ArticleRSC advances2018
Tripterine alleviates lipopolysaccharide-induced airway epithelial barrier dysfunction through suppressing the Hippo pathway.
Article in RSC advances, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
3 citing papers in PubMed, 4 citations in OpenAlex.
- Review
- YES-associated protein-regulated Smad7 worsen epithelial barrier injury of chronic sinusitis with nasal polyps.Immunity, inflammation and disease · 2023Article
- Tripterin liposome relieves severe acute respiratory syndrome as a potent COVID-19 treatment.Signal transduction and targeted therapy · 2022Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recent studies show that airway epithelial barrier dysfunction is closely associated with allergic inflammation and asthma pathogenesis. Tripterine, a pentacyclic triterpenoid isolated from the plant family Celastraceae, possesses anti-inflammatory and anti-oxidant properties. Our study aimed to investigate the effects of tripterine on lipopolysaccharide (LPS)-induced airway epithelial barrier dysfunction and the molecular mechanism involved. Cell viability and apoptosis were evaluated by CCK-8 assay and flow cytometry, respectively. The mRNA expressions and secretion of interleukin (IL)-6, IL-8, IL-1β, and mucin 5AC (MUC5AC) were detected by qRT-PCR and ELISA, respectively. The changes of the Hippo pathway were examined by western blot analyses of phosphorylated yes-associated protein (YAP) and transcriptional coactivator with PDZ-binding motif (TAZ). Results showed that LPS treatment induced viability inhibition and apoptosis in lung bronchial epithelial cell line (16HBE) cells. Exposure to LPS increased the mRNA expression and concentrations of IL-6, IL-8, IL-1β, and MUC5AC in 16HBE cells. However, pretreatment with tripterine attenuated the effects of LPS on 16HBE cells. Tripterine inhibited LPS-induced activation of the Hippo pathway in 16HBE cells. Moreover, knockdown of YAP attenuated LPS-induced airway epithelial barrier dysfunction in 16HBE cells. In conclusion, tripterine attenuated LPS-induced airway epithelial barrier dysfunction through suppressing the Hippo pathway, providing new insight into the mechanism responsible for the effects of tripterine in asthma.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.