11-羰基-β-乙酰乳香酸抑制自发性高血压大鼠血管重构研究  

Research of Acetyl-11-keto-β-boswellic Acid on Vascular Remodeling of Spontaneously Hypertensive Rats

作　　者：尚沛津 窦芳[1] 张一恺[3] 刘天龙[1] 刘文星[1] 许航[1] 牟菲[1] 李玉文[1] 文爱东[1] 

机构地区：[1]第四军医大学西京医院药剂科,陕西西安710032 [2]中国人民解放军第517医院药剂科,山西忻州034000 [3]沈阳军区总医院药剂科,辽宁沈阳110016

出　　处：《现代生物医学进展》2017年第8期1405-1410,共6页Progress in Modern Biomedicine

基　　金：国家自然科学基金项目(81201985;81373947)

摘　　要：目的:观察11-羰基-β-乙酰乳香酸(AKBA)对高血压血管重构的抑制作用。方法:自发性高血压大鼠(SHR)随机分为模型组(SHR),20 mg/kg AKBA低剂量组(AKBA-L),40 mg/kg AKBA高剂量组(AKBA-H)和20 mg/kg替米沙坦组(Telmi),另设Wistar-Kyoto(WKY)空白对照组。各组大鼠分别灌胃给予8周相应药物和蒸馏水。每周监测大鼠收缩压;检测大鼠血液一氧化氮(NO)和血管紧张素Ⅱ(Ang Ⅱ)水平;评估整体炎性反应和氧化应激水平;苏木精-伊红染色观察血管重构情况;马森染色观察血管胶原沉积情况。结果:8周给药期间,SHR血压持续升高,替米沙坦显著降低血压,但AKBA未显示出明显的血压调节作用。与SHR组相比,AKBA和替米沙坦都有效地减少了血管压力,减少Ang Ⅱ分泌,增加NO的产生(P<0.05);其次有效地降低炎性反应和氧化应激,显著改善机体肿瘤坏死因子-α(TNF-α)、单核细胞趋化蛋白-1(MCP-1)、过氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GPx)和丙二醛(MDA)的表达水平(P<0.05)。除此之外,相比SHR组,AKBA显著抑制血管重构,降低血管厚度,横切面积和血管厚度/血管内径比值(P<0.05),减少血管胶原沉积(P<0.05)。结论:AKBA能有效缓解血管压力和氧化应激,减少胶原沉积,从而有效改善血管重构。Objective： To observe the inhibitory effect of Acetyl-11-keto-β-bosweUic acid （AKBA） on vascular remodeling of spontaneously hypertensive rats. Methods： Spontaneously hypertensive rats （SHR） were randomly divided into four groups as follow： the model group （SHR）, 20 mg/kg AKBA group （AKBA-L）, 40 mg/kg （AKBA-H） and 20 mg/kg telmisartan group （Telmi）, in addition, age-matched Wistar-Kyoto rats （WKY） were needed as contrast. Each group was treated by orally gavage with corresponding drugs and water for 8 weeks. Systolic blood pressure was monitored weekly, and vascular contractility was assessed by nitric oxide （NO） and angiotensin II （AnglI）secretion, additionally, systemic inflammatory response and oxidative stress were preliminarily evaluated. Hematoxylin ＆ eosin staining was used to assess vascular morphological alterations, and Masson staining was used to evaluate collagen deposition. Results： Systolic blood pressure of SHR was continuously elevated during 8 w, and AKBA showed no effect on systolic blood pressure. Whereas, AKBA decreased vascular contractility notably through restoring NO and AngII levels （P〈0.05）. Further, AKBA decreased inflammatory response and oxidative stress by restoring tumor necrosis factor-ct （TNF-ct）, monocyte chemoattractant protein-1 （MCP-1）, superoxide dismutase （SOD）, glutathione peroxidase （GPx） and malondialdehyde （MDA） levels significantly （P〈0.05）. AKBA markedly decreased vascular remodeling, decreased vascular wall thickness, vascular cross-sectional area and media/lumen ratio （P〈0. 05）, which were significantly elevated in SHR group. Additionally, AKBA effectively decreased collagen deposition in vascular walls of hypertension. Conclusions： AKBA can effectively decrease vascular contractility and attenuate oxidative stress, and thus decrease collagen deposition and attenuate vascular remodeling.

关 键 词：11-羰基-β-乙酰乳香 高血压 血管重构 

分 类 号：R-33[医药卫生] R544.1