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漆黄素通过介导PI3K/AKT/mTOR信号通路抑制脂多糖诱导的RAW264.7细胞炎症并诱导自噬。

Fisetin inhibits inflammation and induces autophagy by mediating PI3K/AKT/mTOR signaling in LPS-induced RAW264.7 cells.

作者信息

Sun Yue, Qin Hong, Zhang Huihui, Feng Xiangling, Yang Lina, Hou De-Xing, Chen Jihua

机构信息

Xiangya School of Public Health, Central South University, Changsha, China.

Inspecting Agency, Shanghai Municipal Health Commission, Shanghai, China.

出版信息

Food Nutr Res. 2021 Mar 25;65. doi: 10.29219/fnr.v65.6355. eCollection 2021.

DOI:10.29219/fnr.v65.6355
PMID:33841067
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8009086/
Abstract

BACKGROUND

Fisetin, a natural potent flavonoid, has various beneficial, pharmacological activities. In this study, we investigated expression changes of the fisetin regulating genes in lipopolysaccharide (LPS)-treated RAW264.7 cells and explored the role of fisetin in inflammation and autophagy.

METHODS AND RESULTS

Microarray analysis identified 1,071 genes that were regulated by fisetin in LPS-treated RAW264.7 cells, and these genes were mainly related to the process of immune system response. Quantitative real-time polymerase chain reaction and Bio-Plex analysis indicated that fisetin decreased the expression and secretion of several inflammatory cytokines in cells administered with LPS. Western blot analysis and immunofluorescence assay showed that fisetin decreased microtubule-associated protein 1 light-chain 3B (LC3B) and lysosome-associated membrane protein 1 (LAMP1) expression in LPS-treated cells, while the autophagy inhibitor chloroquine (CQ) could partially reverse this effect. In addition, fisetin reduced the elevated expression of p-PI3K, p-AKT and p-mTOR induced by LPS in a concentration-dependent manner.

CONCLUSIONS

Fisetin diminished the expression and secretion of inflammatory cytokines and facilitated autophagosome-lysosome fusion and degradation in LPS-treated RAW264.7 cells via inhibition of the PI3K/AKT/mTOR signaling pathway. Overall, the results of this study provide new clues for the anti-inflammatory mechanism of fisetin and explain the crosstalk between autophagy and inflammation to some extent.

摘要

背景

漆黄素是一种天然强效黄酮类化合物，具有多种有益的药理活性。在本研究中，我们研究了漆黄素调控基因在脂多糖（LPS）处理的RAW264.7细胞中的表达变化，并探讨了漆黄素在炎症和自噬中的作用。

方法与结果

微阵列分析确定了1071个在LPS处理的RAW264.7细胞中受漆黄素调控的基因，这些基因主要与免疫系统反应过程相关。定量实时聚合酶链反应和生物芯片分析表明，漆黄素降低了给予LPS的细胞中几种炎性细胞因子的表达和分泌。蛋白质免疫印迹分析和免疫荧光测定显示，漆黄素降低了LPS处理细胞中微管相关蛋白1轻链3B（LC3B）和溶酶体相关膜蛋白1（LAMP1）的表达，而自噬抑制剂氯喹（CQ）可部分逆转这种作用。此外，漆黄素以浓度依赖性方式降低了LPS诱导的p-PI3K、p-AKT和p-mTOR的表达升高。

结论

漆黄素通过抑制PI3K/AKT/mTOR信号通路，减少了LPS处理的RAW264.7细胞中炎性细胞因子的表达和分泌，并促进了自噬体-溶酶体融合及降解。总体而言，本研究结果为漆黄素的抗炎机制提供了新线索，并在一定程度上解释了自噬与炎症之间的相互作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b541/8009086/659ff8527969/FNR-65-6355-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b541/8009086/361a7d2810f0/FNR-65-6355-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b541/8009086/b6b74a3c4202/FNR-65-6355-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b541/8009086/b5e97968b278/FNR-65-6355-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b541/8009086/896dadfcda0a/FNR-65-6355-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b541/8009086/a0b2a5b9c356/FNR-65-6355-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b541/8009086/659ff8527969/FNR-65-6355-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b541/8009086/361a7d2810f0/FNR-65-6355-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b541/8009086/b6b74a3c4202/FNR-65-6355-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b541/8009086/b5e97968b278/FNR-65-6355-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b541/8009086/896dadfcda0a/FNR-65-6355-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b541/8009086/a0b2a5b9c356/FNR-65-6355-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b541/8009086/659ff8527969/FNR-65-6355-g006.jpg

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