Research Paper Volume 16, Issue 7 pp 6521—6536

Garlic oil supplementation blocks inflammatory pyroptosis-related acute lung injury by suppressing the NF-κB/NLRP3 signaling pathway via H2S generation

Tursunay Dilxat1, , Qiang Shi1, , Xiaofan Chen1, , Xuxin Liu1, ,

  • 1 Xinjiang Agricultural Vocational Technological College, Changji 831100, Xinjiang, China

Received: October 19, 2023       Accepted: March 9, 2024       Published: April 12, 2024
How to Cite

Copyright: © 2024 Dilxat et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.


Acute lung injury (ALI) is a major cause of acute respiratory failure with a high morbidity and mortality rate, and effective therapeutic strategies for ALI remain limited. Inflammatory response is considered crucial for the pathogenesis of ALI. Garlic, a globally used cooking spice, reportedly exhibits excellent anti-inflammatory bioactivity. However, protective effects of garlic against ALI have never been reported. This study aimed to investigate the protective effects of garlic oil (GO) supplementation on lipopolysaccharide (LPS)-induced ALI models. Hematoxylin and eosin staining, pathology scores, lung myeloperoxidase (MPO) activity measurement, lung wet/dry (W/D) ratio detection, and bronchoalveolar lavage fluid (BALF) analysis were performed to investigate ALI histopathology. Real-time polymerase chain reaction, western blotting, and enzyme-linked immunosorbent assay were conducted to evaluate the expression levels of inflammatory factors, nuclear factor-κB (NF-κB), NLRP3, pyroptosis-related proteins, and H2S-producing enzymes. GO attenuated LPS-induced pulmonary pathological changes, lung W/D ratio, MPO activity, and inflammatory cytokines in the lungs and BALF. Additionally, GO suppressed LPS-induced NF-κB activation, NLRP3 inflammasome expression, and inflammatory-related pyroptosis. Mechanistically, GO promoted increased H2S production in lung tissues by enhancing the conversion of GO-rich polysulfide compounds or by increasing the expression of H2S-producing enzymes in vivo. Inhibition of endogenous or exogenous H2S production reversed the protective effects of GO on ALI and eliminated the inhibitory effects of GO on NF-κB, NLRP3, and pyroptotic signaling pathways. Overall, these findings indicate that GO has a critical anti-inflammatory effect and protects against LPS-induced ALI by suppressing the NF-κB/NLRP3 signaling pathway via H2S generation.


ALI: Acute lung injury; ARDS: Acute respiratory distress syndrome; GO: Garlic oil; LPS: Lipopolysaccharide; GSDMD: Gasdermin D; GSDME: Gasdermin E; DATS: Diallyl trisulfide; CBS: Cystathionine β-synthase; CSE: Cystathionine γ-lyase; 3MST: 3-mercaptopyruvate sulphurtransferase; H2S: Hydrogen sulfide; IAM: Iodoacetamide; AOAA: Amino-oxyacetic acid; PAG: DL-propargylglycine; BALF: Bronchoalveolar lavage fluid; H&E: Hematoxylin–eosin; SDS-PAGE: Sodium dodecyl sulfate–polyacrylamide gel electrophoresis.