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논문분류	춘계학술대회 초록집
제목	Glucosylated Albumin Mitigates LPS-Induced Kidney Injury by Rescuing Cells from G1/S Cell Cycle Arrest
저자	Seong Min Lee
출판정보	2025; 2025(1):
키워드	Glc-alb, LPS, AKI, Cell cycle, Inflammation
초록	Acute kidney injury (AKI) arises from multiple pathological mechanisms, including inflammation, cell cycle arrest, and oxidative stress, all of which contribute to the progression of chronic kidney disease. We engineered a glucosylated albumin (Glc-alb) nanoplatform that regulates its half-life in the body while minimizing renal toxicity. In this study, we assessed the therapeutic efficacy of Glc-alb and its underlying mechanisms in an LPS-induced AKI model. C57BL/6 mice were intravenously injected with Glc-alb (200μg/mouse) 1 hour before LPS administration, and kidneys were harvested after 24 hours. For in vitro validation, HK-2 and THP-1 cells were each treated with Glc-alb (30, 300nM) 1 hour before LPS stimulation for 24 hours, using albumin alone as the vehicle control. Glc-alb significantly improved renal function by lowering both BUN and creatinine levels in mice injected with LPS versus albumin alone. These therapeutic effects were further supported by Glc-alb reversing LPS-induced increases in NGAL, ICAM-1, pp65, and pSTAT3 expression, while restoring the G1/S cell cycle marker pCDK4 in the kidney. Glc-alb also reduced the frequency of circulating CD11b+F4/80+macrophages and CD11b+Gr-1+neutrophils induced by LPS in the spleen and downregulated pro-inflammatory markers in THP-1 cells. In HK-2 cells, Glc-alb suppressed LPS-induced reactive oxygen species (ROS) production and enhanced mitochondrial activity and wound healing ability even under hypoxic conditions. These findings suggest that Glc-alb exerts potent renoprotective effects, possibly by regulating ROS production and STAT3-mediated inflammation that impair the cell cycle. Glc-alb exhibits potent therapeutic potential by reducing inflammation, preventing G1/S cell cycle arrest, and alleviating oxidative stress, ultimately protecting against LPS-induced kidney injury.
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