浙江临床医学
浙江臨床醫學
절강림상의학
ZHEJIANG CLINICAL MEDICAL JOURNAL
2014年
2期
178-181
,共4页
肾动脉狭窄%动脉粥样硬化%阿利吉仑%基质金属蛋白酶%斑块稳定性
腎動脈狹窄%動脈粥樣硬化%阿利吉崙%基質金屬蛋白酶%斑塊穩定性
신동맥협착%동맥죽양경화%아리길륜%기질금속단백매%반괴은정성
Aortic stenosis of renal artery%Atherosclerosis%Aliskiren%Matrix metalloproteinase%Plaque stability
目的：通过比较阿利吉仑与生理盐水对一肾一夹（1K1C）及二肾一夹（2K1C）动脉粥样硬化性大鼠大动脉斑块稳定性的影响，探讨阿利吉仑影响动脉粥样硬化性斑块稳定性的机制。方法采用手术复制单双侧肾动脉狭窄并联合高脂饲养及注射VitD3建立动脉粥样硬化合并肾动脉狭窄动物模型，饲养10周后予阿利吉仑50mg/（kg·d）干预4周，免疫组检测主动脉弓斑块部位巨噬细胞特异性标记抗原CD68、血管平滑肌细胞表型标志物α-SMA及基质金属蛋白酶（MMP）1，2，9，比较平均光密度值（MOD）的变化。结果相同造模方式下，阿利吉仑组对斑块部位CD68、α-SMA及MMP1，2，9表达的影响与生理盐水组比较差异均有统计学意义（P<0.05）。结论阿利吉仑可增加斑块部位α-SMA的表达，并抑制斑块部位巨噬细胞CD68、MMP1、MMP2、MMP9的表达，提示阿利吉仑对抑制AS斑块的破裂有显著作用。
目的：通過比較阿利吉崙與生理鹽水對一腎一夾（1K1C）及二腎一夾（2K1C）動脈粥樣硬化性大鼠大動脈斑塊穩定性的影響，探討阿利吉崙影響動脈粥樣硬化性斑塊穩定性的機製。方法採用手術複製單雙側腎動脈狹窄併聯閤高脂飼養及註射VitD3建立動脈粥樣硬化閤併腎動脈狹窄動物模型，飼養10週後予阿利吉崙50mg/（kg·d）榦預4週，免疫組檢測主動脈弓斑塊部位巨噬細胞特異性標記抗原CD68、血管平滑肌細胞錶型標誌物α-SMA及基質金屬蛋白酶（MMP）1，2，9，比較平均光密度值（MOD）的變化。結果相同造模方式下，阿利吉崙組對斑塊部位CD68、α-SMA及MMP1，2，9錶達的影響與生理鹽水組比較差異均有統計學意義（P<0.05）。結論阿利吉崙可增加斑塊部位α-SMA的錶達，併抑製斑塊部位巨噬細胞CD68、MMP1、MMP2、MMP9的錶達，提示阿利吉崙對抑製AS斑塊的破裂有顯著作用。
목적：통과비교아리길륜여생리염수대일신일협（1K1C）급이신일협（2K1C）동맥죽양경화성대서대동맥반괴은정성적영향，탐토아리길륜영향동맥죽양경화성반괴은정성적궤제。방법채용수술복제단쌍측신동맥협착병연합고지사양급주사VitD3건립동맥죽양경화합병신동맥협착동물모형，사양10주후여아리길륜50mg/（kg·d）간예4주，면역조검측주동맥궁반괴부위거서세포특이성표기항원CD68、혈관평활기세포표형표지물α-SMA급기질금속단백매（MMP）1，2，9，비교평균광밀도치（MOD）적변화。결과상동조모방식하，아리길륜조대반괴부위CD68、α-SMA급MMP1，2，9표체적영향여생리염수조비교차이균유통계학의의（P<0.05）。결론아리길륜가증가반괴부위α-SMA적표체，병억제반괴부위거서세포CD68、MMP1、MMP2、MMP9적표체，제시아리길륜대억제AS반괴적파렬유현저작용。
Objective To compare the influences of the stability of atherosclerotic aortic plaques in rats about aliskiren and normal saline on one kidney one clip(1K1C)and two kidney one clip(2K1C),and to explore the mechanism of aliskiren affects the stability of atherosclerotic plaque. Methods Duplicated the single bilateral renal artery stenosis by operation which combined with high fat diet and injection of VitD3 to establish animal models of atherosclerosis and renal artery stenosis,intervened by aliskiren of 50mg/kg.d of 4 weeks which feed after 10 weeks,detected the macrophage-specific marker phenotype of CD68,vascular smooth muscle cell marker α -SMA and matrix metalloproteinase immune group(MMP)1,2,9 of aortic arch plaques,compared the average optical density(MOD)changes with it. Results The expressions of CD68,α -SMA and MMP1,2,9 on plaque site were different significantly compared with the normal saline group and aliskiren group by the same molding way(P<0.05). Conclusions Aliskiren may increase the expression of α -SMA in plaques,and inhibit the expression of macrophages CD68, MMP1,MMP2,MMP9 in plaque,suggesting that aliskiren could significantly inhibit of plaque rupture in AS.
