English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Plus monthly

Global: Zendy Tools annual

Global: Zendy Tools monthly

Global: Zendy Free Plan

Acute lung injury (ALI) is a common respiratory disease and is a serious threat to human health due to the lack of effective treatment. Geniposidic acid (GPA) is an iridoid glucoside extracted from Gardeniae jasminoides Ellis and can treat inflammation-related diseases. This study aimed to investigate the regulatory functions of GPA on lipopolysaccharide (LPS)-induced ALI and its potential mechanism, providing effective strategies for the clinical treatment of ALI. ALI models were constructed by LPS in Sprague-Dawley rats and pulmonary epithelial cells. The function of GPA was investigated by hematoxylin–eosin staining, lung function assessment, Western blot, Masson staining, and Sirius Red staining, quantitative real-time PCR, enzyme-linked immunosorbent assay, cell counting kit-8 assay, apoptosis analysis, and immunofluorescence assays. Functionally, GPA increased survival, relieved pulmonary epithelial function in response to LPS, repressed pulmonary fibrosis and inflammation caused by ALI  in vivo ; GPA also repressed pulmonary epithelial cell injury and inflammation induced by LPS  in vitro . Mechanistically, GPA decreased the protein levels of TLR4 and MyD88 and accelerated the nuclear export of p65, suggesting that GPA repressed the activation of p65. GPA protected LPS-induced ALI through the TLR4/MyD88 signaling pathway.

Geniposidic acid protects lipopolysaccharide-induced acute lung injury via the TLR4/MyD88 signaling pathway in vitro and in vivo