ArticleInflammation2017
JNK Inhibitor SP600125 Attenuates Paraquat-Induced Acute Lung Injury: an In Vivo and In Vitro Study.
Article in Inflammation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 47 citations in OpenAlex.
- Mcl-1 downregulation enhances BCG treatment efficacy in bladder cancer by promoting macrophage polarization.Cancer cell international · 2025Article
- Regulated programmed cell death in acute lung injury: from pathogenesis to therapy.Frontiers in immunology · 2025Review
- Dysregulation of the JNK signaling pathway in tuberculosis: mechanisms and therapeutic strategies.Frontiers in cellular and infection microbiology · 2025Review
- FGF18 alleviates sepsis-induced acute lung injury by inhibiting the NF-κB pathway.Respiratory research · 2024Article
- Roles of oxidative stress/JNK/ERK signals in paraquat-triggered hepatic apoptosis.Current research in toxicology · 2024Article
- Sivelestat sodium attenuates acute lung injury by inhibiting JNK/NF-κB and activating Nrf2/HO-1 signaling pathways.Biomolecules & biomedicine · 2023Article
- Liquiritin exhibits anti-acute lung injury activities through suppressing the JNK/Nur77/c-Jun pathway.Chinese medicine · 2023Article
- Phospho-proteomics identifies a critical role of ATF2 in pseudorabies virus replication.Virologica Sinica · 2022Article
- Anti-high-mobility group box-1 (HMGB1) mediates the apoptosis of alveolar epithelial cells (AEC) by receptor of advanced glycation end-products (RAGE)/c-Jun N-terminal kinase (JNK) pathway in the rats of crush injuries.Journal of orthopaedic surgery and research · 2022Article
- Oxaloacetate acid ameliorates paraquat-induced acute lung injury by alleviating oxidative stress and mitochondrial dysfunction.Frontiers in pharmacology · 2022Article
- Dexmedetomidine Attenuates LPS-Stimulated Alveolar Type II Cells' Injury through Upregulation of miR-140-3p and Partial Suppression of PD-L1 Involving Inactivating JNK-Bnip3 Pathway.Canadian respiratory journal · 2022Article
- Emodin Protects Against Lipopolysaccharide-Induced Acute Lung InjuryFrontiers in pharmacology · 2022Article
- Luteolin delays photoreceptor degeneration in a mouse model of retinitis pigmentosa.Neural regeneration research · 2021Article
- Understanding the role of neutrophils in acute respiratory distress syndrome.Biomedical journal · 2021Review
- Expression of DUSP12 Reduces Lung Vascular Endothelial Cell Damage in a Murine Model of Lipopolysaccharide-Induced Acute Lung Injury via the Apoptosis Signal-Regulating Kinase 1 (ASK1)-Jun N-Terminal Kinase Activation (JNK) Pathway.Medical science monitor : international medical journal of experimental and clinical research · 2021Article
- JNK‑IN‑8 treatment alleviates lipopolysaccharide‑induced acute lung injury via suppression of inflammation and oxidative stress regulated by JNK/NF‑κB signaling.Molecular medicine reports · 2021Article
- Polydatin relieves paraquat-induced human MRC-5 fibroblast injury through inhibiting the activation of the NLRP3 inflammasome.Annals of translational medicine · 2020Article
- Wogonoside inhibits inflammatory cytokine production in lipopolysaccharide-stimulated macrophage by suppressing the activation of the JNK/c-Jun signaling pathway.Annals of translational medicine · 2020Article
- The JNK pathway represents a novel target in the treatment of rheumatoid arthritis through the suppression of MMP-3.Journal of orthopaedic surgery and research · 2020Article
- Role of the MAPK pathway in human lung epithelial-like A549 cells apoptosis induced by paraquat.Genetics and molecular biology · 2020Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute lung injury (ALI) is a major complication soon after paraquat poisoning and rapidly progresses with high mortality. However, the specific mechanism underlying paraquat-induced ALI is still unclear. In this study, the mechanism underlying the protective effects of SP600125 on paraquat-induced ALI was investigated according to oxidative stress, inflammation, and apoptosis. The rats were randomly assigned into the control group (CON), the paraquat poisoning group (PQ), and the PQ + SP600125 group (SP). A549 cells were divided into the Con group, Pq group, and Sp group. H&E staining and detection of lung wet/dry ratio were employed to evaluate lung injury. Annexin V-PI staining was done to evaluate A549 cell apoptosis. Dihydroethidium fluorescence was used to measure reactive oxygen species (ROS) in the lungs and A549 cells. ELISA was performed to detect TNF-α and IL-6 in the supernatant of bronchoalveolar lavage fluid (BALF) and A549 cells. RT-qPCR was done to measure the messenger RNA (mRNA) expression of TNF-α and IL-6 in the lungs and A549 cells. Western blotting assay was performed to detect the protein expression of phospho-JNK, total JNK, and cleaved caspase-3. Electrophoretic mobility shift assay was employed to detect the DNA binding activities of AP-1 and P-p65. JNK inhibitor SP600125 reduced JNK phosphorylation, downregulated cleaved caspase-3 protein level, decreased AP-1 transcriptional activity and ROS level, and reduced the transcription and expression of TNF-α and IL-6, which improved ALI and cell apoptosis after paraquat poisoning. Our results indicate that JNK/AP-1 mediates ALI as well as oxidative stress and inflammation deterioration secondary to paraquat poisoning.
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