ArticleClinical and translational science2019
Tranilast Treatment Attenuates Cerebral Ischemia-Reperfusion Injury in Rats Through the Inhibition of Inflammatory Responses Mediated by NF-κB and PPARs.
Article in Clinical and translational science, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It carries an expression of concern. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 24 citations in OpenAlex.
- Eupatorin interferes with NLRP3 inflammasome activation via modulation of NF-κB signaling pathway in LPS induced macrophages.Immunologic research · 2026Article
- Characterization of TRPV2-associated pathology in Parkinson's disease and therapeutic modulation using Tranilast.Frontiers in cellular neuroscience · 2026Article
- Tranilast Reduces Intestinal Ischemia Reperfusion Injury in Rats Through the Upregulation of Heme-Oxygenase (HO)-1.Journal of clinical medicine · 2025Article
- PANoptosis: Cross-Talk Among Apoptosis, Necroptosis, and Pyroptosis in Neurological Disorders.Journal of inflammation research · 2025Review
- The Role of Transforming Growth Factor-β (TGF-β) in Asthma and Chronic Obstructive Pulmonary Disease (COPD).Cells · 2024Review
- Tumor necrosis factor receptor-associated factor 5 enhances perianal fistulizing Crohn's disease through epithelial-mesenchymal transition.CytoJournal · 2024Article
- M6A Modification and Transcription Analysis of LncRNA in Cerebral Ischemia/Reperfusion Injury.International journal of genomics · 2024Article
- Therapeutic Effects of Long-Term Administration of Tranilast in an Animal Model for the Treatment of Fibroids.International journal of molecular sciences · 2023Article
- Tranilast reduces cardiomyocyte injury induced by ischemia‑reperfusion via Nrf2/HO‑1/NF‑κB signaling.Experimental and therapeutic medicine · 2023Article
- Current Pharmacotherapy and Multi-Target Approaches for Alzheimer's Disease.Pharmaceuticals (Basel, Switzerland) · 2022Review
- Tranilast inhibits angiotensin II-induced myocardial fibrosis through S100A11/ transforming growth factor-β (TGF-β1)/Smad axis.Bioengineered · 2021Article
- Peroxisome Proliferator-Activated Receptor-Gamma (PPAR-ɣ): Molecular Effects and Its Importance as a Novel Therapeutic Target for Cerebral Ischemic Injury.Neurochemical research · 2021Review
- Tranilast: a potential anti-Inflammatory and NLRP3 inflammasome inhibitor drug for COVID-19.Immunopharmacology and immunotoxicology · 2021Review
- Knockdown of lncRNA TTTY15 alleviates ischemia/reperfusion-induced inflammation and apoptosis of PC12 cells by targeting miR-766-5p.Experimental and therapeutic medicine · 2021Article
- Cytokine Storm in COVID-19-Immunopathological Mechanisms, Clinical Considerations, and Therapeutic Approaches: The REPROGRAM Consortium Position Paper.Frontiers in immunology · 2020Article
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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
Ischemia-reperfusion injury (IRI) occurs when blood supply returns to tissue after interruption, which is associated with life-threatening inflammatory response. Tranilast is a widely used antiallergic agent in the treatment against bronchial asthma and keloid. To study the function of tranilast, we used IRI in rat models. The brain tissues of IRI rats with or without tranilast treatment were collected. Neuronal apoptosis in the brain was detected by terminal deoxynucleotidyl transferase nick end labeling assay, and proinflammatory cytokine levels were measured by quantitative real-time polymerase chain reaction and enzyme-linked immunosorbent assay. The expression levels of nuclear factor-kappa B (NF-κB), inhibitor of κB (IκB) and peroxisome proliferator-activated receptors (PPARs) were detected by Western blot. The results showed that tranilast treatment reduced neuronal apoptosis in the brain of IRI rats. Tranilast enhanced the short-term memory and long-term memory to novel object recognition paradigm. Tranilast treatment decreased the messenger RNA (mRNA) and protein levels of multiple proinflammatory cytokines, and affected NF-κB and inhibitor of kappa B protein expressions. Tranilast promoted the expressions of PPAR-α and PPAR-γ. Our findings demonstrate that tranilast treatment could attenuate cerebral IRI by regulating the inflammatory cytokine production and PPAR expression. Tranilast is a potential drug for IRI treatment in the clinic.
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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 Socratic graph.