见AS斑块,斑块面积明显小于模型组;中药组斑块面积显著减少,部分内膜较为光滑。模型组小鼠主动脉组织中TGF-βmRNA表达水平明显低于空白对照组(P<0.01);西药组、中药组小鼠主动脉组织中TGF-βmRNA表达水平明显高于模型对照组(P<0.05或P<0.01),而中药组小鼠主动脉组织中TGF-βmRNA表达水平高于西药组,但2组比较差异无统计学意义(P>0.05)。结论:新活络效灵丹在一定程度上可通过上调保护性因子TGF-β以抑制免疫炎性反应,发挥抗动脉粥样硬化的作用,可能是其防治AS早期斑块的形成机制之一。Objective: To observe the effect of New Huoluo Xiaoling Dan(NHLXLD) on aorta pathological changes in ApoE Knock-out mice and the expressions of Transforming Growth Factor beta(TGF-β),and to explore possible mechanism of anti-AS.Methods: AS model was induced by high lipid diet in ApoE knock-out mice. Forty five ApoE knock-out mice were equally randomized into 3 groups,including control group(CG),western medicine group(WMG) and traditional Chinese medicine group(TCMG). Ten C57 BL/6J mice were also prepared as blank group(BG). During modeling,BG received no intervention; CG took normal saline 0. 3 m L daily; TCMG was treated by NHLXLD 9. 67 g/kg. d,and WMG was administered avarstatin 3. 33 mg/kg. d. The treatment lasted for 13 weeks with gastric lavage once everyday. Then the aortic roots were taken for HE stain and the mRNA levels of TGF-βof each group were assayed. Results: Atherosclerotic plaques were observed obviously in the aorta of CG mice with overwhelming formation of foam cells,lipid core and a large number of macrophages infiltration. There were visible AS plaques on WMG aortic wall; plaque area was significantly lower than the CG; plaque area in TCMG was significantly reduced with the more smooth aortic endometrium. The TGF-β mRNA expressions of CG were lower than BG(P〈 0. 01); The TGF-β mRNA expressions of WMG and TCMG were higher than CG(P〈 0. 05 or P〈 0. 01). While the TGF-β mRNA expressions of TCMG were higher than WMG,but the difference was not statistically significant(P〈 0. 05). Conclusion: NHLXLD suppressed immune inflammatory response in a certain extent by increasing protective factor TGF-β on anti-AS. It might be one of the possible mechanisms preventing the formation of AS plaque.
关 键 词:新活络效灵丹 APOE基因敲除小鼠 动脉粥样硬化 转化生长因子-Β
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