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作 者:刘美之[1] 贾振华[2,3] 魏聪 王宏涛 梁俊清 张军芳 肖维刚 郎艳松 吴以岭[1,2]
机构地区:[1]河北医科大学 [2]河北以岭医药研究院 [3]河北医科大学附属以岭医院 [4]国家中医药管理局心脑血管络病重点研究室 [5]河北省络病重点实验室
出 处:《中医杂志》2015年第3期240-245,共6页Journal of Traditional Chinese Medicine
基 金:国家重点基础研究发展计划("973"计划)(2012CB518606)
摘 要:目的探讨通心络超微粉对兔动脉粥样硬化早期外膜微血管新生的影响及可能作用机制。方法采用颈动脉套管术联合高脂饮食喂养建立兔动脉粥样硬化早期颈动脉损伤的模型。将造模成功的90只新西兰白兔随机分为空白组、模型组、阿托伐他汀组和通心络高、中、低剂量组,每组15只。通心络高、中、低剂量组分别给予通心络超微粉0.60、0.30、0.15 g/(kg·d),阿托伐他汀组给予阿托伐他汀溶液2.50 mg/(kg·d),空白组与模型组按3 ml/(kg·d)给予0.5%羧甲基纤维素钠溶液。各组连续灌胃4周。各组取兔术侧颈动脉标本,观察血管病理特征,检测颈动脉外膜微血管密度(MVD)、血清超氧化物歧化酶(SOD)活力、丙二醛(MDA)含量、血管外膜组织中超氧阴离子(O-·2)、颈动脉组织p38MAPK及pp38MAPK蛋白的表达水平。结果 HE染色显示通心络高、中剂量组和阿托伐他汀组术侧颈动脉损伤均较模型组有不同程度减轻。与模型组比较,通心络高、中剂量组和阿托伐他汀组血清SOD活力升高,MDA含量、颈动脉外膜MVD、O-·2、p-p38MAPK蛋白表达水平降低(P<0.05或P<0.01)。结论通心络超微粉具有抑制兔动脉粥样硬化早期外膜微血管新生作用,其机制可能与提高血管系统和外膜组织的抗氧化能力、抑制p38MAPK通路激活有关。Objective To investigate the influence of Tongxinluo( TXL) ultrafine power on rabbit early atherosclerotic epicardial angiogenesis and its possible mechanisms. Methods Carotid artery cannula and high fat diet were used to build early atherosclerotic carotid artery injury rabbit model. Ninety New Zealand white rabbit models were randomly divided into control group,model group,atorvastatin group and TXL high,medium and low dose group,with 15 in each. The TXL high,medium and low dose group was given TXL ultrafine powder 0. 60,0. 30,0. 15 g /( kg·d) respectively. The atorvastatin group were given atorvastatin solution 2. 50 mg /( kg·d),while the control group and model group were given 0. 5% sodium carboxymethyl cellulose solution 3 ml /( kg·d). All groups were treated with gastric perfusion for 4 weeks. Carotid artery samples from the operation side were obtained to observe pathological features of vascular morphology. Microvessel density( MVD) of carotid artery adventitia,activity of serum superoxide dismutase( SOD),malondialdehyde( MDA) content,the expression levels of superoxide anion(O2-) in adventitia tissues,p38 MAPK and p-p38 MAPK protein in carotid artery tissues were detected. Results HE staining showed the carotid artery injuries of the TXL high and middle dose group and atorvastatin group were milder in varying degrees comparing with the model group. Also compared with the model group,the activity of serum SOD in the TXL high dose group and atorvastatin group increased,while MDA content,MVD of carotid adventitia,the expression levels of O2^-,p-p38 MAPK protein were decreased( P〈0. 05 or P〈0. 01). Conclusion TXL ultrafine powder can inhibit epicardial neovascularization in the early stage of atherosclerosis,its mechanism might be related to increase of antioxidant capacity of the vascular system and adventitia tissue and inhibite on p38 MAPK pathway activation.
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