| 尚沛津,窦 芳,张一恺,刘天龙,刘文星,许 航,牟 菲,李玉文,文爱东.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[J].,2017,17(8):1405-1410 |
| 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 |
| 投稿时间：2016-08-18 修订日期：2016-09-10 |
| DOI：10.13241/j.cnki.pmb.2017.08.002 |
| 中文关键词: 11-羰基-β-乙酰乳香 高血压 血管重构 |
| 英文关键词: Acetyl-11-keto-β-boswellic acid Hypertension Vascular remodeling |
| 基金项目:国家自然科学基金项目（81201985；81373947） |
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| 中文摘要: |
| 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（AngII）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AngII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。 |
| 英文摘要: |
| ABSTRACT Objective: To observe the inhibitory effect of Acetyl-11-keto-β-boswellic 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（AngII）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-α (TNF-α), 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. Conclusion: AKBA can effectively decrease vascular contractility and attenuate oxidative stress, and thus decrease collagen deposition and attenuate vascular remodeling. |
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