深入了解碱性磷酸酶的抗炎机制。
Insights into Alkaline Phosphatase Anti-Inflammatory Mechanisms.
作者信息
Balabanova Larissa, Bondarev Georgii, Seitkalieva Aleksandra, Son Oksana, Tekutyeva Liudmila
机构信息
G.B. Elyakov Pacific Institute of Bioorganic Chemistry, Far Eastern Branch, Russian Academy of Sciences, Prospect 100-Letya Vladivostoka 152, 690022 Vladivostok, Russia.
Youth Research Laboratory of Recombinant DNA Technologies, Advanced Engineering School, Institute of Biotechnology, Bioengineering and Food Systems, Far Eastern Federal University, 10 Ajax Bay, Russky Island, 690922 Vladivostok, Russia.
出版信息
Biomedicines. 2024 Nov 1;12(11):2502. doi: 10.3390/biomedicines12112502.
BACKGROUND
The endogenous ecto-enzyme and exogenously administered alkaline phosphatase (ALP) have been evidenced to significantly attenuate inflammatory conditions, including Toll-like receptor 4 (TLR4)-related signaling and cytokine overexpression, barrier tissue dysfunction and oxidative stress, and metabolic syndrome and insulin resistance, in experimental models of colitis, liver failure, and renal and cardiac ischemia-reperfusion injury. This suggests multiple mechanisms of ALP anti-inflammatory action that remain to be fully elucidated.
METHODS
Recent studies have contributed to a deeper comprehension of the role played by ALP in immune metabolism. This review outlines the established effects of ALP on lipopolysaccharide (LPS)-induced inflammation, including the neutralization of LPS and the modulation of purinergic signaling.
RESULTS
The additional mechanisms of anti-inflammatory activity of ALP observed in different pathologies are proposed.
CONCLUSIONS
The anti-inflammatory pathways of ALP may include a scavenger receptor (CD36)-mediated activation of β-oxidation and oxidative phosphorylation, caveolin-dependent endocytosis, and selective autophagy-dependent degradation.
背景
内源性外切酶和外源性碱性磷酸酶（ALP）已被证明在结肠炎、肝衰竭以及肾和心脏缺血再灌注损伤的实验模型中能显著减轻炎症状态，包括Toll样受体4（TLR4）相关信号传导和细胞因子过度表达、屏障组织功能障碍和氧化应激，以及代谢综合征和胰岛素抵抗。这表明ALP抗炎作用的多种机制仍有待充分阐明。
方法
近期研究有助于更深入理解ALP在免疫代谢中的作用。本综述概述了ALP对脂多糖（LPS）诱导炎症的既定影响，包括LPS的中和以及嘌呤能信号传导的调节。
结果
提出了在不同病理状态下观察到的ALP抗炎活性的其他机制。
结论
ALP的抗炎途径可能包括清道夫受体（CD36）介导的β氧化和氧化磷酸化激活、小窝蛋白依赖性内吞作用以及选择性自噬依赖性降解。
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