ArticleMolecular medicine reports2021
JNK‑IN‑8 treatment alleviates lipopolysaccharide‑induced acute lung injury via suppression of inflammation and oxidative stress regulated by JNK/NF‑κB signaling.
Article in Molecular medicine reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 14 citations in OpenAlex.
- Mechanism of Action ofBiology · 2026Article
- Article
- Epimedin C: A promising neuroprotective agent that can participate in mediating the JNK/Nrf2/HO-1 signaling pathway to prevent neurodegenerative diseases.Experimental and therapeutic medicine · 2026Article
- TMPRSS11E-mediated TFR1 cleavage influences IFN-γR2 internalization and the macrophage innate response.Communications biology · 2025Article
- The Protective Effects of Annexin A1 in Acute Lung Injury Mediated by Nrf2.Immunity, inflammation and disease · 2025Article
- JNK-IN-8 treatment improves ARDS-induced cognitive impairment by inhibiting JNK/NF-κB-mediated NLRP3 inflammasome.Brain and behavior · 2023Article
- Silencing circPalm2 inhibits sepsis-induced acute lung injury by sponging miR-376b-3p and targeting MAP3K1.Toxicological research · 2023Article
- Fecal microbiota transplantation from HUC-MSC-treated mice alleviates acute lung injury in mice through anti-inflammation and gut microbiota modulation.Frontiers in microbiology · 2023Article
- Lnc90386 Sponges miR-33-5p to MediateFrontiers in immunology · 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
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
JNK serves critical roles in numerous types of inflammation‑ and oxidative stress‑induced disease, including acute lung injury (ALI). JNK‑IN‑8 is the first irreversible JNK inhibitor that has been described. However, whether JNK‑IN‑8 can prevent lipopolysaccharide (LPS)‑induced ALI by inhibiting JNK activation and its downstream signaling is poorly understood. The objective of the present study was to investigate the specific therapeutic effects of JNK‑IN‑8 on LPS‑induced ALI and the molecular mechanisms involved. JNK‑IN‑8 attenuated myeloperoxidase activity, malondialdehyde and superoxide dismutase content and the lung wet/dry ratio, and improved the survival rate following lethal injection of LPS. Additionally, JNK‑IN‑8 decreased bronchoalveolar lavage fluid protein levels, lactate dehydrogenase activity, neutrophil infiltration and the number of macrophages (as demonstrated by flow cytometry), as well as the production of TNF‑α, IL‑6 and IL‑1β (as evaluated via ELISA). In addition, reverse transcription‑quantitative PCR and ELISA showed that JNK‑IN‑8 attenuated LPS‑induced inflammatory cytokine production and oxidative stress in primary murine peritoneal macrophages and RAW264.7 cells
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