Beijing Key Laboratory of Pharmacology of Chinese Materia Region, Institute of Basic Medical Sciences, Xiyuan Hospital, China Academy of Chinese Medical Sciences, National Clinical Research Center of Cardiovascular Disease of Traditional Chinese Medicine, Beijing 100000, China.
the National Key Facility for Crop Gene Resources and Genetic Improvement, Institute of Crop Science, Chinese Academy of Agricultural Science, Beijing 100098, China.
J Tradit Chin Med. 2024 Jun;44(3):554-563. doi: 10.19852/j.cnki.jtcm.20240408.001.
To investigate the underlying protein molecular mechanisms of " stagnation and blood stasis syndrome" (QS) and " deficiency and blood stasis syndrome" (QD), as two subtypes of coronary artery disease (CAD) in Traditional Chinese Medicine (TCM), following percutaneous coronary intervention (PCI).
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.
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.
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.
探究经皮冠状动脉介入治疗(PCI)后,中医“气滞血瘀证”(QS)和“气虚血瘀证”(QD)两种冠心病(CAD)亚型的潜在蛋白分子机制。
本研究纳入 227 例 QS 型 CAD 患者和 211 例 QD 型 CAD 患者,所有患者均接受 PCI。采用无标记定量蛋白质组学技术分析两种 CAD 亚型患者 PCI 前后血清变化,旨在阐明 PCI 治疗两种不同中医证候 CAD 的干预机制。
PCI 后两组患者肿瘤坏死因子-α、高密度脂蛋白胆固醇、血瘀临床症状观察和 Gensini 评分均有明显变化;蛋白质组学分析发现 QS 组和 QD 组患者分别与对照组相比有 79 个和 95 个差异表达蛋白;补体 C8α链、补体因子 H、载脂蛋白 H、载脂蛋白 B、纤溶酶原、碳酸酐酶 2 和补体因子 I 在两组比较中均发生改变。此外,富集分析表明,PCI 后 QS 患者的细胞黏附和连接相关过程发生变化,而 QD 组则发生脂质代谢相关途径的变化,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。蛋白质-蛋白质相互作用网络分析进一步富集了 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。这些蛋白的功能网络可能有助于解释中医证候型 CAD 的病理生理学。
本定量蛋白质组学研究初步鉴定了不同中医证型 CAD 经 PCI 治疗的生物标志物,为理解各种中医证型 CAD 治疗相关的蛋白谱奠定了基础。