ArticleMolecular medicine reports2022
Tranilast attenuates lipopolysaccharide‑induced lung injury via the CXCR4/JAK2/STAT3 signaling pathway.
Article in Molecular medicine reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 15 citations in OpenAlex.
- AhR as a Common Denominator in Immunity and Inflammation in Chronic Lung Diseases: Molecular and Clinical Insights.Diseases (Basel, Switzerland) · 2026Review
- The CXCL12/CXCR4 Axis in Sepsis-Induced Acute Lung Injury: Mechanisms and Therapeutic Potential.Current issues in molecular biology · 2025Review
- Targeting PANoptosis: a promising therapeutic strategy for ALI/ARDS.Apoptosis : an international journal on programmed cell death · 2025Review
- Effect of the MIAT/microRNA 130a-3p/Pdgfra axis on retinal microglia activation in mice with chronic retinal hypoperfusion injury.Cell biology and toxicology · 2025Article
- The Role and the Regulation of NLRP3 Inflammasome in Irritable Bowel Syndrome: A Narrative Review.Microorganisms · 2025Review
- Article
- Protective effect and mechanism of Sufentanil on acute lung injury in septic mice.Frontiers in pharmacology · 2024Article
- Long Non-Coding RNA Dancr Affects Myocardial Fibrosis in Atrial Fibrillation Mice via the MicroRNA-146b-5p/Smad5 Axis.Acta Cardiologica Sinica · 2023Article
- Avenanthramide Improves Colonic Damage Induced by Food Allergies in Mice through Altering Gut Microbiota and Regulating Hsp70-NF-κB Signaling.Nutrients · 2023Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It has been reported that the expression of C‑X‑C motif chemokine receptor 4 (CXCR4) is increased in patients with lung injury, while CXCR4 downregulation can improve sepsis‑induced lung injury. Previous studies have shown that tranilast can inhibit CXCR4 mRNA expression. Therefore, the present study aimed to investigate whether tranilast could protect against lipopolysaccharide (LPS)‑induced lung injury via the CXCR4/Janus kinase 2 (JAK2)/STAT3 signaling pathway. A Cell Counting Kit‑8 assay was performed to evaluate the effect of different concentrations of tranilast on the viability of LPS‑induced BEAS‑2B cells. The mRNA and protein expression levels of the inflammatory factors, TNFα, IL‑1β, IL‑6, cytochrome c oxidase subunit II and inducible nitric oxide synthase were detected using reverse transcription‑quantitative PCR and western blot analysis, respectively. In addition, the cell apoptosis rate and the expression levels of apoptosis‑related proteins were analyzed using a TUNEL staining assay and western blot analysis, respectively. The expression levels of the CXCR4/JAK2/STAT3 signaling pathway‑related proteins were also determined using western blot analysis. Furthermore, the effects of tranilast on cell viability, inflammation and apoptosis were also evaluated in LPS‑stimulated BEAS‑2B cells following CXCR4 overexpression, which were pre‑treated with tranilast. The results demonstrated that tranilast could alleviate LPS‑induced cell viability, the secretion of inflammatory cytokines and cell apoptosis. In addition, cell treatment with tranilast inhibited the expression of CXCR4/JAK2/STAT3 signaling‑related proteins in LPS‑induced BEAS‑2B cells. Following CXCR4 overexpression, the alleviating effect of tranilast on cell viability, inflammatory response and apoptosis was notably attenuated. Overall, the current study suggested that tranilast could attenuate LPS‑induced lung injury via the CXCR4/JAK2/STAT3 signaling pathway, suggesting that tranilast could be considered as a promising agent for treating sepsis‑induced acute lung injury.
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