ArticleWorld journal of gastroenterology2002
Anti-inflammatory effect of cholecystokinin and its signal transduction mechanism in endotoxic shock rat.
Article in World journal of gastroenterology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 41 citations in OpenAlex.
- A Review of Vagus Nerve Stimulation for Disease: Comprehensive Theory and Evidence for Mechanisms of Action.Comprehensive physiology · 2026Review
- The Role of Peptides in Asthma-Obesity Phenotype.International journal of molecular sciences · 2024Review
- Article
- Review
- Cholecystokinin and the hormone concept.Endocrine connections · 2021Review
- Review
- Neuropeptides Modulate Local Astrocytes to Regulate Adult Hippocampal Neural Stem Cells.Neuron · 2020Article
- Activation of a nerve injury transcriptional signature in airway-innervating sensory neurons after lipopolysaccharide-induced lung inflammation.American journal of physiology. Lung cellular and molecular physiology · 2020Article
- Gastrin, Cholecystokinin, Signaling, and Biological Activities in Cellular Processes.Frontiers in endocrinology · 2020Review
- Investigating the Protein Signature of Adamantinomatous Craniopharyngioma Pediatric Brain Tumor Tissue: Towards the Comprehension of Its Aggressive Behavior.Disease markers · 2019Article
- Effects of CCK-8 and Cystathionine γ-Lyase/Hydrogen Sulfide System on Acute Lung Injury in Rats.Inflammation · 2017Article
- Cholecystokinin-From Local Gut Hormone to Ubiquitous Messenger.Frontiers in endocrinology · 2017Review
- Role of p38 MAPK and STAT3 in lipopolysaccharide-stimulated mouse alveolar macrophages.Experimental and therapeutic medicine · 2014Article
- Cholecystokinin inhibits inducible nitric oxide synthase expression by lipopolysaccharide-stimulated peritoneal macrophages.Mediators of inflammation · 2014Article
- Diet-induced obesity reprograms the inflammatory response of the murine lung to inhaled endotoxin.Toxicology and applied pharmacology · 2013Article
- Article
- Parallel changes in gene expression in peripheral blood mononuclear cells and the brain after maternal separation in the mouse.BMC research notes · 2009Article
- Enteroendocrine cells express functional Toll-like receptors.American journal of physiology. Gastrointestinal and liver physiology · 2007Article
- Expression of NF-kappaB and human telomerase reverse transcriptase in gastric cancer and precancerous lesions.World journal of gastroenterology · 2004Article
- Fos expression in tyrosine hydroxylase-containing neurons in rat brainstem after visceral noxious stimulation: an immunohistochemical study.World journal of gastroenterology · 2003Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimTo study the anti-inflammatory effects of cholecystokinin-octapeptide (CCK-8) on lipopolysaccharide (LPS)-induced endotoxic shock (ES) and further investigate its signal transduction pathways involving p38 mitogen-activated protein kinase (MAPK) and IkappaB-alpha.
methodsEighty-four rats were divided randomly into four groups: LPS (8 mg.kg(-1), iv) induced ES; CCK-8 (40 microg.kg(-1), iv) pretreatment 10 min before LPS (8 mg.kg(-1)); CCK-8 (40 microg.kg(-1), iv) or normal saline (control) groups. The inflammatory changes of lung and spleen, phagocytic function of alveolar macrophage, quantification of inflammatory cells in bronchoalveolar lavage (BAL) were investigated in rats by using hematoxylin and eosin (HE) staining, phagocytosis of Candida albicans and differential cell counting. Nitric oxide (NO) production in serum, lung and spleen was measured with the Griess reaction. The mechanism involving p38 MAPK and IkappaB-alpha signal pathways was investigated by Western blot.
resultsInflammatory changes of lung and spleen induced by LPS were alleviated by CCK-8, the increase of NO induced by LPS in serum, lung and spleen was significantly inhibited and the neutrophil infiltration in BAL was significantly reduced by CCK-8. The number of neutrophils was (52+/-10)X10(6) cells. (-1) in LPS group, while it decreased to (18+/-4)X10(6) cells. (-1) in CCK-8+LPS (P<0.01). The phagocytic rate of CCK-8 group increased to (62.49+/-9.49) %, compared with control group (48.16+/-14.20) %, P<0.05. The phagocytosis rate was (85.14+/-4.64) % in LPS group, which reduced to (59.33+/-3.14) % in CCK-8+LPS group (P<0.01). The results of phagocytosis indexes showed similar changes. CCK-8 may play an important role in increasing the expression of p38 MAPK and decreasing the degradation of IkappaB-alpha in lung and spleen of ES rats.
conclusionCCK-8 can result in anti-inflammatory effects, which may be related to activation of p38 MAPK and inhibition on the degradation of IkappaB-alpha.
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