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DOI: 10.12201/bmr.202507.00074

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  Abstract: 随着透析龄的逐渐延长,尿毒症毒素的积累,腹腔内导管的机械刺激,长期接触生物不相容性透析液,慢性心力衰竭、代谢性酸中毒、胰岛素抵抗等能造成PD患者持续微炎症状态。微炎症是一种持续的低水平炎症状态,临床表现为炎症因子水平升高,长期持续的微炎症状态进一步导致PD患者预后不良。β2-MG在PD患者中的积累被认为是引发微炎症状态的重要因素之一,其作用机制涉及多个途径和分子通路。研究证明β2-MG通过非经典转化生长因子-β(Transforming growth factor-β, TGF β ) , 激活单核细胞中的TGF-β信号传导,促使其向M1型巨噬细胞分化并分泌肿瘤坏死因子- α(Tumor necrosis factor- α, TNF- α ) 、白介素-1 β( Interleukin-1 β, IL-1 β ) 以及白介素-6(Interleukin-6, IL-6)等炎性因子5,这些促炎因子通过自分泌或旁分泌机制活化NF-κB通路,进一步刺激腹膜细胞,加剧局部和全身炎症反应。Heiko Bruns等人将研究聚焦到β2-MG与炎症小体上,从体内外实验证明了β2-MG作为一种被巨噬细胞吞噬后的内源性介质,会形成淀粉样纤维,这使得溶酶体肿胀破裂,激活NLRP3炎性小体,进而促使IL-1β和IL-18分泌过度,表明β2-MG代表巨噬细胞无菌炎症的诱导剂6。既往研究表明氧化应激反应可以加剧炎症反应,PD患者早期肾功能衰竭有氧化应激反应参与,长期持续的氧化应激反应导致持续的微炎症反应。研究表明,β2-MG可以作为氧化应激的新型生物标志物7,有学者将120例早期2型糖尿病肾病患者纳入研究,发现β2-MG水平与早期2型糖尿病肾病患者氧化应激程度呈正相关8。有研究结果表明抑制β2-MG有助于增加抗氧化物的含量,能够降低氧化应激的产生和相关因子的释放,从而缓解氧化应激对肾损伤的影响9。由此可见,β2-MG通过加剧氧化应激反应促进患者全身微炎症反应,由此推断,这种现象在PD患者中表现得更明显。

  Key words: ; ; ; 

  Submit time: 27 July 2025

  Copyright: The copyright holder for this preprint is the author/funder, who has granted biomedRxiv a license to display the preprint in perpetuity.
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