Abstract
Chronic obstructive pulmonary disease (COPD) is a common chronic pulmonary disease with multiple etiologies and pathological changes. PYK2 expression is significantly increased in lipopolysaccharide-induced lung injury, but it mediates chronic lung inflammation. The mechanism of its occurrence remains unclear. Quanzhenyiqitang is often used in clinical treatment of COPD, so this study explored the mechanism of its treatment of lipopolysaccharide-induced lung injury. In this study, transfection, flow cytometry, QRT-PCR, and Western blotting methods were used to study the mechanism of Quanzhenyiqitang lipopolysaccharide-induced lung injury. The results showed that the mechanism of occurrence remains unclear. Our novel observations imply that the PYK2/p38MAPK/HDAC2/CK2 pathway is one of the fundamental underlying mechanisms that mediate the pathogenic progression of COPD, and Quanzhenyiqitang may be the therapeutic drug to prevent chronic inflammation and delay the progression of COPD by inhibiting PYK2 signaling pathways.
Highlights
Macrophages are an important component of the human body’s innate immunity
In the process of lung inflammation, macrophages continue to interact with epithelial cells, microvascular endothelial cells, neutrophils, lymphocytes, fibroblasts, and stem cells or tissue progenitor cells to regulate the stability of the lung environment and the pathogens [5]. e polarized states of alveolar macrophages are not mutually exclusive, and cells can simultaneously display two subtypes of M1 and M2 macrophages according to environmental signals
LPS-stimulated Pyk2/p38MAPK/HDAC2/CK2 signaling pathway in rat alveolar macrophage. e results showed that the expression of p-Pyk2, p-p38MAPK, and CK2 was activated, while HDAC2 was downregulated after LPS stimulation of rat alveolar macrophages, and Quanzhenyiqitangtreated serum significantly inhibited this progression (Figure 1(a)). e same result was obtained in the expression levels of HDAC2 and CK2 mRNA (Figure 1(b))
Summary
Macrophages are an important component of the human body’s innate immunity It was originated in the yolk sac and liver precursor cells during embryonic development and entered into the lungs and settled to form alveolar macrophages [1]. Alveolar macrophages are mostly distributed in the alveolar cavity, accounting for 80% of the alveolar resident cells It is the only inner cell group that contacts with air in the human body in the first line of defense against pollutants and pathogenic bacteria [2]. It can secrete more than one hundred types of inflammatory mediators. In the process of lung inflammation, macrophages continue to interact with epithelial cells, microvascular endothelial cells, neutrophils, lymphocytes, fibroblasts, and stem cells or tissue progenitor cells to regulate the stability of the lung environment and the pathogens [5]. e polarized states of alveolar macrophages are not mutually exclusive, and cells can simultaneously display two subtypes of M1 and M2 macrophages according to environmental signals
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