Licorice and dried ginger decoction inhibits inflammation and alleviates mitochondrial dysfunction in chronic
Sensen Li1, Juan Cao1, Zhongjie Yang2
1Department of Scientific Research Section, the First People's Hospital of Zhumadian, Affiliated Hospital of Huanghuai University, Zhumadian, Henan 463000, China; Zhumadian Key Laboratory of Chronic Disease Research, School of Medicine, Huanghuai University, Zhumadian, Henan 463000, China.
Background:
Chronic obstructive pulmonary disease (COPD) is a chronic respiratory disease. Licorice and dried ginger decoction (LGD) is traditional Chinese medicine prescription with multiple effects. Glycyrrhetinic acid (GA) is the main bioactive components of LGD, which has been proven to have a relieving effect on various inflammatory diseases. Siglec-1 is a cell surface sialoadhesin and has been confirmed to be overexpressed in COPD and facilitate inflammatory reaction. This study is aimed to probe the interaction between LGD, GA, and siglec-1.
Methods:
Cigarette smoke (CS) combined with lipopolysaccharide (LPS) treatment was utilized to construct a COPD rat model. Cigarette smoke extract (CSE) was utilized to induce alveolar macrophage NR8383 to construct a COPD cell model. HE staining was applied for measuring histopathological changes of COPD rats. Enzyme-linked immunosorbent assay (ELISA), reverse transcription real-time polymerase chain reaction (RT-qPCR), and western blot were applied for testing the concentrations and expressions of proinflammatory factors. High performance liquid chromatography-tandem mass spectrometry (HPLC-MS) analysis was utilized to determine the combination between siglec-1 and GA. JC-1 assay was utilized to evaluate mitochondrial function. Reactive oxygen species (ROS) production was tested by dichloro-dihydro-fluorescein diacetate (DCFH-DA) staining.
Results:
LGD treatment notably alleviated lung injury and inflammatory response in COPD rats. In CSE-induced cells, LGD treatment suppressed the contents of tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6, and IL-8. Sialic-acid-binding Ig-like lectin 1 (Siglec-1) expression induced by CS was decreased after LGD treatment. Furthermore, we proved that GA could target siglec-1 to regulate the inflammatory response in COPD rats and cells. Additionally, GA could reduce ROS production and alleviate mitochondrial dysfunction to suppress COPD progression.
Conclusion:
LGD inhibits inflammation and alleviates mitochondrial dysfunction in COPD by targeting siglec-1.
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