Protective Effects of Platycodin D3 on Airway Remodeling and Inflammation via Modulating MAPK/NF- κ B Signaling Pathway in Asthma Mice

Feng Peng; Fengchun Xiao; Long Lin

doi:10.1155/2022/1612829

Protective Effects of Platycodin D3 on Airway Remodeling and Inflammation via Modulating MAPK/NF- κ B Signaling Pathway in Asthma Mice

Evid Based Complement Alternat Med. 2022 Aug 10:2022:1612829. doi: 10.1155/2022/1612829. eCollection 2022.

Authors

Feng Peng^{1

2}, Fengchun Xiao³, Long Lin^{1

2}

Affiliations

¹ Department of Pediatrics, Affiliated Hangzhou Chest Hospital, Zhejiang University School of Medicine, Hangzhou 310003, China.
² Department of Pediatrics, Zhejiang Hospital of Integrated Traditional Chinese and Western Medicine, Hangzhou 310003, China.
³ Department of Pathology, The First Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou 310016, China.

Abstract

Background: Asthma is a disease with airway hyperresponsive and airway inflammation. Platycodin D is a triterpenoid saponin extracted from Platycodon grandiflorus root, which has various pharmacological activities. The study mainly explored the effects of platycodin D3 (PD₃) in airway remodeling and inflammation of asthma.

Methods: The ovalbumin (OVA)-induced asthma mice were given PD3 (20 mg/kg, 40 mg/kg, and 80 mg/kg) in different groups. The asthma mice administrated with dexamethasone (DXM) were enrolled as the positive control group, and the normal control mice and asthma model mice separately received the same volume of saline. Mouse airway lung dynamic compliance (Cdyn) and total airway resistance (RL) were measured by the EMKA animal lung function analysis system. The inflammation factor levels were estimated by ELISA. Histopathological changes were tested by HE and PAS staining. The protein and phosphorylation levels of NF-κBp65, p38, ERK1/2, and JNK1/2 were detected by Western blot.

Results: In asthmatic mice, PD3 enhanced the airway Cdyn and decreased RL to improve the airway hyperreactivity and alleviated the pathological injury of lung tissues. In addition, PD3 could reduce the infiltration of inflammatory cells in BALF and suppress the levels of eotaxin, IL-4, IL-5, IL-13, IFN-γ, and IgE. Furthermore, PD3 treatment inhibited the phosphorylation of NF-κBp65, p38, ERK1/2, and JNK1/2 proteins in asthma mice.

Conclusion: PD3 treatment alleviated the airway remodeling and inflammation in asthmatic mice, which might be related to downregulating the phosphorylated proteins in the MAPK/NF-κB signaling pathway.