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目的 探讨氟伐他汀抑制再狭窄的作用机制。方法 将 48只大白兔随机分为 3组 ,正常对照组 :喂饲基础饲料 ;单纯球囊损伤组 :喂饲基础饲料 +球囊损伤右颈总动脉 ;氟伐他汀干预后球囊损伤组 :喂饲基础饲料 +氟伐他汀 10mg·kg-1 ·d-1 +球囊损伤右颈总动脉。各组又分为 3d、7d、14d、3 0d组 ,分别于第 3d、7d、14d、3 0d采用原位杂交方法检测血管损伤后基质金属蛋白酶 -9(MMP -9)和金属蛋白酶组织抑制剂 -2 (TIMP -2 )mRNA表达情况。结果 MMP -9和TIMP -2mRNA在正常对照组几乎不表达 ;血管损伤后中膜第 3d开始表达 ,第 7d达高峰 ,第 14d、3 0d内膜有少量表达 ,氟伐他汀干预后MMP -9明显降低 (P <0 0 5 ,P <0 0 1) ,但TIMP -2mRNA表达无明显变化。结论 氟伐他汀可通过减少血管损伤后基质金属蛋白酶 -9的表达 ,抑制平滑肌细胞增殖、迁移 ,从而达到防治再狭窄的作用
Objective To investigate the mechanism of fluvastatin inhibiting restenosis. Methods 48 rabbits were randomly divided into 3 groups: normal control group, fed basal diet, simple balloon injury group, fed basal diet and balloon injury, right common carotid artery, balloon injury group treated with fluvastatin, Feed basal diet + fluvastatin 10mg · kg-1 · d-1 + balloon injury of the right common carotid artery. Each group was further divided into 3d, 7d, 14d and 30d groups, respectively. The in situ hybridization was used to detect the expression of matrix metalloproteinase-9 (MMP -9) and metalloproteinase (TIMP-1) on the 3rd, 7th, 14th, 2 (TIMP-2) mRNA expression. Results MMP-9 and TIMP-2 mRNA were almost not expressed in normal control group. The expression of MMP-9 and TIMP-2 mRNA was detected on the 3rd day after vascular injury and reached its peak on the 7th day. (P <0.05, P <0.01), but TIMP-2 mRNA expression did not change significantly. Conclusion Fluvastatin can inhibit the restenosis by reducing the expression of MMP-9 after vascular injury and inhibiting the proliferation and migration of smooth muscle cells