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.

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Publication Details

Journal
Journal of Asian Natural Products Research
Published
2025-05-27
DOI
https://doi.org/10.1080/10286020.2025.2506181
Citations
3
Primary Topic
Eicosanoids and Hypertension Pharmacology
Type
article
Field-Weighted Citation Impact
3.34

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article

Chlorogenic acid targets SLC37A2 to inhibit macrophage activation via ER-dependent NF-κB and NLRP3 signaling pathways against sepsis-induced acute lung injury

Tiantian Wei, Meimei Zhao, Wei Yu, Ke‐Wu Zeng et al.
3 citations
Journal of Asian Natural Products Research
Eicosanoids and Hypertension Pharmacology
3.34
article

Chlorogenic acid targets SLC37A2 to inhibit macrophage activation via ER-dependent NF-κB and NLRP3 signaling pathways against sepsis-induced acute lung injury

Tiantian Wei, Meimei Zhao, Wei Yu, Ke‐Wu Zeng, Zheng­ping Liu, Bo Han, Yang Liu, Xiaowen Zhang, Ling Li, Chen Yang
article en
3 citations

Abstract

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.

Journal of Asian Natural Products ResearchVol. 28(3)
Shihezi University (CN), Beijing University of Chinese Medicine (CN), Peking University (CN), Feed Control (Norway) (NO), Peking University Third Hospital (CN), Shandong Academy of Pharmaceutical Sciences (CN)
Natural Science Foundation of Shandong Province, Beijing Municipal Natural Science Foundation
Good health and well-being
Openalex Percentile: Top 9%
Eicosanoids and Hypertension Pharmacology
3.34
DOISourceOpenAlex
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