降钙素基因相关肽抑制动脉损伤后NF-κB表达及其对新生内膜增殖的影响

赵然尊; 龙仙萍; 刘志江; 盛瑾; 王冬梅; 石蓓

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降钙素基因相关肽抑制动脉损伤后NF-κB表达及其对新生内膜增殖的影响

论著 | 更新时间：2026-01-09

- 降钙素基因相关肽抑制动脉损伤后NF-κB表达及其对新生内膜增殖的影响
- Effect of calcitonin gene-related peptide on NF-κB expression and neointima formation after artery injury in vivo and in vitro
- 陆军军医大学学报 2014年36卷第14期页码：1472-1476
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  中图分类号： R341;R363.22;R543.4
- 纸质出版：2014
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赵然尊,龙仙萍,刘志江,盛瑾,王冬梅,石蓓.降钙素基因相关肽抑制动脉损伤后NF-κB表达及其对新生内膜增殖的影响[J].陆军军医大学学报(原第三军医大学学报),2014,36(14):1472-1476.

　Zhao Ranzun,Long Xianping,Liu Zhijiang,Sheng Jin,Wang Dongmei,Shi Bei.Effect of calcitonin gene-related peptide on NF-κB expression and neointima formation after artery injury in vivo and in vitro[J].J Amry Med Univ (J Third Mil Med Univ),2014,36(14):1472-1476.
赵然尊,龙仙萍,刘志江,盛瑾,王冬梅,石蓓.降钙素基因相关肽抑制动脉损伤后NF-κB表达及其对新生内膜增殖的影响[J].陆军军医大学学报(原第三军医大学学报),2014,36(14):1472-1476. DOI：

　Zhao Ranzun,Long Xianping,Liu Zhijiang,Sheng Jin,Wang Dongmei,Shi Bei.Effect of calcitonin gene-related peptide on NF-κB expression and neointima formation after artery injury in vivo and in vitro[J].J Amry Med Univ (J Third Mil Med Univ),2014,36(14):1472-1476. DOI：

摘要

目的通过降钙素基因相关肽（calcitonin gene related peptide，CGRP）处理血管平滑肌细胞（vascular smooth muscle cells，VSMCs）和颈动脉损伤大鼠模型，探讨NF-κB在CGRP调节VSMCs表型改变和动脉损伤后新生内膜增殖中的作用。方法建立颈动脉损伤大鼠模型，并分为对照组和CGRP组(n=24)，通过HE染色观察新生内膜形成情况，并Western blot检测两组动物损伤动脉中NF-κB p65蛋白表达情况。以组织块贴壁培养法获得VSMCs，并分为对照组、IL-1β组（给予IL-1β处理）、CGRP组（给予IL-1β+CGRP处理）和CGRP8-37组（在IL-1β+CGRP基础上，加CGRP8-37）(n=24)，Western blot法检测细胞内NF-κB p65蛋白和细胞表型标志蛋白表达变化，MTT法检测细胞增殖能力。结果 ①对照组大鼠的颈动脉损伤后7 d时新生内膜明显增加，至28 d时基本稳定，而CGRP组7 d和28 d时新生内膜面积较对照组同时间点显著降低[7d: (2.09±0.26) vs (3.76±0.33)；14 d：(3.52 ±0.41) vs (6.38±0.61)，

0.05

]

；且与对照组比较，CGRP组1周时NF-κB p65蛋白表达水平明显降低（

0.05），而28 d时两组NF-κB p65表达水平无差异（

0.05）。②在体外培养VSMCs中，IL-1β处理显著激活细胞NF-κB p65蛋白表达（

0.05），伴随着VSMCs收缩表现标志蛋白SM α-actin表达减少和OPN表达增加（

0.05）；同时再给予CGRP处理后，则显著减弱IL-1β诱导的NF-κB p65蛋白表达（

0.05），且使VSMCs合成表现标志蛋白OPN表达减少。RT-PCR分析获得相一致的结果。同时，CGRP显著抑制IL-1β引起的VSMCs增殖。③CGRP受体阻断剂CGRP8-37可以阻断CGRP减弱IL-1β诱导的NF-κB p65蛋白表达作用，并抑制CGRP对VSMC表达蛋白调节作用。结论 CGRP与受体结合后抑制NF-κB激活，促进VSMCs分化标志基因表达，从而抑制细胞增殖，降低动脉损伤后新生内膜增殖，这对于防治动脉粥样硬化和血管成形术后再狭窄可能具有重要应用价值。

Abstract

Objective To investigate the effects of calcitonin gene-related peptide (CGRP) on nuclear factor-κB (NF-κB) expression and neointima formation after artery injury through CGRP treatment of vascular smooth muscle cells (VSMCs) in vitro and rats with balloon-injured carotid arteries in vivo. Methods Rats with balloon-injured carotid arteries were divided into a control group(n=24) and a CGRP group(n=24). Neointima formation was observed by HE staining. The expression of NF-κB p65 protein in the injured arteries was detected by Western blot. Furthermore

VSMCs were obtained by aortic tissue adherent culture and divided into a control group

an interleukin-1β (IL-1β) group

an IL-1β+CGRP group and an CGRP8-37 (a receptor blocker of CGRP) group (IL-1β+CGRP+CGRP8-37). The expression of phenotypic proteins of VSMCs and NF-κB p65 was detected by Western blotting. Cell proliferation was determined by MTT assay. Results As compared to the control group

both the area of neointima formation at 7 d and 28 d (7 d: 2.09±0.26 vs 3.76±0.33; 14 d: 3.52±0.41 vs 6.38±0.61

0.05) and the expression of NF-κB p65 protein at 7 d (

0.05) (but not 28 d

0.05) significantly reduced in the CGRP group. In in vitro cultured VSMCs

IL-1β induced obvious expression up-regulation of NF-κB p65 along with the expression decrease of SM α-actin (the contractile phenotypic marker of VSMCs) and the expression increase of osteopontin (the synthetic phenotypic marker of VSMCs) (

0.05). However

CGRP treatment significantly alleviated the effects of IL-1β-induced up-regulation of NF-κB p65 and induced the down-regulation of osteopontin. Similar results were found by RT-PCR. Also

CGRP significantly inhibited the effect of IL-1β-induced VSMCs proliferation by MTT assay. The use of CGRP8-37 blocked the above-mentioned effects of CGRP on the expression NF-κB p65 and the phenotypic proteins of VSMCs. Conclusion CGRP binds its receptor and subsequently inhibits the activa

tion of NF-κB

and then contributes to the expression of VSMCs differentiation genes

the inhibition of cell proliferation and the reduction of neointima formation

which may be important in the treatment of atherosclerosis and restenosis after angioplasty.

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