Tripterygium glycosides alleviate CSE-induced lung injury by inhibiting IL-33 in bronchial epithelial cells.

Abstract

Chronic obstructive pulmonary disease (COPD) is characterized by airway remodeling and inflammation. Cigarette smoke extract (CSE) induces apoptosis, inflammation, and oxidative stress in COPD. Tripterygium glycosides (TG) are an active compound found in the root extracts of Tripterygium wilfordii Hook F (TWHF) that possesses anti-inflammatory and immunosuppressive effects. However, its role in COPD remains elusive. Herein, 2.5% CSE was used to treat human bronchial epithelial cells (BEAS-2B) to construct a cell injury model. Cell viability, apoptosis, and proliferation were assessed using MTT, flow cytometry, and EdU. Gene expression was analyzed using ELISA, Western blot, and RT-qPCR. TG treatment abolished 2.5% CSE-induced BEAS-2B cell viability and proliferation inhibition, apoptosis and inflammatory response promotion, and IL-33 level increase. Moreover, the repression of TG treatment on 2.5% CSE-triggered BEAS-2B cell damage was abrogated by IL-33 overexpression. Phosphorylation of JNK, ERK1/2, and p38 in 2.5% CSE-treated BEAS-2B cells was enhanced, manifesting that MAPK signaling pathways were activated. TG administration attenuated 2.5% of CSE-activated MAPK pathways through IL-33 upregulation. TG treatment repressed CSE-induced BEAS-2B cell damage partly by regulating the IL-33-mediated MAPK signaling pathway, providing a better understanding of the role of TG in the anti-inflammatory therapeutics for COPD treatment.