目的:探讨气滞血瘀证(QS)和气虚血瘀证(QD)的蛋白质分子机制,作为中医冠心病(CAD)的两种亚型,经皮冠状动脉介入治疗(PCI)后。
方法:在本研究中,共纳入227例有QS的CAD患者和211例有QD的CAD患者;所有参与者均接受PCI.采用无标记定量蛋白质组学方法分析两种亚型冠心病患者PCI术前和术后6个月的血清变化,旨在阐明PCI治疗两种不同中医证型冠心病的干预机制。
结果:生化分析显示肿瘤坏死因子-α有显著变化,高密度脂蛋白胆固醇,血瘀证临床症状观察,PCI后两组患者的Gensini水平;蛋白质组学分析确定了QS和QD患者组中79和95个差异表达蛋白,分别,与对照组相比。补体C8α链,补体因子H,载脂蛋白H,载脂蛋白B,纤溶酶原,在两个对照组中,碳酸酐酶2和补体因子I均发生了变化。此外,富集分析表明,QS患者PCI术后细胞粘附和连接相关过程发生改变,包括过氧化物酶体增殖物激活受体信号通路和细胞外基质受体相互作用,QD组发生改变。蛋白质相互作用网络分析进一步丰富了52个节点蛋白,包括载脂蛋白B,脂蛋白(a),补体C5,载脂蛋白A4,补体C8α链,补体C8β链,补体C8γ链,载脂蛋白H,载脂蛋白A-Ⅱ,白蛋白,补体C4-B,载脂蛋白C3等。这些蛋白质的功能网络被认为有助于以中医证型为特征的CAD的病理生理学。
结论:目前的定量蛋白质组学研究已经初步确定了接受PCI治疗的不同中医亚型中CAD的生物标志物,为理解与各种中医亚型治疗CAD相关的蛋白质谱奠定了基础。
OBJECTIVE: To investigate the underlying protein molecular mechanisms of \"Qi stagnation and blood stasis syndrome\" (QS) and \"Qi deficiency and blood stasis syndrome\" (QD), as two subtypes of coronary artery disease (CAD) in Traditional Chinese Medicine (TCM), following percutaneous coronary intervention (PCI).
METHODS: In this study, a total of 227 CAD patients with QS and 211 CAD patients with QD were enrolled; all participants underwent PCI. Label-free quantification proteomics were employed to analyze the changes in serum in two subtypes of CAD patients before and 6 months after PCI, aiming to elucidate the intervention mechanism of PCI in treating CAD characterized by two different TCM syndromes.
RESULTS: Biochemical analysis revealed significant changes in tumor necrosis factor-α, high density lipoprotein cholesterol, blood stasis clinical symptoms observation, and Gensini levels in both patient groups post-PCI; Proteomic analysis identified 79 and 95 differentially expressed proteins in the QS and QD patient groups, respectively, compared to their control groups. complement C8 alpha chain, complement factor H, apolipoprotein H, apolipoprotein B, plasminogen, carbonic anhydrase 2, and complement factor I were altered in both comparison groups. Furthermore, enrichment analysis demonstrated that cell adhesion and connectivity-related processes underwent changes in QS patients post-PCI, whereas lipid metabolism-related pathways, including the peroxisome proliferator-activated receptor signaling pathway and extracellular matrix receptor interaction, underwent changes in the QD group. The protein-protein interaction network analysis further enriched 52 node proteins, including apolipoprotein B, lipoprotein (a), complement C5, apolipoprotein A4, complement C8 alpha chain, complement C8 beta chain, complement C8 gamma chain, apolipoprotein H, apolipoprotein A-Ⅱ, albumin, complement C4-B, apolipoprotein C3, among others. The functional network of these proteins is posited to contribute to the pathophysiology of CAD characterized by TCM syndromes.
CONCLUSIONS: The current quantitative proteomic study has preliminarily identified biomarkers of CAD in different TCM subtypes treated with PCI, potentially laying the groundwork for understanding the protein profiles associated with the treatment of various TCM subtypes of CAD.