慢性肺源性心脏病患者血清TGF-β1水平的临床意义
郭金叶，何士杰
（1.承德医学院，河北 承德，067000；2.承德市中心医院呼吸内科，河北 承德，067000）
浏览次数：114次 下载次数：374次
摘要：
目的 探讨慢性肺源性心脏病患者血清TGF-β1水平的临床价值。方法 选取慢性肺源性心脏病急性加重期患者40例作为急性加重期组，经常规治疗缓解后作为稳定期组。同时选取40例体检的健康人为正常对照组。采用酶联免疫吸附法测 定各组血清TGF-β1水平。结果 慢性肺源性心脏病急性加重期组和稳定期组血清TGF-β1水平均高于正常对照组（P<0.05）；稳定期组血清TGF-β1水平明显低于急性加重期组（P<0.05）。结论 TGF-β1参与了慢性肺源性心脏病的病理生理过程，血清TGF-β1水平可间接反应慢性肺源性心脏病的严重程度，可作为监测病情、观察疗效的一个良好指标。
关键词：慢性肺源性心脏病；肺动脉高压；转化生长因子-β1
中图分类号：R541.5文献标志码：A文章编号：2096-1413(2017)06-0042-02
The clinical significance of serum TGF-β1 in patients with chronic cor pulmonale
GUO Jin-ye 1, HE Shi-jie 2
(1. Chengde Medical College, Chengde 067000; 2. Department of Respiratory Medicine, Chengde Central Hospital,
Chengde 067000, China)
ABSTRACT: Objective To explore the clinical value of the expression levels of serum TGF-β1 in patients with chronic cor pulmonale. Methods A total of 40 patients with chronic cor pulmonale in the acute exacerbation were selected as the acute exacerbation group, and patients alleviated after conventional treatment were selected as the stable group. At the same time, 40 healthy people were selected as the normal control group. The serum TGF-β1 levels in the three groups were measured by enzyme-linked immunosorbent assay. Results The levels of serum TGF-β1 in acute exacerbation group and stable group were higher than those in the normal control group (P<0.05). The level of serum TGF-β1 in the stable group was significantly lower than that in the acute exacerbation group (P<0.05). Conclusion TGF-β1 participates in the pathophysiology of chronic cor pulmonale, and serum TGF-β1 levels may be an indirect response to the severity of chronic cor pulmonale, which can be used as a good indicator to monitor the condition and observe the curative effect.
KEYWORDS: chronic cor pulmonale; pulmonary hypertension; transforming growth factor-β1
参考文献：
[1] 中华医学会呼吸病学分会慢性阻塞性肺疾病学组.慢性阻塞性肺疾病诊治指南(2013 年修订版)[J].中华结核和呼吸,2013,36(4):255-264.
[2] 葛均波,徐永健,梅长林,等.内科学[M].8版,北京:人民卫生出版社,2013:115.
[3] MIZUNO S,BOGAARD HJ,KRASKAUSKAS D,et al.P53 Gene deficiency promotes hypoxia-induced pulmonary hypertension and vascular remodeling in mice[J].Am J Physiol Lung Cell Mol Physiol,2011,300(5): 753-761.
[4] 王金星,魏裔君,李慧.TGF-β1 与慢性肺疾病研究进展[J].当代医学,2009,15(3):40.
[5] 胡义杰,李志平,陈建明,等.低氧诱导肺动脉内皮细胞转分化的初步机制研究[J].局解手术学杂志,2013,22(6):594-596.
[6] BRADBURY DA,NEWTON R,ZHU YM,et al.Effert of bradykinin, TGF-β1, IL-1β, and hypoxia on COX-2 expression in pulmonary artery smooth muscle cells[J].Am J Physiol Lung Cell Mol Physiol,2002,283(4): 717-725.
[7] 马绍骏,蔡文玮,盛净.转化生长因子β1与体外血管外膜成纤维细 胞的增殖和迁移[J].中国组织工程研究与临床康复,2011,15(7):1195-1198.
[8] 蒋永亮,戴爱国,李启芳,等.转化生长因子与诱导型一氧化氮合酶相互调控对大鼠低氧性肺动脉高压的作用[J].中华结核和呼吸杂志,2005,28(7):453-457.
[9] KAPUR NK,PARUCHURI V,ARONOVITZ MJ,et al.Biventricular remodeling in murine models of right ventricular pressure overload[J].PLoS One,2013,8(7):e70802.
[10] WU YP,CHE DY,ZHANG WR,et al.Role of the pericytes of intra-acinar pulmonary artery in the structural remodeling of pulmonary vessels[J].J Tongji Med Univ,1995,15(1):16-18.