白俐 张林 郭道保

【摘要】 目的：观察胰激肽原酶对血管损伤后兔血管形态及MMP-2、TIMP-2、P53蛋白表达的影响。方法：18只西新兰兔随机分为假手术组、模型组及胰激肽原酶组，每组6只。通过球囊损伤制备兔腹主动脉损伤模型，并进行3周的胰激肽原酶治疗，之后观察血管形态及检测MMP-2、TIMP-2、P53蛋白表达的变化。结果：与假手术组相比，模型组内膜增生明显（P<0.05）;与模型组相比，胰激肽原酶组内膜增生有改善（P<0.05）。模型组MMP-2、TIMP-2表达均较假手术组升高，胰激肽原酶组MMP-2表达较模型组下降，差异均有统计学意义（P<0.05）;胰激肽原酶组TIMP-2表达与模型组比较，差异无统计学意义（P>0.05）;模型组P53表达较假手术组下降，胰激肽原酶组P53表达较模型组升高，差异均有统计学意义（P<0.05）。结论：胰激肽原酶具有抑制血管损伤后内膜增生，与促进P53蛋白表达及抑制MMP-2表达相关。

【关键词】 胰激肽原酶 血管损伤 再狭窄 内膜增殖

Effects of Pancreatic Kininogenase on Intimal Proliferation and Apoptosis in Restenosis after Vascular Injury/BAI Li， ZHANG Lin， GUO Daobao. //Medical Innovation of China， 2021， 18（12）： 0-020

[Abstract] Objective： To observe the effect of Pancreatic Kininogenase on vascular morphology and MMP-2，

TIMP-2， P53 protein expression in rabbits after vascular injury. Method： A total of 18 rabbits were randomly divided into sham operation group， model group and Pancreatic Kininogenase group， 6 rabbits in each group. The abdominal aortic injury model was prepared by balloon injury and treated with Pancreatic Kiniogenase for 3 weeks. The blood vessel morphology and MMP-2， TIMP-2， P53 protein expression were observed. Result： Compared with the sham group， the intima hyperplasia in model group was obvious （P<0.05）， and compared with the model group， the intimal hyperplasia in the Pancreatic Kininogenase group was improved （P<0.05）. The MMP-2， TIMP-2 expression in the model group were higher than those in the sham operation group， the MMP-2 in the Pancreatic Kininogenase group was lower than that in the model group， and the differences were statistically significant （P<0.05）， and the TIMP-2 expression showed no difference between the Pancreatic Kininogenase group and the model group （P>0.05）. And the P53 expression in the model group was lower than that in the sham operation group， the P53 expression in the Pancreatic Kininogenase group was higher than that in the model group， the differences were statistically significant （P<0.05）. Conclusion： Pancreatic Kininogenase can inhibit intimal hyperplasia after vascular injury， related to promoting P53 protein expression and inhibiting MMP-2 expression.

[Key words] Pancreatic Kininogenase Vascular injury Restenosis Intimal proliferation

First-authors address： Guangzhou Xinhai Hospital， Guangzhou 510000， China

doi：10.3969/j.issn.1674-4985.2021.12.004

随着技术发展，经皮腔内冠状动脉成形术（PTCA）目前成为治疗冠心病常规療法，但其术后3～6个月再狭窄（RS）发生率高，即使使用药物洗脱支架后再狭窄率仍达6.4%[1]。故如何防治PTCA术后再狭窄成为大家探索的热点话题。其中基质金属蛋白酶（MMPs）及其抑制剂（TIMPs）、凋亡相关因子P53、bcl-2/bax等证实均参与PTCA术后再狭窄发生，而近年研究发现胰激肽原酶有调控凋亡蛋白、抗纤维化、氧化应激等作用，从而对高心病心肌重构、肾脏纤维化等产生影响[2-4]。本研究旨在通过胰激肽原酶对兔腹主动脉球囊损伤术后血管形态观察及MMPs、TIMPs、P53检测而探讨其对血管再狭窄影响，为PTCA术后再狭窄防治提供新的思路。现报道如下。

1 材料与方法

1.1 材料 本实验从2019年5月开始人员培训和试剂、动物准备等前期工作，至2020年11月完成动物实验、各指标检测及数据收集。新西兰兔，雄性，18只，体重2.5～3.5 kg，平均（2.87±0.51）kg，单笼、恒温、恒湿度饲养，实验动物使用许可证号：SYXK（粤）2017-0125。

1.2 药物与试剂 注射……