Journal ArticleDOI
Nuclear factor-κB and TNF-α mediate gastric ulceration induced by phorbol myristate acetate
Tetsu Takeuchi,Soichiro Miura,Lin Wang,Keita Uehara,Misa Mizumori,Hiroshi Kishikawa,Ryota Hokari,Hajime Higuchi,Masayuki Adachi,Hiromasa Nakamizo,Hiromasa Ishii +10 more
TLDR
In this paper, the authors determined whether nuclear factor-kappaB and tumor necrosis factor-alpha (TNF-alpha) play role in the formation of gastric ulcer induced by phorbol-12-myristate-13-alphacetate (PMA) in rats.Abstract:
Phorbol esters induce inflammation in rodents by activating protein kinase C. We determined whether nuclear factor-kappaB (NF-kappaB) and tumor necrosis factor-alpha (TNF-alpha) play role in the formation of gastric ulcer induced by phorbol-12-myristate-13-alphacetate (PMA) in rats. Subserosally injected PMA dose-dependently induced gastric mucosal ulcer. Activation of NF-kappaB in the gastric mucosa corresponding to the PMA injection sites was observed before the ulcers became obvious as assessed by an in situ fluorescence DNA binding assay and electrophoretic mobility shift assay. The NF-kappaB activation and subsequent ulcer formation were significantly inhibited by injection of pyrrolidine dithiocarbamate, proteasome inhibitor (MG132), or NF-kappaB decoy. Antibody against TNF-alpha significantly inhibited ulcer formation without attenuating NF-kappaB activation. These results suggest that both NF-kappaB activation followed by TNF-alpha release contribute to tissue damage in PMA-induced gastric ulcer formation.read more
Citations
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Network pharmacology-based strategy to investigate pharmacological mechanisms of Zuojinwan for treatment of gastritis.
TL;DR: ZJW could alleviate gastritis through the molecular mechanisms predicted by network pharmacology, and this research demonstrates that the network pharmacological approach can be an effective tool to reveal the mechanisms of traditional Chinese medicine from a holistic perspective.
Peptic ulcer: a review on etiology and pathogenesis
TL;DR: The main aim of this review article has to summarize the ulcerogenic mechanisms of various mediators involved in Pept ic ulcer disease.
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Chronic treatment with agents that stabilize cytosolic IκB-α enhances survival and improves resting membrane potential in MDX muscle fibers subjected to chronic passive stretch
TL;DR: Results are consistent with the hypothesis that passive stretch activates an NFkappaB-mediated pathogenic mechanism in dystrophic muscle and suggest that agents which stabilize cytosolic IkappB-alpha levels may be useful for treating Duchenne and related muscular dystrophies.
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Gastroprotective and anti‐ulcer effects of oxymatrine against several gastric ulcer models in rats: Possible roles of antioxidant, antiinflammatory, and prosurvival mechanisms
TL;DR: The results reveal that OXY has remarkable protective effects on gastric ulcers, and provides evidence for the beneficial effects of OXY for treating peptic ulcers.
Journal ArticleDOI
Transcriptional activation of the human claudin-18 gene promoter through two AP-1 motifs in PMA-stimulated MKN45 gastric cancer cells.
TL;DR: It is found that phorbol 12-myristate 13-acetate (PMA) treatment of MKN45 human gastric cancer cell line increased claudin-18a2 expression and Protein kinase C (PKC) and mitogen-activated protein kinase (MAPK) inhibitors suppressed the upregulation of claudins 18a2.
References
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The role of protein kinase C in cell surface signal transduction and tumour promotion
TL;DR: Protein kinase C probably serves as a receptor for the tumour promoters and further exploration of the roles of this enzyme may provide clues for understanding the mechanism of cell growth and differentiation.
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NF-κB: Ten Years After
TL;DR: The manuscript and the Figures and Table are based on a manuscript originally written by Gordon C. Dickinson in 2012 and then edited by David I. Dickinson and revised by David A. Dickinson.