虾青素通过抑制小鼠炎症反应和调节 SOCS3/JAK2/STAT3 信号通路改善脂多糖诱导的急性肺损伤,Food & Function

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虾青素通过抑制小鼠炎症反应和调节 SOCS3/JAK2/STAT3 信号通路改善脂多糖诱导的急性肺损伤
Food & Function ( IF 5.1 ) Pub Date : 2022-10-18 , DOI: 10.1039/d2fo02182j
Li Zhu ₁ , Huihui Wu ₁ , Zhenbo Ma ₂ , Decheng Dong ₁ , Ze Yang ₁ , Jing Tian ₁

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急性肺损伤 (ALI) 是一种全身性炎症过程。大量研究表明，虾青素（ASTA）具有很强的抗炎作用，几乎无毒副作用。本研究的目的是探讨 ASTA 对脂多糖 (LPS) 诱导的小鼠 ALI 的影响及其机制。结果显示，与 LPS 组相比，呼吸阻力（Re）、吸气阻力（Ri）、动态肺顺应性（Cdyn）、湿/干重（W/D）比值、白蛋白（BA/SA ASTA预处理组的）比值和髓过氧化物酶（MPO）活性显着降低，细胞总数、中性粒细胞和巨噬细胞计数显着降低。HE染色结果显示肺泡间质水肿、出血及红细胞渗出减少。与LPS组相比，ASTA预处理组Th17细胞比例及白细胞介素（IL）-17和肿瘤坏死因子-α（TNF-α）含量显着降低，而转化生长因子（ TGF)-β和Treg细胞的百分比显着增加。Western blot分析表明，ASTA可上调细胞因子信号抑制因子3（SOCS3）的表达水平，下调磷酸化Janus激酶2（p-JAK2）、磷酸化信号转导因子和转录激活因子3的表达水平(p-STAT3) 在肺组织中。结果表明，ASTA对LPS诱导的小鼠急性肺损伤具有保护作用，其保护机制是通过激活SOCS3/JAK2/STAT3信号通路，

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Astaxanthin ameliorates lipopolysaccharide-induced acute lung injury via inhibition of inflammatory reactions and modulation of the SOCS3/JAK2/STAT3 signaling pathways in mice

Acute lung injury (ALI) is a systemic inflammatory process. A large number of studies have shown that astaxanthin (ASTA) has strong anti-inflammatory effects and almost non-toxic side effects. The purpose of this study was to explore the effect of ASTA on lipopolysaccharide (LPS)-induced ALI in mice and its underlying mechanism. The result showed that compared with the LPS group, the expression levels of the respiratory resistance (Re), inspiratory resistance (Ri), dynamic lung compliance (Cdyn), wet/dry weight (W/D) ratio, albumin (BA/SA) ratio and myeloperoxidase (MPO) activity in the ASTA pretreatment group were significantly reduced, and total cell, neutrophil and macrophage counts were significantly decreased. HE staining results showed that alveolar interstitial edema, bleeding and erythrocyte exudation were reduced. Compared with the LPS group, the percentage of Th17 cells and the content of interleukin (IL)-17 and tumor necrosis factor-α (TNF-α) in the ASTA pretreatment group were significantly decreased, while the content of the transforming growth factor (TGF)-β and the percentage of Treg cells were significantly increased. Western blot analysis showed that ASTA could up-regulate the expression level of the suppressor of cytokine signaling-3 (SOCS3) and down-regulate the expression levels of phosphorylated Janus kinase 2 (p-JAK2), phosphorylated signal transducer and activator of transcription 3 (p-STAT3) in lung tissue. The results showed that ASTA had a protective effect on LPS-induced acute lung injury in mice, and its protective mechanism was through activating the SOCS3/JAK2/STAT3 signaling pathway, promoting Treg cell differentiation and reducing inflammatory reactions and Th17 cell differentiation, which provided a theoretical basis for the clinical treatment of ALI.

更新日期：2022-10-18

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