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International immunopharmacology. 2024 Sep 30:139:112668. doi: 10.1016/j.intimp.2024.112668 Q14.72025

SKLB023 protects against inflammation and apoptosis in sepsis-associated acute kidney injury via the inhibition of toll-like receptor 4 signaling

SKLB023通过抑制 Toll 样受体4信号传导保护内毒素诱导的急性肾损伤中的炎症和细胞凋亡 翻译改进

Hui Li  1, Qian Ren  1, Yao Hu  2, Fan Guo  1, Rongshuang Huang  1, Lin Lin  3, Zhouke Tan  4, Liang Ma  5, Ping Fu  1

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作者单位

  • 1 Department of Nephrology, Institute of Kidney Diseases, West China Hospital of Sichuan University, Chengdu 610041, PR China.
  • 2 Department of Medicine Renal Division, Affiliated Hospital & Clinical Medical College of Chengdu University, Chengdu 610041, PR China.
  • 3 West-district Outpatient Department, West China Hospital of Stomatology, Sichuan University, Chengdu 610041, PR China. Electronic address: linlin_stomatology@foxmail.com.
  • 4 Department of Nephrology, Organ Transplant Center, Guizhou Province Key Laboratory of Cell Engineering, Affiliated Hospital of ZunYi Medical University, ZunYi 563003, PR China. Electronic address: tanzhouke@zmu.edu.cn.
  • 5 Department of Nephrology, Institute of Kidney Diseases, West China Hospital of Sichuan University, Chengdu 610041, PR China. Electronic address: liang_m@scu.edu.cn.

    • DOI: 10.1016/j.intimp.2024.112668 PMID: 39008938

    摘要 中英对照阅读

    Sepsis-associated acute kidney injury (SA-AKI) is one of common critical illnesses with high morbidity and mortality. At present, effective therapeutic drugs for SA-AKI are remain lacking. SKLB023 is a synthetic small-molecule compound which exerts potent anti-inflammatory effects in our previous studies. Here, this study aimed to characterize the protective effect of SKLB023 on SA-AKI and explore its underlying mechanism. The SA-AKI experimental models ha... ...点击完成人机验证后继续浏览

    Sepsis相关的急性肾损伤（SA-AKI）是一种常见的严重疾病，具有高发病率和死亡率。目前，针对SA-AKI的有效治疗药物仍然缺乏。SKLB023是我们之前研究中显示有强大抗炎作用的合成小分子化合物。本研究旨在探讨SKLB023对SA-AKI的保护效应及其潜在机制。通过结扎/穿刺盲肠（CLP）和脂多糖（LPS）注射在雄性C57BL/6J小鼠中建立SA-AKI实验模型。在建模前3天以及建模当天提前30分钟，通过灌胃给予SKLB023（CLP模型中剂量为50或25 mg/kg，在LPS模型中剂量为50 mg/kg）。我们的结果显示，SKLB023治疗能够改善SA-AKI小鼠的存活率，并减轻两种类型败血症AKI小鼠的肾病理损伤、炎症和细胞凋亡。机制上，SKLB023降低了由LPS触发的肾小管上皮细胞中TLR4的表达，并抑制了下游通路包括NF-κB和MAPK通路的激活。本研究表明，SKLB023有望成为预防和治疗败血症AKI的潜在药物。

    关键词：急性肾损伤；细胞凋亡；炎症；SKLB023；败血症； Toll-like受体4

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    期刊名：International immunopharmacology

    缩写：INT IMMUNOPHARMACOL

    ISSN：1567-5769

    e-ISSN：1878-1705

    IF/分区：4.7/Q1

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    SKLB023 protects against inflammation and apoptosis in sepsis-associated acute kidney injury via the inhibition of toll-like receptor 4 signaling