ArticleBMC gastroenterology2012
Lubiprostone stimulates small intestinal mucin release.
Article in BMC gastroenterology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- The ClC-2 Chloride Channel Activator, Lubiprostone, Improves Intestinal Barrier Function in Biopsies from Crohn's Disease but Not Ulcerative Colitis Patients.Pharmaceutics · 2023Article
- Receptor-mediated activation of CFTR via prostaglandin signaling pathways in the airway.American journal of physiology. Lung cellular and molecular physiology · 2022Article
- Gastrointestinal Dysfunction in Parkinson's Disease: Current and Potential Therapeutics.Journal of personalized medicine · 2022Review
- Chronic Kidney Disease, Gut Dysbiosis, and Constipation: A Burdensome Triplet.Microorganisms · 2020Review
- A quantitative systems pharmacology model of colonic motility with applications in drug development.Journal of pharmacokinetics and pharmacodynamics · 2019Article
- Article
- Alteration of the Intestinal Environment by Lubiprostone Is Associated with Amelioration of Adenine-Induced CKD.Journal of the American Society of Nephrology : JASN · 2015Article
- Lubiprostone in constipation: clinical evidence and place in therapy.Therapeutic advances in chronic disease · 2015Review
- Impaired viscosity of gastric secretion and its mucin content as potential contributing factors to the development of chronic constipation.Digestive diseases and sciences · 2014Article
- Irritable bowel syndrome: the evolution of multi-dimensional looking and multidisciplinary treatments.World journal of gastroenterology · 2014Review
- ClC-2 regulation of intestinal barrier function: Translation of basic science to therapeutic target.Tissue barriersReview
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Authors and funding
1 author.
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Abstract
backgroundLubiprostone is a synthetic bicyclic fatty acid derivative of prostaglandin E1 (PGE1) used for chronic constipation. The best known action of lubiprostone is simulation of Cl- dependent fluid secretion. In a mouse model of the genetic disease cystic fibrosis, we previously showed that in vivo administration of lubiprostone resulted in greater mucus accumulation in the small intestine. The aim of this study was to directly test whether lubiprostone stimulates intestinal mucin release.
methodsMucin release was measured by mounting segments (4-5 cm) of mouse proximal-mid small intestine in an organ bath, allowing access to the perfusate (luminal) and the bath (serosal) solutions. Nifedipine (10-6 M) and indomethacin (10-5 M) were included in all solutions to inhibit smooth muscle activity and endogenous prostaglandin production, respectively. The tissue was equilibrated under flow for 30 min, using the perfusate collected during the final 10 min of the equilibration period to measure unstimulated release rate. Stimulus was then added to either the perfusate or the bath and the perfusate was collected for another 30 min to measure the stimulated mucin release rate. Mucin in perfusates was quantified by periodic acid-Schiff's base dot-blot assay, using purified pig gastric mucin as a standard.
resultsWhen applied luminally at 1 μM lubiprostone was ineffective at stimulating mucin release. When added to the serosal solution, 1 μM lubiprostone stimulated mucin release to ~300% of the unstimulated rate. As a positive control, serosal 1 μM prostaglandin E2 increased mucin release to ~400% of the unstimulated rate.
conclusionsThese results support the idea that lubiprostone has prostaglandin-like actions on the intestine, which includes stimulation of mucin release. Stimulation of mucin release by lubiprostone may be protective in gastrointestinal conditions where loss of mucus is believed to contribute to pathogenesis. Thus, in addition to chronic constipation, there is greater potential for the therapeutic applications of lubiprostone.
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