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Ophiopogonin D attenuates PM2.5-induced inflammation via suppressing the AMPK/NF-?B pathway in mouse pulmonary epithelial cells.

ABSTRACT: Exposure to fine particulate matter, such as particulate matter of ?2.5 µm in diameter (PM2.5), causes pulmonary in?ammation and injury to other organs. It has been reported that Ophiopogonin D (OP-D) has anti-inflammatory activity. The aim of the present study was to investigate this anti-inflammatory activity of OP-D on PM2.5-induced acute airway inflammation and its underlying mechanisms. The viability of PM2.5-treated mouse lung epithelial (MLE-12) cells with or without OP-D treatment was determined using a Cell Counting Kit-8 assay. The corresponding levels of IL-1?, IL-6, IL-8 and TNF-? were examined via ELISA. Subcellular localization of NF-?Bp65 was detected using immunofluorescence staining. The expression levels of AMP-activated protein kinase (AMPK), phosphorylated (p)-AMPK, NF-?Bp65 and p-NF-?Bp65 were analyzed using western blotting. The selective AMPK inhibitor Compound C (CC) was utilized to investigate the involvement of AMPK in the protection against PM2.5-induced cell inflammation by OP-D treatment. The results demonstrated that OP-D significantly ameliorated the PM2.5-stimulated release of proinflammatory cytokines (TNF-?, IL-1?, IL-6 and IL-8) and inhibited the translocation of NF-?Bp65 from the cytoplasm to the nucleus in MLE-12 cells. Moreover, OP-D significantly prevented the PM2.5-triggered phosphorylation of NF-?Bp65 and upregulated AMPK activity. The anti-inflammatory activity of OP-D could also be attenuated by the AMPK-specific inhibitor CC. The present results suggested that the anti-inflammatory activity of OP-D was mediated via AMPK activation and NF-?B signaling pathway downregulation, which ameliorated the expression of proinflammatory cytokines. Therefore, OP-D could be a candidate drug to treat PM2.5-induced airway inflammation.

SUBMITTER: Wang Y

PROVIDER: S-EPMC7571316 | biostudies-literature | 2020 Dec

REPOSITORIES: biostudies-literature

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Ophiopogonin D attenuates PM2.5-induced inflammation via suppressing the AMPK/NF-κB pathway in mouse pulmonary epithelial cells.

Wang Ying Y Li Dan D Song Lei L Ding Hui H

Experimental and therapeutic medicine 20201005 6

Exposure to fine particulate matter, such as particulate matter of ≤2.5 µm in diameter (PM2.5), causes pulmonary inﬂammation and injury to other organs. It has been reported that Ophiopogonin D (OP-D) has anti-inflammatory activity. The aim of the present study was to investigate this anti-inflammatory activity of OP-D on PM2.5-induced acute airway inflammation and its underlying mechanisms. The viability of PM2.5-treated mouse lung epithelial (MLE-12) cells with or without OP-D treatment was de ...[more]

PMID: 33093877

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Project description:Acute respiratory distress syndrome (ARDS) is a common destructive syndrome with high morbidity and mortality rates. Currently, few effective therapeutic interventions for ARDS are available. Clinical trials have shown that the effectiveness of aspirin is inconsistent. The contribution of platelets to the inflammatory response leading to the development of ARDS is increasingly recognized. The antiplatelet agent aspirin reportedly exerts a protective effect on acid- and hyperoxia-induced lung injury in murine models. Our previous study showed that pretreatment with aspirin exerts protective effects on hyperoxia-induced lung injury in mice. However, the mechanisms and therapeutic efficacy of aspirin in the posttreatment of hyperoxia-induced acute lung injury (ALI) remain unclear. In this study, we used a homozygous NF-κB-luciferase+/+ transgenic mouse model and treated mice with low-dose (25 μg/g) or high-dose (50 μg/g) aspirin at 0, 24, and 48 h after exposure to hyperoxia (inspired oxygen fraction (FiO2) > 95%). Hyperoxia-induced lung injury significantly increased the activation of NF-κB in the lung and increased the levels of macrophages infiltrating the lung and reactive oxygen species (ROS), increased the HO-1, NF-κB, TNF-α, IL-1β, and IL-4 protein levels, and reduced the CC10, SPC, eNOS, Nrp-1, and IκBα protein levels in the lung tissue. Pulmonary edema and alveolar infiltration of neutrophils were also observed in the lung tissue of mice exposed to hyperoxia. However, in vivo imaging revealed that posttreatment with aspirin reduced luciferase expression, suggesting that aspirin might reduce NF-κB activation. Posttreatment with aspirin also reduced hyperoxia-induced increases in the numbers of lung macrophages, intracellular ROS levels, and the expression of TNF-α, IL-1β, and IL-4; it also increased CC10, SPC and Nrp-1 levels compared with hyperoxia exposure alone. Lung histopathology also indicated that the aspirin posttreatment significantly reduced neutrophil infiltration and lung edema compared with hyperoxia exposure alone. Aspirin effectively induces an anti-inflammatory response in a model of hyperoxia-induced lung injury. Thus, aspirin may have potential as a novel treatment for hyperoxia-induced ALI.

Dataset Information

Ophiopogonin D attenuates PM2.5-induced inflammation via suppressing the AMPK/NF-?B pathway in mouse pulmonary epithelial cells.

Publications

Ophiopogonin D attenuates PM2.5-induced inflammation via suppressing the AMPK/NF-κB pathway in mouse pulmonary epithelial cells.

Similar Datasets

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