服用富血小板血浆对稳定型冠心病患者内皮祖细胞增殖和分化的影响

Ronald Rendy Hehanusa
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摘要

内皮祖细胞(EPCs)是内皮细胞的重要前体,在调节血管结构和维持血管平衡以防止炎症和血栓形成方面发挥着关键作用,从而导致冠心病(CHD)的稳定。生长因子可刺激 EPC 增殖和分化过程中的信号转导。富血小板血浆(PRP)含有公认的血管生成生长因子。我们的研究旨在分析 PRP 对稳定型心脏病患者 EPC 增殖和分化的影响。采用实验后试验对照组设计,用 M-199 培养基培养外周血中的单核细胞(MNCs),将其分为 PRP 组、血小板贫血浆组(PPP)和对照组,培养 14 天。采用方差分析法利用 CD34 标记对 EPC 增殖进行量化。7 天后,使用 Mann-Whitney U 检验用 von Willebrand Factor(vWF)标记对分化细胞进行计数。与 PPP 组(0.762 ± 0.19)和对照组(0.068 ± 0.05,P=0.000)相比,PRP 组的 EPC 增殖(1.052 ± 0.16)显著增加。然而,与 PPP(0.00-0.30 vs. 0.00-0.20,p=0.565)或对照组(0.00-0.30 vs. 0.00-0.00,p=0.064)相比,PRP 组的 EPC 分化没有显著增加。此外,与对照组相比(0.00-0.20 vs. 0.00-0.00,p = 0.144),PPP 组的 EPC 分化没有明显增加。与PPP组和对照组相比,PRP能明显促进稳定型冠心病患者外周血中EPC的增殖,但不能明显促进其分化。
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THE EFFECT OF PLATELET-RICH PLASMA ADMINISTRATION ON PROLIFERATION AND DIFFERENTIATION OF ENDOTHELIAL PROGENITOR CELLS IN PATIENTS WITH STABLE CORONARY HEART DISEASE
Endothelial Progenitor Cells (EPCs) are crucial precursors to endothelial cells, playing a key role in regulating blood vessel structure and maintaining homeostasis to protect against inflammation and thrombosis, contributing to stable coronary heart disease (CHD). Growth factors stimulate signal transduction during EPC proliferation and differentiation. Platelet-Rich Plasma (PRP) contains widely recognized growth factors in angiogenesis. Our research aimed to analyze PRP's effects on EPC proliferation and differentiation in stable CHD patients. Using an experimental post-test control group design, mononuclear cells (MNCs) from peripheral blood were cultured with M-199 medium, divided into PRP, Platelet Poor Plasma (PPP), and control groups, and incubated for 14 days. EPC proliferation was quantified with CD34 markers using ANOVA. After 7 days, differentiated cells were counted with von Willebrand Factor (vWF) markers using the Mann-Whitney U test.EPC proliferation significantly increased in the PRP group (1.052 ± 0.16) compared to PPP (0.762 ± 0.19) and the control (0.068 ± 0.05, p=0.000). However, EPC differentiation showed no significant increase in the PRP group compared to PPP (0.00-0.30 vs. 0.00-0.20, p = 0.565) or the control (0.00-0.30 vs. 0.00-0.00, p = 0.064). Additionally, no significant increase in EPC differentiation was observed in the PPP group compared to the control (0.00-0.20 vs. 0.00-0.00, p = 0.144). PRP significantly enhanced EPC proliferation but did not significantly enhance differentiation in the peripheral blood of stable CHD patients compared to PPP and control groups.
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