ArticleBioMed research international2013
Glutamine and alanyl-glutamine increase RhoA expression and reduce Clostridium difficile toxin-a-induced intestinal epithelial cell damage.
Article in BioMed research international, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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The trial behind it
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Who cites it
11 citing papers in PubMed, 16 citations in OpenAlex.
- Article
- Clostridioides difficile Infection in Aged Mice Decreases Memory Function, Which Can Be Protected with Alanyl-Glutamine Supplementation.The Journal of nutrition · 2025Article
- Alanyl-glutamine supplementation forBMJ open · 2023Article
- Host and Clostridioides difficile-Response Modulated by Micronutrients and Glutamine: An Overview.Frontiers in nutrition · 2022Review
- Article
- Novel therapies and preventative strategies for primary and recurrent Clostridium difficile infections.Annals of the New York Academy of Sciences · 2019Review
- [RhoA/Rho-kinase contributes to chronic pain following thoracotomy by up-regulating glutaminase 1 expression in rat spinal dorsal cord].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2017Article
- Protection of rat liver against hepatic ischemia-reperfusion injury by a novel selenocysteine-containing 7-mer peptide.Molecular medicine reports · 2016Article
- Review
- Baicalein reduces the occurrence of cirrhotic endotoxemia by reducing intestinal mucosal apoptosis.BMC complementary and alternative medicine · 2015Article
- Small GTPases of the Ras superfamily regulate intestinal epithelial homeostasis and barrier function via common and unique mechanisms.Tissue barriers · 2013Review
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
Abstract
Clostridium difficile is a major cause of antibiotic-associated colitis and is associated with significant morbidity and mortality. Glutamine (Gln) is a major fuel for the intestinal cell population. Alanyl-glutamine (Ala-Gln) is a dipeptide that is highly soluble and well tolerated. IEC-6 cells were used in the in vitro experiments. Cell morphology was evaluated by atomic force microscopy (AFM) and scanning electron microscopy (SEM). Cell proliferation was assessed by WST-1 and Ki-67 and apoptosis was assessed by TUNEL. Cytoskeleton was evaluated by immunofluorescence for RhoA and F-actin. RhoA was quantified by immunoblotting. TcdA induced cell shrinkage as observed by AFM, SEM, and fluorescent microscopy. Additionally, collapse of the F-actin cytoskeleton was demonstrated by immunofluorescence. TcdA decreased cell volume and area and increased cell height by 79%, 66.2%, and 58.9%, respectively. Following TcdA treatment, Ala-Gln and Gln supplementation, significantly increased RhoA by 65.5% and 89.7%, respectively at 24 h. Ala-Gln supplementation increased cell proliferation by 137.5% at 24 h and decreased cell apoptosis by 61.4% at 24 h following TcdA treatment. In conclusion, TcdA altered intestinal cell morphology and cytoskeleton organization, decreased cell proliferation, and increased cell apoptosis. Ala-Gln and Gln supplementation reduced intestinal epithelial cell damage and increased RhoA expression.
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