论文部分内容阅读
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。
AIM: To observe the inhibitory effect of 11-carbonyl-β-acetobutyric acid (AKBA) on vascular remodeling in hypertensive rats. Methods SHR, AKBA-L 20 mg / kg, AKBA-H 40 mg / kg and AKBA-H 20 mg / kg were randomly divided into three groups: / kg telmisartan, another Wistar-Kyoto (WKY) blank control group. The rats in each group were given gavage for 8 weeks respectively with the corresponding drugs and distilled water. The systolic blood pressure of rats was monitored weekly. The levels of blood nitric oxide (NO) and angiotensin Ⅱ (Ang Ⅱ) in rats were measured. The levels of total inflammatory reaction and oxidative stress were evaluated. The levels of blood vessels were observed by hematoxylin-eosin staining Structure conditions; Mason staining vascular deposition deposition. RESULTS: During the 8 weeks of treatment, the blood pressure of SHR continued to increase, telmisartan significantly reduced blood pressure, but AKBA did not show obvious blood pressure regulation. Compared with SHR group, both AKBA and telmisartan effectively reduced the blood pressure, reduced the secretion of Ang Ⅱ and increased the production of NO (P <0.05), and then effectively reduced the inflammatory reaction and oxidative stress, and significantly improved the body Tumor necrosis factor-α (TNF-α), monocyte chemoattractant protein-1 (MCP-1), superoxide dismutase (SOD), glutathione peroxidase (GPx) and malondialdehyde MDA) (P <0.05). In addition, AKBA significantly inhibited vessel remodeling, decreased vascular thickness, cross-sectional area, and ratio of vessel thickness / vessel diameter (P <0.05) and decreased collagen deposition (P <0.05). Conclusion: AKBA can effectively relieve vascular pressure and oxidative stress, reduce collagen deposition, thereby effectively improving vascular remodeling.