Feikang granules ameliorate pulmonary inflammation in the rat model of chronic obstructive pulmonary disease via TLR2/4-mediated NF-κB pathway

Abstract

Purpose: Several reports have shown that traditional Chinese medicine could be an alternative therapeutic approach for COPD patients, but the mechanism remains unknown. The present study aimed to examine the effects of Feikang granules in a COPD model rat and investigate the possible mechanisms via Toll-like receptor (TLR)/ nuclear factor kappa B (NF-κB) signaling. Methods: The COPD model rats were treated with Feikang granules, dexamethasone, or normal saline. The pulmonary function; lung tissue histology; levels of inflammatory cytokines; mRNA levels of TNFα, IL-6, TLR4, and TLR2; and protein levels of TLR4, TLR2, p-IκB, IκB and P65 in lung tissues were evaluated. Results: The present study confirmed that the pro-inflammatory cytokines, TNF-α, IL-1β, IL-6, and IL-17 levels were elevated and the pulmonary function and morphology are altered in COPD model rats. The TLR2 and TLR4-mediated NF-kB signaling pathway plays a role in the mechanism of action. Feikang granules, a type of Chinese herbal medicine, significantly reduced LPS induced inflammatory cytokines release from lung tissue and alveolar macrophage in a dosedependent manner. These medical herbs also prevented TLR2/4 and IκB downregulation and reversed the p-IκB and NF-κB p65 upregulation of the lung tissue in the COPD rats. Feikang granules were also found to protect against pulmonary dysfunction and pathological changes in the COPD rats. Conclusion: The Chinese herbal medicine formula Feikang granules prevent pulmonary inflammation and improve pulmonary function, suggesting that Feikang granules may be an effective treatment for chronic pulmonary diseases, such as COPD.

Baicalin Inhibits Inflammation in Rats with Chronic Obstructive Pulmonary Disease by the TLR2/MYD88/NF-κBp65 Signaling Pathway

“…e TLR2/MYD88/NF-κB signaling pathway is currently a more recognized pathway to regulate inflammatory cells [31]. A previous study has shown that the TLR2/4 mediated NF-κB pathway could improve lung inflammation in COPD model rats [32]. Li et al found that the TLR2/MYD88/NF-κB signaling pathway reduced pulmonary fibrosis [33].…”

Efficacy evaluation and potential pharmacological mechanism of tanreqing injection in the treatment of COPD combined with respiratory failure based on meta-analysis and network pharmacology

“…TNF-α can disrupt epithelial cells as a physical barrier to airway inflammation and promote the release of inflammatory factors, such as IL-6 and IL-8 in bronchial epithelial cells, and high levels of IL-6 are associated with decreased lung function. TNF-α usually activates JNK, NF-κBp65, and p38 MAPK after promoting the production of many inflammatory mediators to further aggravate the inflammatory response in airway epithelial cells [ 57 ]. Activation of MAPK and NF-κB signaling pathways can upregulate inflammatory genes in airway epithelial cells.…”

Perilla Leaf Extract (PLE) Attenuates COPD Airway Inflammation via the TLR4/Syk/PKC/NF-κB Pathway In Vivo and In Vitro

“…Previously, it was found that TLR4, Syk, PKC, and NF-κB play critical roles in inflammatory diseases ( Slomiany and Slomiany, 2018 ; Yang H. et al, 2020 ; Ma et al, 2020 ), and the PLE and its several Syk affinitive components have been proved to act on Syk to relieve allergic airway inflammation ( Yang H. et al, 2020 ) ( Yang et al, 2021 ). TLR4 leads to initiation of Syk-, PKC-, and NF-κB p65-dependent signal cascades in COPD ( Zhang et al, 2018 ; Fan et al, 2019 ; Yang L. et al, 2020 ). TLR4 is a receptor that mediates inflammatory responses to ligands, such as LPS from Gram-negative bacteria.…”