Mechanism of pulmonary platycoside E ameliorates fibrosis by inhibiting JAK/STAT signaling to inhibit macrophage M2 polarization
10.3969/j.issn.1000-484X.2025.04.006
- VernacularTitle:桔梗皂苷E通过抑制JAK/STAT信号阻抑巨噬细胞M2极化改善肺纤维化的机制
- Author:
Yunyun LIU
1
;
Yaru LI
;
Xiao LI
;
Ningyi JIN
;
Yiquan LI
;
Guangze ZHU
Author Information
1. 长春中医药大学中西医结合学院,长春 130117
- Publication Type:Journal Article
- Keywords:
Pulmonary fibrosis;
Macrophages;
Platycoside E;
Inflammation
- From:
Chinese Journal of Immunology
2025;41(4):803-807
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To investigate the role of Platycoside E(PE)in a mouse model of bleomycin(BLM)-induced pulmonary fibrosis by targeting the JAK/STAT signaling pathway to suppress macrophage M2 polarization.Methods:Forty BALB/c mice were randomly assigned to five experimental groups:blank control group,model group,pirfenidone(PDF)experimental group,PE high-dose group and PE low-dose experimental group,each with eight mice.After adaptive feeding,except for blank control group,all mice were used in the model of BLM nasal drip-induced pulmonary fibrosis.HE and Masson staining were employed to examine pathological alterations of lung tissue in mice;ELISA to detect concentrations of IL-10,IL-4,IL-17A and TNF-α in mice serum;expressions of CD206 and CD11b in lung tissue were detected by immunofluorescence.Western blot to detect protein expressions of JAK1,p-JAK1,STAT6 and p-STAT6 in lung tissues.Results:Compared with blank control group,tissues in model group showed distorted structure and thickened alveolar walls,fibrotic foci were formed,and alveolar inflammatory fraction and collagen volume fraction were significantly increased(P<0.01).ELISA showed that concentrations of IL-4,IL-10,IL-6 and TNF-α in serum were significantly reduced compared to those of model group.Immunofluorescence showed that fluorescence intensity of CD11b and CD206 treated by PE were decreased significantly.Western blot showed that expressions of JAK1,p-JAK,STAT6 and p-STAT6 proteins were significantly elevated in lung tissues of model mice.Following PE treatment,levels of the above proteins were diminished.Conclusion:PE can effectively improve lung fibrosis induced by BLM in mice,the mechanism may be related to the inhibition of JAK/STAT pathway to block macrophage M2 polarization.
