ArticleInflammopharmacology2023
Suppressing NLRP3 activation and PI3K/AKT/mTOR signaling ameliorates amiodarone-induced pulmonary fibrosis in rats: a possible protective role of nobiletin.
Article in Inflammopharmacology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 33 citations in OpenAlex.
- Norcantharidin attenuates amiodarone-induced pulmonary fibrosis via modulating miRNA-30a/GSK-3β/β-catenin and oxidative-inflammatory pathways.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Nobiletin attenuates LPS-induced acute lung injury via a STING-dependent signaling pathway.Archives of pharmacal research · 2026Article
- Cilostazol mitigates amiodarone-induced pulmonary toxicity and fibrosis by regulating the cAMP/TGF-β1 pathway-mediated epithelial-to-mesenchymal transition in rats.Scientific reports · 2026Article
- Nobiletin's role in idiopathic pulmonary fibrosis via the PI3K/AKT/MDM2/p53 signaling pathway.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Modulation of AMPK/NLRP3 Signaling Mitigates Radiation-Induced Lung Inflammation by a Synthetic Lipoxin A4 Analogue.International journal of molecular sciences · 2025Article
- Nobiletin alleviates hypoxia-induced pulmonary hypertension by inhibiting calcium-sensing receptor.Journal of natural medicines · 2025Article
- Modulating NLRP3 Inflammasomes in Idiopathic Pulmonary Fibrosis: A Comprehensive Review on Flavonoid-Based Interventions.Cell biochemistry and biophysics · 2025Review
- Ubiquitination in hepatocellular carcinoma immunity.Journal of translational medicine · 2025Review
- NR4A1 silencing alleviates high-glucose-stimulated HK-2 cells pyroptosis and fibrosisWorld journal of diabetes · 2025Article
- circ0066187 promotes pulmonary fibrogenesis through targeting STAT3-mediated metabolism signal pathway.Cellular and molecular life sciences : CMLS · 2025Article
- Exosomes derived from liver failure patients' plasma stimulated mesenchymal stem cells alleviate acute liver failure.Stem cell research & therapy · 2025Article
- Nobiletin and Eriodictyol Suppress Release of IL-1β, CXCL8, IL-6, and MMP-9 from LPS, SARS-CoV-2 Spike Protein, and Ochratoxin A-Stimulated Human Microglia.International journal of molecular sciences · 2025Article
- Ferroptosis in pulmonary fibrosis: pathogenesis and traditional Chinese medicine-driven therapeutic approaches.Frontiers in cell and developmental biology · 2025Review
- Therapeutic framework nucleic acid complexes targeting oxidative stress and pyroptosis for the treatment of osteoarthritis.Materials today. Bio · 2024Article
- NLRP3 Inflammasome in Acute and Chronic Liver Diseases.International journal of molecular sciences · 2024Review
- Non-apoptotic programmed cell deaths in diabetic pulmonary dysfunction: the new side of advanced glycation end products.Frontiers in endocrinology · 2023Review
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Amiodarone (AMD), a medicine used to treat life-threatening arrhythmias, is frequently linked to pulmonary fibrosis (PF). Despite the involvement of NLRP3 inflammasome and PI3K/Akt/mTOR axis in fibrosis modulation and development, their significance in the etiology of AMD-induced PF remains uncertain. Nobiletin (NOB), a citrus flavonoid, has recently gained attention for its ability to reduce fibrotic processes in a variety of organs through inhibiting NLRP3-associated inflammation and suppressing PI3K/AKT/mTOR fibrotic pathway. Therefore, this research aimed to investigate the possible beneficial impact of NOB against AMD-induced PF, taking into account the roles of NLRP3 and PI3K/AKT/mTOR axis in its pathogenesis. Twenty-four rats were randomly specified into Vehicle; NOB 20 mg/kg; AMD 30 mg/kg, and NOB + AMD. All treatments were administered orally once a day for 4 weeks. The lung oxidant/antioxidant status, as well as the expression of inflammatory and fibrotic markers were all assessed. The results revealed that NOB, by improving Nrf2/HO-1 pathway, could reduce ROS production and NLRP3 activation, which in turn hindered IL-1β release, prohibited TGF-β1-related PI3K/AKT/mTOR cascade, suppressed α-SMA expression, and impeded collagen deposition. These findings point to a novel strategy by which NOB may alleviate the AMD-prompted NLRP3 inflammatory responses and associated PF through blocking PI3K/AKT/mTOR signaling.
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