Lin Yi-Wen, Tsai Chien-Sung, Huang Chun-Yao, Tsai Yi-Ting, Shih Chun-Ming, Lin Shing-Jong, Li Chi-Yuan, Lin Cheng-Yen, Sung Shih-Ying, Lin Feng-Yen
Institute of Oral Biology, National Yang Ming Chiao Tung University, Taipei 112, Taiwan.
Taipei Heart Institute, Taipei Medical University, Taipei 110, Taiwan.
Biomedicines. 2022 May 7;10(5):1089. doi: 10.3390/biomedicines10051089.
Orthotopic allograft transplantation (OAT) is a major strategy for solid heart and kidney failure. However, the recipient's immunity-induced chronic rejection induces OAT vasculopathy that results in donor organ failure. With the exception of immunosuppressive agents, there are currently no specific means to inhibit the occurrence of OAT vasculopathy. On the other hand, far-infrared (FIR) therapy uses low-power electromagnetic waves given by FIR, with a wavelength of 3-25 μm, to improve human physiological functions. Previous studies have shown that FIR therapy can effectively inhibit inflammation. It has also been widely used in adjuvant therapy for various clinical diseases, especially cardiovascular diseases, in recent years. Thus, we used this study to explore the feasibility of FIR in preventing OAT vasculopathy. In this study, the model of transplantation of an aorta graft from PVG/Seac rat to ACI/NKyo rat, and in vitro model of human endothelial progenitor cells (EPCs) was used. In this report, we presented that FIR therapy decreased the serious of vasculopathy in OAT-recipient ACI/NKyo rats via inhibiting proliferation of smooth muscle cells, accumulation of collagen, and infiltration of fibroblast in the vessel wall; humoral and cell-mediated immune responses were decreased in the spleen. The production of inflammatory proteins/cytokines also decreased in the plasma. Additionally, FIR therapy presented higher mobilization and circulating EPC levels associated with vessel repair in OAT-recipient ACI/NKyo rats. In vitro studies demonstrated that the underlying mechanisms of FIR therapy inhibiting OAT vasculopathy may be associated with the inhibition of the Smad2-Slug axis endothelial mesenchymal transition (EndoMT). Thus, FIR therapy may be the strategy to prevent chronic rejection-induced vasculopathy.
原位同种异体移植（OAT）是治疗实体心脏和肾脏衰竭的主要策略。然而，受者免疫诱导的慢性排斥反应会引发OAT血管病变，导致供体器官衰竭。除免疫抑制剂外，目前尚无抑制OAT血管病变发生的特异性方法。另一方面，远红外线（FIR）疗法利用波长为3 - 25μm的FIR发出的低功率电磁波来改善人体生理功能。先前的研究表明，FIR疗法可有效抑制炎症。近年来，它还被广泛用于各种临床疾病的辅助治疗，尤其是心血管疾病。因此，我们开展本研究以探索FIR在预防OAT血管病变方面的可行性。在本研究中，采用了将PVG/Seac大鼠的主动脉移植物移植到ACI/NKyo大鼠的模型以及人内皮祖细胞（EPCs）的体外模型。在本报告中，我们指出FIR疗法通过抑制平滑肌细胞增殖、胶原蛋白积累和成纤维细胞在血管壁的浸润，减轻了OAT受体ACI/NKyo大鼠血管病变的严重程度；脾脏中的体液和细胞介导免疫反应降低。血浆中炎症蛋白/细胞因子的产生也减少。此外，FIR疗法使OAT受体ACI/NKyo大鼠中与血管修复相关的EPC动员和循环水平升高。体外研究表明，FIR疗法抑制OAT血管病变的潜在机制可能与抑制Smad2 - Slug轴内皮间充质转化（EndoMT）有关。因此，FIR疗法可能是预防慢性排斥反应诱导的血管病变的策略。
