苯磺酸左旋氨氯地平對(duì)兔內(nèi)皮損傷術(shù)后內(nèi)膜增生與斑塊穩(wěn)定的影響
發(fā)布時(shí)間:2018-06-03 18:25
本文選題:苯磺酸左旋氨氯地平 + 瑞舒伐他汀; 參考:《臨床心血管病雜志》2015年01期
【摘要】:目的:觀察苯磺酸左旋氨氯地平對(duì)新西蘭兔腹主動(dòng)脈球囊內(nèi)皮損傷術(shù)后動(dòng)脈粥樣硬化(AS)的影響,從抗炎和穩(wěn)定斑塊的角度探討相關(guān)機(jī)制。方法:42只新西蘭兔隨機(jī)分為假手術(shù)組、模型組、左旋氨氯地平組以及瑞舒伐他汀組。模型采用高脂飲食聯(lián)合腹主動(dòng)脈球囊內(nèi)皮損傷術(shù)制作。ELISA法檢測(cè)各組術(shù)前與術(shù)后8周的血脂、血管炎癥性及斑塊穩(wěn)定性相關(guān)指標(biāo),如超敏C反應(yīng)蛋白(hs-CRP)、脂蛋白磷脂酶A2(Lp-PLA2)以及1型纖溶酶原激活物抑制物(PAI-1),術(shù)后8周處死后取腹主動(dòng)脈病變組織,行HE染色分析斑塊厚度及內(nèi)膜增生系數(shù)(IHI)以及免疫組織化學(xué)法檢測(cè)斑塊內(nèi)金屬基質(zhì)蛋白酶(MMP-3)表達(dá)。結(jié)果:左旋氨氯地平組血清低密度脂蛋白膽固醇(LDL-C)水平較模型組有降低趨勢(shì)(16.24mmol/L∶19.41mmol/L,P=0.08)。左旋氨氯地平組的腹主動(dòng)脈斑塊厚度、IHI與模型組無(wú)顯著性差異(313μm∶405μm、0.68∶0.66,均P0.05),而瑞舒伐他汀組的斑塊厚度、IHI明顯低于模型組(273.75μm∶405.93μm、0.52∶0.68,均P0.05)。左旋氨氯地平組的血清hs-CRP、Lp-PLA2以及PAI-1水平與模型組無(wú)明顯差異(P0.05),而左旋氨氯地平組斑塊內(nèi)MMP-3陽(yáng)性表達(dá)面積百分比顯著小于模型組(52.45%∶70.84%,P0.05)。結(jié)論:左旋氨氯地平具有降低血清LDL-C趨勢(shì),對(duì)抑制兔腹主動(dòng)脈球囊內(nèi)皮損傷術(shù)后的內(nèi)膜增生無(wú)明顯作用,但可通過(guò)抑制斑塊內(nèi)MMP-3的表達(dá)從而增加斑塊穩(wěn)定性。
[Abstract]:Aim: to observe the effect of levamlodipine on atherosclerosis (ASS) after balloon endothelial injury of abdominal aorta in New Zealand rabbits and to explore the mechanism of anti-inflammatory and stable plaque. Methods 42 New Zealand rabbits were randomly divided into sham operation group, model group, levamlodipine group and resuvastatin group. The serum lipids, vascular inflammation and plaque stability were measured by high fat diet combined with balloon endothelial injury of abdominal aorta by Elisa before and 8 weeks after operation. For example, hypersensitive C-reactive protein (hs-CRPN), lipoprotein phospholipase A2P (Lp-PLA2) and plasminogen activator inhibitor type 1 (PAI-1) were taken from abdominal aorta after 8 weeks of operation. The thickness of plaque, intimal hyperplasia coefficient (IHI) and the expression of metalloproteinase 3 (MMP-3) in plaque were detected by HE staining and immunohistochemistry. Results: compared with the model group, the serum LDL-C level of the L-amlodipine group decreased to 16.24 mmol / L ~ (19.41) mmol / L ~ (0.08) mg 路L ~ (-1) 路L ~ (-1) 路L ~ (-1) 路L ~ (-1) 路L ~ (-1) 路L ~ (-1). There was no significant difference in the thickness of abdominal aortic plaque (IHI) between the levamlodipine group and the model group. There was no significant difference between the model group and the model group (313 渭 m: 405 渭 m or 0.68: 0.66, P < 0.05), while the thickness of the plaque in the rosuvastatin group was significantly lower than that in the model group (273.75 渭 m vs 405.93 渭 m: 0.520.68, P 0.05 5). There was no significant difference in the levels of hs-CRPnLp-PLA2 and PAI-1 between the L-amlodipine group and the model group, but the percentage of MMP-3 positive area in the L-amlodipine group was significantly lower than that in the model group (52.45: 70.84). Conclusion: L-amlodipine can decrease the trend of serum LDL-C and has no effect on intimal hyperplasia after abdominal aortic balloon endothelial injury in rabbits, but it can increase plaque stability by inhibiting the expression of MMP-3 in plaque.
【作者單位】: 暨南大學(xué)附屬第一醫(yī)院心內(nèi)科;
【基金】:廣東省科技計(jì)劃項(xiàng)目(No:2011B031800336)
【分類號(hào)】:R965
【參考文獻(xiàn)】
相關(guān)期刊論文 前4條
1 陳海生;劉卓敏;;左旋氨氯地平與厄貝沙坦對(duì)原發(fā)性高血壓早期腎小球?yàn)V過(guò)率和微量白蛋白的影響[J];中國(guó)心血管雜志;2006年05期
2 曹雅e,
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