Galectin-3 in septic acute kidney injury: a translational study.
Galectin-3 in septic acute kidney injury: a translational study.
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Galectin-3 在脓毒症急性肾损伤中的作用：一项转化研究
DOI：
10.1186/s13054-021-03538-0
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发表时间：
2021-03-18
期刊：
影响因子：
--
通讯作者：
Eliaz I
中科院分区：
文献类型：
--
作者：
Sun H;Jiang H;Eliaz A;Kellum JA;Peng Z;Eliaz I
半乳糖凝集素-3 （Gal-3）是一种多效聚糖结合蛋白，与脓毒症和急性肾损伤（AKI）有关。然而，其在脓毒症相关AKI （S-AKI）中的作用从未被阐明。我们的目的是探索Gal-3在S-AKI中的作用及其作为治疗靶点的潜在效用。在57例入住重症监护病房（ICU）的脓毒症患者中，研究了血清Gal-3作为ICU死亡率和AKI发展的预测因子。在盲肠结扎穿刺（CLP）诱导的S-AKI大鼠模型中，在CLP后2、8和24小时(h)检测7天死亡率和血清Gal-3、白细胞介素-6 （IL-6）和肌酐。两个实验组分别给予Gal-3抑制剂修饰柑橘果胶（P-MCP） 400 mg/kg/d和1200 mg/kg/d，对照组只给予水（每组18只）。57例患者中，27例发生AKI， 8例在ICU死亡。血清Gal-3是控制年龄、AKI、急性生理和慢性健康评估（APACHE II）评分前后AKI （OR = 1.2 [95% CI 1.1-1.4], p = 0.01）和ICU死亡率（OR = 1.4 [95% CI 1.1-2.2], p = 0.04）的独立预测因子。在CLP大鼠实验中，血清Gal-3峰值早于IL-6。血清Gal-3在clp后2小时显著低于对照组（400 mg: p = 0.003; 1200 mg: p = 0.002）， IL-6在所有时间点均显著低于对照组，在clp后24小时差异最大（400 mg: p = 0.015; 1200 mg: p = 0.02）。在Gal-3抑制剂组中，7天死亡率从对照组的61%显著降低到28% （400 mg p - mcp: p = 0.03）和22% （1200 mg p - mcp: p = 0.001）。根据RIFLE标准，AKI发生率从对照组的89%显著降低到p - mcp组的44% （400 mg: p = 0.007; 1200 mg: p = 0.007）。这项转化研究证明了Gal-3在S-AKI发病机制中的重要性，以及它作为治疗靶点的潜在效用。
Galectin-3 (Gal-3) is a pleiotropic glycan-binding protein shown to be involved in sepsis and acute kidney injury (AKI). However, its role has never been elucidated in sepsis-associated AKI (S-AKI). We aimed to explore Gal-3’s role and its potential utility as a therapeutic target in S-AKI. In 57 patients admitted to the intensive care unit (ICU) with sepsis, serum Gal-3 was examined as a predictor of ICU mortality and development of AKI. In a rat model of S-AKI induced by cecal ligation and puncture (CLP), 7-day mortality and serum Gal-3, Interleukin-6 (IL-6), and creatinine were examined at 2, 8, and 24 hours (h) post-CLP. Two experimental groups received the Gal-3 inhibitor modified citrus pectin (P-MCP) at 400 mg/kg/day and 1200 mg/kg/day, while the control group received water only (n = 18 in each group). Among 57 patients, 27 developed AKI and 8 died in the ICU. Serum Gal-3 was an independent predictor of AKI (OR = 1.2 [95% CI 1.1–1.4], p = 0.01) and ICU mortality (OR = 1.4 [95% CI 1.1–2.2], p = 0.04) before and after controlling for age, AKI, and acute physiology and chronic health evaluation (APACHE II) score. In the CLP rat experiment, serum Gal-3 peaked earlier than IL-6. Serum Gal-3 was significantly lower in both P-MCP groups compared to control at 2 h post-CLP (400 mg: p = 0.003; 1200 mg: p = 0.002), and IL-6 was significantly lower in both P-MCP groups at all time points with a maximum difference at 24 h post-CLP (400 mg: p = 0.015; 1200 mg: p = 0.02). In the Gal-3 inhibitor groups, 7-day mortality was significantly reduced from 61% in the control group to 28% (400 mg P-MCP: p = 0.03) and 22% (1200 mg P-MCP: p = 0.001). Rates of AKI per RIFLE criteria were significantly reduced from 89% in the control group to 44% in both P-MCP groups (400 mg: p = 0.007; 1200 mg: p = 0.007). This translational study demonstrates the importance of Gal-3 in the pathogenesis of S-AKI, and its potential utility as a therapeutic target.
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DOI：
10.1186/s13054-015-0941-6
发表时间：
2015-05-06
期刊：
Critical care (London, England)
影响因子：
--
作者：
Dai X;Zeng Z;Fu C;Zhang S;Cai Y;Chen Z
通讯作者：
Chen Z
影响因子：
3.7
作者：
Dieplinger, Benjamin;Egger, Margot;Mueller, Thomas
通讯作者：
Mueller, Thomas
影响因子：
6.2
作者：
Dang, Zexu;MacKinnon, Alison;Sethi, Tariq
通讯作者：
Sethi, Tariq
影响因子：
3.7
作者：
Kolatsi-Joannou M;Price KL;Winyard PJ;Long DA
通讯作者：
Long DA
DOI：
10.1186/cc5783
发表时间：
2007
期刊：
Critical care (London, England)
影响因子：
--
作者：
Bozza FA;Salluh JI;Japiassu AM;Soares M;Assis EF;Gomes RN;Bozza MT;Castro-Faria-Neto HC;Bozza PT
通讯作者：
Bozza PT