Chrysosplenol D protects mice against LPS-induced acute lung injury by inhibiting oxidative stress, inflammation, and apoptosis via TLR4-MAPKs/NF-κB signaling pathways
| Autor: | Yaxin Lv, Bing Cao, Xiaoke Zheng, Beibei Zhang, Chenxin Zhao, Shi Jingya, Mengnan Zeng, Qinqin Zhang, Yifan Ding, Mengya Wang, Aozi Feng |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2021 |
| Předmět: |
Lipopolysaccharides
p38 mitogen-activated protein kinases Immunology Acute Lung Injury Inflammation Lung injury medicine.disease_cause Microbiology Mice medicine Animals Molecular Biology chemistry.chemical_classification Reactive oxygen species medicine.diagnostic_test Chemistry lipopolysaccharide apoptosis NF-kappa B Cell Biology Original Articles RC581-607 Flavones Molecular biology chrysosplenol D Toll-Like Receptor 4 Oxidative Stress Infectious Diseases Bronchoalveolar lavage Apoptosis TLR4 Immunologic diseases. Allergy medicine.symptom Oxidative stress Signal Transduction |
| Zdroj: | Innate Immunity Innate Immunity, Vol 27 (2021) |
| ISSN: | 1753-4267 1753-4259 |
| Popis: | This study investigated the effect and mechanism of chrysosplenol D (CD) on LPS-induced acute lung injury in mice. Histological changes in the lungs were measured by hematoxylin-eosin staining. The levels of IL-6, IL-1β, and TNF-α in the bronchoalveolar lavage fluid were detected by ELISA. The levels of oxidative stress were detected by the cuvette assay. Immune cells in peripheral blood, the levels of reactive oxygen species, and apoptosis of primary lung cells were detected by flow cytometry. The mRNA levels of TLR4, MyD88, IL-1β, and NLRP3 were measured by quantitative real-time polymerase chain reaction. The levels of proteins in apoptosis and the TLR4-MAPKs/NF-κB signaling pathways were detected by Western blot. Hematoxylin-eosin staining showed that CD could improve lung injury; decrease the levels of inflammatory factors, oxidative stress, reactive oxygen species, and cell apoptosis; and regulate the immune system. Moreover, CD could down-regulate the mRNA levels of TLR4, MyD88, NLRP3, and IL-1β in lung, and the protein levels of Keap-1, Cleaved-Caspase-3/Caspase-3, Cleaved-Caspase-9/Caspase-9, TLR4, MyD88, p-ERK/ERK, p-JNK/JNK, p-p38/p38, p-p65/p65, NLRP3, and IL-1β, and up-regulated the levels of Bcl-2/Bax, p-Nrf2/Nrf2, and HO-1. The results suggested that CD could protect mice against LPS-induced acute lung injury by inhibiting oxidative stress, inflammation, and apoptosis via the TLR4-MAPKs/NF-κB signaling pathways. |
| Databáze: | OpenAIRE |
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