首页> 中文期刊> 《实用医学杂志》 >颈总动脉损伤大鼠血管蛋白激酶C与核因子-κB的表达及辛伐他汀对其的影响

颈总动脉损伤大鼠血管蛋白激酶C与核因子-κB的表达及辛伐他汀对其的影响

         

摘要

目的:探讨蛋白激酶C(PKC)与核因子-κB(NF-κB)在血管损伤后狭窄中的作用及辛伐他汀对其的影响.方法:建立颈总动脉损伤动物模型:雄性SD大鼠48只,分为假手术组、手术组、低剂量和高剂量辛伐他汀组,低、高剂量辛伐他汀组术前3 d分别用5 mg/(kg·d)和10 mg/(kg·d)辛伐他汀灌胃,术后14 d处死.HE染色观察血管形态学的变化;Western blot检测血管PKCα与NF-κB蛋白的表达.结果:与假手术组比较,手术组血管平滑肌细胞(VSMC)增殖显著,管腔严重狭窄;与手术组相比,辛伐他汀处理后VSMC排列趋于规整,管腔狭窄程度较轻.与假手术组比较,手术组PKCα与NF-κB蛋白差异显著(P < 0.01);与手术组比较,高剂量组PKCα与NF-κB蛋白表达显著降低(P < 0.01),低剂量组的表达差异无统计学意义(P > 0.05);高剂量组与低剂量组有明显差异(P < 0.05).结论:PKCα与NF-κB参与血管损伤后狭窄的形成,辛伐他汀具有抗血管狭窄作用,其机制可能与下调PKCα与NF-κB表达有关.%Objective To explore the effect of simvastatin on the expression of PKCa and NF-kB in vessel after carotid artery injury in rats. Methods Animal model of carotid artery injury was established, the rats were randomly divided into; sham group, operation group, low doses group and high doses simvastatin groups, the rats of low and high doses groups were respectively lavaged with 5 mg/(kg-d) and 10 mg/(kg-d) simvastatin, all used animals were dead after 14 days. The changes of tunica media vasorum was observed by HE staining; the expression changes of PKCA and NF-kB proteins were detected by Western blot. Results Compared with sham group,the VSMC was obviously proliferated and the lumen of the carotid artery became stenosis in operation group; The proliferation of VSMC was regularly arrangement and the stenosis degree became slight by simvastatin. Compared with the sham group, the expression of PKCa and NF-kB was significantly increased in operation group (P < 0.01); Compared with operation group, the expression of PKCa and NF-kB was significantly decreased in high doses group (P<0.01), while it was unconspicuous in low doses group(P > 0.05), there was significant difference between low doses group and high doses simvastatin group (P < 0.05). Conclusions PKCa and NF-kB involved in the formation of stenosis after vascular injury. Simvastatin might inhibit the expression of PKCa and NF-kB to suppress VSMC proliferation and reduce the role of vascular stenosis.

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