神经营养因子3及其受体TrkC在缺氧性肺动脉高压病理发展中的作用研究  

The Role of Neurotrophin-3 and its Receptor TrkC in the Pathological Development of Hypoxic Pulmonary Hypertension

作　　者：侯继野 边文山 马勇[2,3] 李永涛 郭林娜[2,3] 沈雷 金海峰[2,3] 姜杨 HOU Jiye;BIAN Wenshan;MA Yong;LI Yongtao;GUO Linna;SHEN Lei;JIN Haifeng;JIANG Yang(Department of Interventional Therapy,Qiqihar Heping Hospital,Qiqihar 161006,Heilongjiang,China;Department of Anatomy,Qiqihar Medical University,Qiqihar 161006,Heilongjiang,China;Key Laboratory of Medicinal and Edible Resources and Prevention and Treatment of Metabolic Diseases in Heilongjiang Province,Qiqihar 161006,Heilongjiang,China)

机构地区：[1]齐齐哈尔市和平医院介入科,黑龙江齐齐哈尔161006 [2]齐齐哈尔医学院解剖学教研室,黑龙江齐齐哈尔161006 [3]黑龙江省药食同源资源与代谢性疾病防治重点实验室,黑龙江齐齐哈尔161006

出　　处：《系统医学》2025年第4期1-5,共5页Systems Medicine

基　　金：黑龙江省省属高等学校基本科研业务费科研项目(2020-KYYWF-0009)。

摘　　要：目的研究神经营养因子3(neurotrophin-3,NT-3)及其受体TrkC在缺氧性肺动脉高压(hypoxic pulmonary hypertension,HPH)病理进程中的作用及其机制。方法选取2023年3月—2023年12月齐齐哈尔医学院的12只雄性SD大鼠,采用随机数字表法分为对照组和HPH组(将大鼠置于低氧箱中,建立HPH大鼠模型),每组6只。测量两组大鼠右心室收缩压(right ventricular systolic pressure,RVSP)、肺动脉厚度百分比、血清NT-3水平、肺动脉中层平滑肌中磷酸化原肌球蛋白受体激酶C型(phosphorylated tropomyosin receptor kinase C,p-TrkC)阳性细胞数,观察不同浓度NT-3及其受体TrkC在肺动脉增生中的作用机制。结果HPH组RVSP为(31.21±5.08)mmHg、肺动脉厚度百分比为(42.35±6.16)%,高于对照组的(13.95±1.97)mmHg、(17.69±3.06)%,差异有统计学意义(t=-5.579、-8.782,P均<0.05)。HPH组的血清NT-3水平和肺动脉中层平滑肌中P-TrkC阳性细胞百分比均高于对照组,差异有统计学意义(P均<0.05)。NT-3促进肺动脉平滑肌细胞(pulmonary arterial smooth muscle cells,PASMC)增生,在给予TrkC抑制剂后,NT-3促进PASMC的增生受到有效抑制。结论在HPH病理发展过程中,NT-3通过结合其受体TrkC促进PASMC的增殖。Objective To investigate the role and mechanism of neurotrophin-3(NT-3)and its receptor TrkC in the pathological process of hypoxic pulmonary hypertension(HPH).Methods Twelve male SD rats in Qiqihar Medical College from March 2023 to December 2023 were selected and divided into control group and HPH group(Rats were placed in a hypoxic chamber to establish HPH rat model)by random number table method,with six rats in each group.To measure right ventricular systolic pressure(RVSP),percentage medial wall thickness,serum NT-3 level and phosphorylated tropomyosin receptor kinase C(p-TrkC)positive cells in pulmonary artery smooth muscle.Investigation of the mechanism of action of different concentrations of NT-3 and its receptor TrkC in pulmonary artery proliferation Results The RVSP and the percentage of pulmonary artery thicknes in HPH group were(31.21±5.08)mmHg,(42.35±6.16)%,which was higher than(13.95±1.97)mmHg and(17.69±3.06)%of control group,the differences were statistically significant(t=-5.579,-8.782,both P<0.05).The serum NT-3 level and the percentage of phosphorylated TrkC positive cells in the middle smooth muscle of pulmonary artery in HPH group were higher than those in control group,the differences were statistically significant(both P<0.05).NT-3 promotes pulmonary arterial smooth muscle cells(PASMC)proliferation,and after the administration of TrkC inhibitors,NT-3 promotes PASMC proliferation and is effectively inhibited.Conclusion During the pathological development of HPH,NT-3 promotes the proliferation of PASMCs by binding to its receptor TrkC.

关 键 词：缺氧性肺动脉高压 神经营养因子3 磷酸化原肌球蛋白受体激酶C型 肺动脉平滑肌细胞 增生 

分 类 号：R544[医药卫生—心血管疾病]