Li Dan, Li Fangyan, Zhou Yaping, Tang Yiping, Hu Zuomin, Wu Qi, Xie Tiantian, Lin Qinlu, Wang Hanqing, Luo Feijun
Hunan Key Laboratory of Grain-Oil Deep Process and Quality Control, Hunan Key Laboratory of Forestry Edible Resources Safety and Processing, National Research Center of Rice Deep Processing and Byproducts, College of Food Science and Engineering, Central South University of Forestry and Technology, Changsha 410004, China.
Hunan Engineering Research Center of Full Life-Cycle Energy-Efficient Buildings and Environmental Health, School of Civil Engineering, Central South University of Forestry and Technology, Changsha 410004, China.
Foods. 2024 Sep 20;13(18):2984. doi: 10.3390/foods13182984.
Excessive inflammatory reactions are the most important pathological injury factor in acute lung injury (ALI). Our recent study found that sialic acid had an anti-colitis effect. In this study, the effect of sialic acid (SA) on acute lung inflammation was investigated. A lipopolysaccharide (LPS)-induced ALI animal model and LPS-stimulated HUVEC cell model were used to evaluate the anti-inflammatory effect of SA and study its molecular mechanisms. Compared with the LPS group, the lung index of the SA group decreased from 0.79 ± 0.05% to 0.58 ± 0.06% (LPS + 50 SA) and 0.62 ± 0.02% (LPS + 100 SA), with < 0.01, suggesting that SA could improve the pulmonary edema of mice and alleviate LPS-induced lung injury. Transcriptome research identified 26 upregulated genes and 25 downregulated genes involved in the protection of SA against ALI. These genes are mainly related to the MAPK and NF-κB signaling pathways. Our study also proved that SA markedly downregulated the expression of inflammatory factors and blocked the JNK/p38/PPAR-γ/NF-κB pathway. Meanwhile, SA treatment also upregulated the expression of HO-1 and NQO1 in ALI mice. In vitro, SA obviously repressed the expressions of inflammatory cytokines and the JNK/p38-NF-κB/AP-1 pathway. SA also regulated the expression of oxidative stress-related genes through the Nrf2 pathway. Taken together, SA exhibits a protective role by modulating the anti-inflammatory and anti-oxidation pathways in ALI, and it may be a promising candidate for functional foods to prevent ALI.
过度的炎症反应是急性肺损伤（ALI）中最重要的病理损伤因素。我们最近的研究发现，唾液酸具有抗结肠炎作用。在本研究中，研究了唾液酸（SA）对急性肺炎症的影响。使用脂多糖（LPS）诱导的ALI动物模型和LPS刺激的人脐静脉内皮细胞（HUVEC）模型来评估SA的抗炎作用并研究其分子机制。与LPS组相比，SA组的肺指数从0.79±0.05%降至0.58±0.06%（LPS + 50 SA）和0.62±0.02%（LPS + 100 SA），P < 0.01，表明SA可改善小鼠肺水肿并减轻LPS诱导的肺损伤。转录组研究确定了26个上调基因和25个下调基因参与SA对ALI的保护作用。这些基因主要与丝裂原活化蛋白激酶（MAPK）和核因子κB（NF-κB）信号通路相关。我们的研究还证明，SA显著下调炎症因子的表达并阻断JNK/p38/过氧化物酶体增殖物激活受体γ（PPAR-γ）/NF-κB通路。同时，SA处理还上调了ALI小鼠中血红素加氧酶-1（HO-1）和醌氧化还原酶1（NQO1）的表达。在体外，SA明显抑制炎症细胞因子的表达以及JNK/p38-NF-κB/活化蛋白-1（AP-1）通路。SA还通过核因子E2相关因子2（Nrf2）通路调节氧化应激相关基因的表达。综上所述，SA通过调节ALI中的抗炎和抗氧化途径发挥保护作用，它可能是预防ALI的功能性食品的一个有前景的候选物。
