Madeng’ai Ethyl Acetate Extract Attenuates Lipopolysaccharide-Induced Inflammation and Acute Lung Injury
4 affiliations
- 1The First Clinical Medical College, Ningxia Medical University, Yinchuan 750004, China
- 2Hunan Provincial Key Laboratory of Dong Medicine, Hunan University of Medicine, Huaihua 418000, China
- 3College of Biological Resources and Environmental Sciences, Jishou University, Jishou 416000, China
- 4Traditional Chinese Medicine (TCM) and Ethnomedicine Innovation & Development International Laboratory, School of Pharmacy, Hunan University of Chinese Medicine, Changsha 410208, China
Abstract
Madeng’ai, the dried root of Potentilla freyniana Bornm., is used in Dong medicine for infections and wound care. This study examined the chemical composition and prophylactic protective effects of the ethyl acetate fraction of its ethanolic root extract (referred to as MEA) in lipopolysaccharide (LPS)-induced acute lung injury (ALI). Ultra-high-performance liquid chromatography coupled to Q-Exactive Orbitrap mass spectrometry detected 77 constituents, comprising 13 compounds authenticated with reference standards and 64 constituents tentatively annotated from accurate mass and tandem mass spectrometry (MS/MS) fragmentation. Network pharmacology prioritized six candidate compounds, 120 overlapping targets, and nine hub targets, and molecular docking explored theoretical interactions with inflammation-related proteins. MEA was evaluated in LPS-stimulated MH-S alveolar macrophages and in male C57BL/6J mice receiving oral pretreatment for seven days prior to intraperitoneal LPS challenge. In MH-S cells, MEA pretreatment reduced nitrite, interleukin (IL)-1β, IL-6, tumor necrosis factor (TNF)-α, 2′,7′-dichlorodihydrofluorescein diacetate (DCFH-DA)-detectable intracellular oxidative fluorescence, and Nlrp3, Pycard, Casp1, and Gsdmd mRNA levels. In mice, seven-day oral pretreatment with MEA attenuated qualitative histological lung injury, pulmonary edema, and serum cytokine elevation, accompanied by lower lung protein levels of NOD-like receptor family pyrin domain-containing 3 (NLRP3), apoptosis-associated speck-like protein containing a CARD (ASC), pro-caspase-1, and the ~30 kDa N-terminal fragment of gasdermin D (GSDMD-N), together with related transcripts. These findings indicate that prophylactic MEA administration attenuates LPS-induced macrophage inflammation and experimental lung injury, accompanied by reduced intracellular oxidative stress and decreased expression of NLRP3–GSDMD pathway-associated markers.
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BibTeX
@article{zhang2026madengai,
title = {{Madeng’ai Ethyl Acetate Extract Attenuates Lipopolysaccharide-Induced Inflammation and Acute Lung Injury}},
author = {Yanbin Zhang and Wenbin Ji and Liang Cao and Yan Wang and Wei Wang and Zaiqi Zhang},
journal = {International Journal of Molecular Sciences},
year = {2026},
month = oct,
doi = {10.3390/ijms27219430},
url = {https://www.mdpi.com/1422-0067/27/21/9430},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Madeng’ai Ethyl Acetate Extract Attenuates Lipopolysaccharide-Induced Inflammation and Acute Lung Injury
AU - Yanbin Zhang
AU - Wenbin Ji
AU - Liang Cao
AU - Yan Wang
AU - Wei Wang
AU - Zaiqi Zhang
PY - 2026
DA - 2026/10/22
JO - International Journal of Molecular Sciences
DO - 10.3390/ijms27219430
UR - https://www.mdpi.com/1422-0067/27/21/9430
AB - Madeng’ai, the dried root of Potentilla freyniana Bornm., is used in Dong medicine for infections and wound care. This study examined the chemical composition and prophylactic protective effects of the ethyl acetate fraction of its ethanolic root extract (referred to as MEA) in lipopolysaccharide (LPS)-induced acute lung injury (ALI). Ultra-high-performance liquid chromatography coupled to Q-Exactive Orbitrap mass spectrometry detected 77 constituents, comprising 13 compounds authenticated with reference standards and 64 constituents tentatively annotated from accurate mass and tandem mass spectrometry (MS/MS) fragmentation. Network pharmacology prioritized six candidate compounds, 120 overlapping targets, and nine hub targets, and molecular docking explored theoretical interactions with inflammation-related proteins. MEA was evaluated in LPS-stimulated MH-S alveolar macrophages and in male C57BL/6J mice receiving oral pretreatment for seven days prior to intraperitoneal LPS challenge. In MH-S cells, MEA pretreatment reduced nitrite, interleukin (IL)-1β, IL-6, tumor necrosis factor (TNF)-α, 2′,7′-dichlorodihydrofluorescein diacetate (DCFH-DA)-detectable intracellular oxidative fluorescence, and Nlrp3, Pycard, Casp1, and Gsdmd mRNA levels. In mice, seven-day oral pretreatment with MEA attenuated qualitative histological lung injury, pulmonary edema, and serum cytokine elevation, accompanied by lower lung protein levels of NOD-like receptor family pyrin domain-containing 3 (NLRP3), apoptosis-associated speck-like protein containing a CARD (ASC), pro-caspase-1, and the ~30 kDa N-terminal fragment of gasdermin D (GSDMD-N), together with related transcripts. These findings indicate that prophylactic MEA administration attenuates LPS-induced macrophage inflammation and experimental lung injury, accompanied by reduced intracellular oxidative stress and decreased expression of NLRP3–GSDMD pathway-associated markers.
SN - 1422-0067
ER -