ArticleNaunyn-Schmiedeberg's archives of pharmacology2026
Genkwanin alleviates paraquat-induced acute lung injury by activating SIRT1-mediated Nrf2/HO-1 signaling pathway.
Article in Naunyn-Schmiedeberg's archives of pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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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.
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Who cites it
2 citing papers in PubMed.
- A Novel SIRT1 Activator Hydroxygenkwanin Alleviates Osteoporosis by Inhibiting Ferroptosis and Lactylation in Skeletal Stem/Progenitor Cells.Antioxidants (Basel, Switzerland) · 2026Article
- Genkwanin mitigates renal fibrosis by reprogramming profibrotic signaling and restoring TFEB-mediated autophagy.Frontiers in pharmacology · 2026Article
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Paraquat (PQ) mainly damages the lungs, leading to acute lung injury (ALI) and even pulmonary fibrosis. Genkwanin (GEN) is demonstrated to possess anti-inflammatory and antioxidant activities in several diseases. This study aims to elucidate the protective effect of GEN against PQ-induced ALI and to decipher its underlying molecular mechanism. C57BL/6 J mice were injected intraperitoneally with 20 mg/kg PQ to induce an in vivo ALI model. BEAS-2B cells were treated with PQ to mimic an in vitro ALI model. The results showed that GEN alleviated PQ-induced lung pathologic damage, lung injury score, wet/dry weight ratio, myeloperoxidase (MPO) activity, and inflammatory cytokine production. GEN inhibited the expression of malondialdehyde (MDA) and 4-hydroxynonenal (4-HNE) and enhanced the activities of superoxide dismutase (SOD) and catalase (CAT) in lung tissues of PQ-treated mice. Also, GEN decreased PQ-induced apoptosis of lung tissues by downregulating Bax and Cleaved caspase 3 and elevating Bcl-2. Moreover, GEN repressed inflammatory factor levels, reactive oxygen species (ROS) production, and apoptosis in PQ-stimulated BEAS-2B cells. Additionally, GEN treatment led to the increase of sirtuin 1 (SIRT1) expression in both PQ-treated mice and BEAS-2B cells. Inhibition of SIRT1 largely reversed the inhibitory effects of GEN on PQ-induced inflammation, oxidative stress, and apoptosis in mice and cells. Furthermore, GEN activated the Nrf2/HO-1 signaling by upregulating SIRT1 in mice and BEAS-2B cells administered with PQ. In conclusion, GEN ameliorates lung inflammation, oxidative stress, and apoptosis in PQ-induced ALI by inducing SIRT1 to activate the Nrf2/HO-1 signaling. Our findings highlight the potential of GEN to resist PQ poisoning.
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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.