ArticleYonsei medical journal2015
Jak1/Stat3 is an upstream signaling of NF-κB activation in Helicobacter pylori-induced IL-8 production in gastric epithelial AGS cells.
Article in Yonsei medical journal, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 37 citations in OpenAlex.
- Helicobacter pylori promote M1 macrophage polarization via JAK3-mediated activation of the SOCS3/IL2RA axis to suppress host immunity.Archives of microbiology · 2026Article
- Review
- NF-κB Signaling Pathway in Rheumatoid Arthritis: Mechanisms and Therapeutic Potential.Molecular neurobiology · 2025Review
- Plant-derived extracts or compounds for Helicobacter-associated gastritis: a systematic review of their anti-Helicobacter activity and anti-inflammatory effect in animal experiments.Chinese medicine · 2025Review
- NF-κB signaling pathway in osteosarcoma: from signaling networks to targeted therapy.Frontiers in oncology · 2025Review
- Article
- Molecular mechanisms underlying methotrexate-induced intestinal injury and protective strategies.Naunyn-Schmiedeberg's archives of pharmacology · 2024Review
- Yiqi Jiedu Huayu decoction inhibits precancerous lesions of chronic atrophic gastritis by inhibiting NLRP3 inflammasome-mediated pyroptosis.World journal of gastrointestinal oncology · 2024Article
- PJ‑001, a small‑molecule proteolysis‑targeting chimera, ameliorates atopic dermatitis‑like inflammation in mice by inhibiting the JAK2/STAT3 pathway and repairing the skin barrier.Experimental and therapeutic medicine · 2024Article
- Galantamine mitigates testicular injury and disturbed spermatogenesis in adjuvant arthritic rats via modulating apoptosis, inflammatory signals, and IL-6/JAK/STAT3/SOCS3 signaling.Inflammopharmacology · 2024Article
- Reactive Oxygen Species andAntioxidants (Basel, Switzerland) · 2023Review
- The NF-κB Pathway: a Focus on Inflammatory Responses in Spinal Cord Injury.Molecular neurobiology · 2023Review
- Molecular characterization and function of JAK/STAT pathway in IPEC-J2 cells during Clostridium perfringens beta2 toxin stimulation.Veterinary research communications · 2023Article
- Astaxanthin inhibits integrin α5 expression by suppressing activation of JAK1/STAT3 in Helicobacter pylori‑stimulated gastric epithelial cells.Molecular medicine reports · 2023Article
- Review
- Astaxanthin Inhibits Matrix Metalloproteinase Expression by Suppressing PI3K/AKT/mTOR Activation inNutrients · 2022Article
- Dietary intake of walnut preventedJournal of clinical biochemistry and nutrition · 2021Article
- Antimicrobial and Immunomodulatory Activity of Herb Extracts Used in Burn Wound Healing: "San Huang Powder".Evidence-based complementary and alternative medicine : eCAM · 2021Article
- Walnut polyphenol extracts inhibitJournal of clinical biochemistry and nutrition · 2020Article
- COVID-19 and Parkinson's Disease: Shared Inflammatory Pathways Under Oxidative Stress.Brain sciences · 2020Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Helicobacter pylori (H. pylori) induces the activation of nuclear factor-kB (NF-κB) and cytokine expression in gastric epithelial cells. The Janus kinase/signal transducers and activators of transcription (Jak/Stat) cascade is the inflammatory signaling in various cells. The purpose of the present study is to determine whether H. pylori-induced activation of NF-κB and the expression of interleukin-8 (IL-8) are mediated by the activation of Jak1/Stat3 in gastric epithelial (AGS) cells. Thus, gastric epithelial AGS cells were infected with H. pylori in Korean isolates (HP99) at bacterium/cell ratio of 300:1, and the level of IL-8 in the medium was determined by enzyme-linked immonosorbent assay. Phospho-specific and total forms of Jak1/Stat3 and IκBα were assessed by Western blot analysis, and NF-κB activation was determined by electrophoretic mobility shift assay. The results showed that H. pylori induced the activation of Jak1/Stat3 and IL-8 production, which was inhibited by a Jak/Stat3 specific inhibitor AG490 in AGS cells in a dose-dependent manner. H. pylori-induced activation of NF-κB, determined by phosphorylation of IκBα and NF-κB-DNA binding activity, were inhibited by AG490. In conclusion, Jak1/Stat3 activation may mediate the activation of NF-κB and the expression of IL-8 in H. pylori-infected AGS cells. Inhibition of Jak1/Stat3 may be beneficial for the treatment of H. pylori-induced gastric inflammation, since the activation of NF-κB is inhibited and inflammatory cytokine expression is suppressed.
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