Yang Chen, Xiao-Wen Zhang, Mei-Mei Zhao, Ling Li, Yang Liu, Tian-Tian Wei, Wei Yu, Bo Han, Zheng-Ping Liu, Ke-Wu Zeng
{"title":"绿原酸靶向SLC37A2,通过er依赖性NF-κB和NLRP3信号通路抑制巨噬细胞活化,对抗败血症诱导的急性肺损伤。","authors":"Yang Chen, Xiao-Wen Zhang, Mei-Mei Zhao, Ling Li, Yang Liu, Tian-Tian Wei, Wei Yu, Bo Han, Zheng-Ping Liu, Ke-Wu Zeng","doi":"10.1080/10286020.2025.2506181","DOIUrl":null,"url":null,"abstract":"<p><p>Sepsis-induced acute lung injury (SI-ALI) requires urgent treatment due to severe inflammation. Our study found chlorogenic acid (CGA) suppressed LPS-induced macrophage activation by lowering NO, TNF-α, and IL-6. TPP-based strategies identified SLC37A2 as the direct target of CGA, validated by CETSA/MST. Molecular docking indicated CGA-SLC37A2 hydrogen bonding. CGA alleviated endoplasmic reticulum stress via SLC37A2, inhibiting TLR4/NF-κB and NLRP3 pathways to reduce inflammation. In SI-ALI mice and zebrafish models, CGA mitigated lung injury through these mechanisms taken together. This work highlights the therapeutic potential of CGA for SI-ALI and the critical role of SLC37A2 in combating infectious pneumonia.</p>","PeriodicalId":15180,"journal":{"name":"Journal of Asian Natural Products Research","volume":" ","pages":"1-22"},"PeriodicalIF":1.3000,"publicationDate":"2025-05-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Chlorogenic acid targets SLC37A2 to inhibit macrophage activation via ER-dependent NF-κB and NLRP3 signaling pathways against sepsis-induced acute lung injury.\",\"authors\":\"Yang Chen, Xiao-Wen Zhang, Mei-Mei Zhao, Ling Li, Yang Liu, Tian-Tian Wei, Wei Yu, Bo Han, Zheng-Ping Liu, Ke-Wu Zeng\",\"doi\":\"10.1080/10286020.2025.2506181\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Sepsis-induced acute lung injury (SI-ALI) requires urgent treatment due to severe inflammation. Our study found chlorogenic acid (CGA) suppressed LPS-induced macrophage activation by lowering NO, TNF-α, and IL-6. TPP-based strategies identified SLC37A2 as the direct target of CGA, validated by CETSA/MST. Molecular docking indicated CGA-SLC37A2 hydrogen bonding. CGA alleviated endoplasmic reticulum stress via SLC37A2, inhibiting TLR4/NF-κB and NLRP3 pathways to reduce inflammation. In SI-ALI mice and zebrafish models, CGA mitigated lung injury through these mechanisms taken together. This work highlights the therapeutic potential of CGA for SI-ALI and the critical role of SLC37A2 in combating infectious pneumonia.</p>\",\"PeriodicalId\":15180,\"journal\":{\"name\":\"Journal of Asian Natural Products Research\",\"volume\":\" \",\"pages\":\"1-22\"},\"PeriodicalIF\":1.3000,\"publicationDate\":\"2025-05-27\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Journal of Asian Natural Products Research\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1080/10286020.2025.2506181\",\"RegionNum\":3,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q3\",\"JCRName\":\"CHEMISTRY, APPLIED\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Asian Natural Products Research","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1080/10286020.2025.2506181","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"CHEMISTRY, APPLIED","Score":null,"Total":0}
Chlorogenic acid targets SLC37A2 to inhibit macrophage activation via ER-dependent NF-κB and NLRP3 signaling pathways against sepsis-induced acute lung injury.
Sepsis-induced acute lung injury (SI-ALI) requires urgent treatment due to severe inflammation. Our study found chlorogenic acid (CGA) suppressed LPS-induced macrophage activation by lowering NO, TNF-α, and IL-6. TPP-based strategies identified SLC37A2 as the direct target of CGA, validated by CETSA/MST. Molecular docking indicated CGA-SLC37A2 hydrogen bonding. CGA alleviated endoplasmic reticulum stress via SLC37A2, inhibiting TLR4/NF-κB and NLRP3 pathways to reduce inflammation. In SI-ALI mice and zebrafish models, CGA mitigated lung injury through these mechanisms taken together. This work highlights the therapeutic potential of CGA for SI-ALI and the critical role of SLC37A2 in combating infectious pneumonia.
期刊介绍:
The Journal of Asian Natural Products Research (JANPR) publishes chemical and pharmaceutical studies in the English language in the field of natural product research on Asian ethnic medicine. The journal publishes work from scientists in Asian countries, e.g. China, Japan, Korea and India, including contributions from other countries concerning natural products of Asia. The journal is chemistry-orientated. Major fields covered are: isolation and structural elucidation of natural constituents (including those for non-medical uses), synthesis and transformation (including biosynthesis and biotransformation) of natural products, pharmacognosy, and allied topics. Biological evaluation of crude extracts are acceptable only as supporting data for pure isolates with well-characterized structures.
All published research articles in this journal have undergone rigorous peer review, based on initial editor screening and anonymized refereeing by at least two expert referees.