ArticleMolecular and cellular biochemistry2011
The role of glucagon-like peptide-2 on apoptosis, cell proliferation, and oxidant-antioxidant system at a mouse model of intestinal injury induced by tumor necrosis factor-alpha/actinomycin D.
Article in Molecular and cellular biochemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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13 citing papers in PubMed, 39 citations in OpenAlex.
- Development of a Mechanism of Action-Reflective Cell-Based Reporter Gene Assay for Measuring Bioactivities of Therapeutic Glucagon-like Peptide-2 Analogues.Molecules (Basel, Switzerland) · 2025Article
- Oxidative stress, hormones, and effects of natural antioxidants on intestinal inflammation in inflammatory bowel disease.Frontiers in endocrinology · 2023Review
- Mechanisms of mucosal healing: treating inflammatory bowel disease without immunosuppression?Nature reviews. Gastroenterology & hepatology · 2022Review
- Intestinal Adaptation upon Chemotherapy-Induced Intestinal Injury in Mice Depends on GLP-2 Receptor Activation.Biomedicines · 2021Article
- Role of glucagon-like peptides in inflammatory bowel diseases-current knowledge and future perspectives.Naunyn-Schmiedeberg's archives of pharmacology · 2019Review
- Glucagon-like peptide-2 rescues memory impairments and neuropathological changes in a mouse model of dementia induced by the intracerebroventricular administration of streptozotocin.Scientific reports · 2019Article
- Choice of Allograft in Patients Requiring Intestinal Transplantation: A Critical Review.Canadian journal of gastroenterology & hepatology · 2017Review
- A synthetic lethal screen identifies ATR-inhibition as a novel therapeutic approach for POLD1-deficient cancers.Oncotarget · 2016Article
- GLP-2 Prevents Intestinal Mucosal Atrophy and Improves Tissue Antioxidant Capacity in a Mouse Model of Total Parenteral Nutrition.Nutrients · 2016Article
- Glucagon-like peptide-2 exhibits protective effect on hepatic ischemia-reperfusion injury in rats.Frontiers of medicine · 2015Article
- The concept of gut rehabilitation and the future of visceral transplantation.Nature reviews. Gastroenterology & hepatology · 2015Review
- In vitro antimicrobial, antioxidant and cytotoxic properties of Streptomyces lavendulae strain SCA5.BMC microbiology · 2014Article
- Experimental diabetes treated with trigonelline: effect on key enzymes related to diabetes and hypertension, β-cell and liver function.Molecular and cellular biochemistry · 2013Article
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Authors and funding
2 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Tumor necrosis factor-alpha (TNF-α) is a multifunctional cytokine, which has the ability to produce cytotoxicity via induction of cell death and cell cycle arrest. Blocking the synthesis of protective proteins through a transcriptional inhibitor such as actinomycin D (Act D) sensitizes many cell types to TNF-α toxicity. Teduglutide, h[Gly(2)]GLP-2, is a protease-resistant synthetic analog of glucagon-like peptide-2 (GLP-2) which is an intestinotrophic peptide. In this study, we evaluated this potential of GLP-2 on apoptosis, cell proliferation, and oxidant-antioxidant system on a mouse model of intestinal injury induced by TNF-α/Act D. The intestinal injury was induced by intraperitoneal administration of 15 μg/kg TNF-α and 800 μg/kg Act D per mouse. Animals were injected subcutaneously 200 μg/kg h[Gly(2)]GLP-2 every 12 h for 10 consecutive days prior to the administration of TNF-α and Act D. The model of intestinal injury induced by TNF-α/Act D, which is the new animal model for the intestinal disorders, was characterized by the degeneration of intestinal mucosa, an increase in apoptotic index, expression of active caspase-3, lipid peroxidation and glutathione (GSH) levels, glutathione peroxidase (GPx) and superoxide dismutase (SOD) activities; a decrease in cell proliferation and catalase (CAT) activity. h[Gly(2)]GLP-2 pretreatment prevented the TNF-α/Act D-induced oxidative injury by a significant reduction in the intestinal injury, apoptotic index, expression of active caspase-3, lipid peroxidation and GSH levels, GPx and SOD activities; a markedly increase in cell proliferation, and CAT activity. These results demonstrate that GLP-2 has a protective, antiapoptotic, proliferative, and antioxidant effects against to TNF-α/Act D-induced intestinal injury. It is suggested that GLP-2 may potentially be useful as a therapeutic agent in TNF-α-mediated intestinal disorders.
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