Background: An overwhelming production of reactive oxygen species concomitant with a decrease in antioxidative capacity plays an important role in modulation of the immune system in critically ill patients. The purpose of this study was to assess the influence of a combined oral supply of the antioxidants R-alpha-lipoic acid (LA) and glutamine (GLN) on the immunity of endotoxemic mice, with a special focus on tissue glutathione levels.
Methods: Female Balb/c mice were fed diets enriched with GLN (3 g/100 kcal), LA (0.74 mg/100 kcal), a combination of GLN and LA, or an isocaloric and isonitrogenous control diet for 10 days. On day 7, the mice were challenged intraperitoneally with 25 microg lipopolysaccharide. Seventy-two hours later, the number and phenotype of lymphocytes in Peyer's patches (PP) and spleen of the endotoxemic mice were measured. In addition, glutathione levels were determined in the small intestine, spleen and liver.
Results: In PP only the combined supply of GLN and LA significantly increased the total cell yield (+19%), which was predominantly due to an increased number of B cells. In the spleen, both LA (+17%) and the combination of GLN and LA (+22%) were able to enhance total cell yield. The glutathione content of the small intestine was increased by feeding LA alone, whereas in the spleen GLN plus LA was most effective.
Conclusion: Supplying combined GLN and LA to endotoxemic mice is effective in selectively increasing the number of systemic and intestinal B lymphocytes. Furthermore, LA augmented the level of the main intracellular antioxidant glutathione in the small intestine. On the basis of these data we recommend investigation of the effects of LA and GLN supplementation in patients with sepsis.
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http://dx.doi.org/10.1007/s00508-006-0568-3 | DOI Listing |
Naunyn Schmiedebergs Arch Pharmacol
January 2025
Department of Zoology, University of Allahabad, Senate House, University Road, Old Katra, Prayagraj, Uttar Pradesh, 211002, India.
This study was designed to evaluate the dose-dependent efficacy of neurotensin receptor-1 (NTSR1) agonist PD149163 in the amelioration of the lipopolysaccharide (LPS)-induced apoptosis in the gastrointestinal tract (GIT) of mice. PD149163 is an analogue of NTS, a GIT tri-decapeptide with anti-inflammatory and anti-oxidative effects. Swiss-albino mice (female/8 weeks/25 ± 2.
View Article and Find Full Text PDFPediatr Surg Int
October 2024
Department of Pediatric General and Urogenital Surgery, Juntendo University School of Medicine, 2-1-1 Hongo, Bunkyo-ku, Tokyo, 113-8421, Japan.
Purpose: Angiopoietin-1 (Ang1) mitigates inflammation as a proangiogenic growth factor. Action of Ang1 on lipopolysaccharide (LPS)-induced endotoxemic inflammation was investigated in endothelin receptor-B null Hirschsprung's disease mice (KO).
Methods: LPS or saline was injected intraperitoneally in KO (KO-LPS; n = 9, KO-sal; n = 5) and wild-type (WT) (WT-LPS; n = 6, WT-sal; n = 6) pups obtained within 24 h of birth.
Drug Chem Toxicol
October 2024
Department of Zoology, University of Allahabad, Prayagraj, India.
The multistrain probiotics' efficacy in ameliorating the endotoxemic effect in Lipopolysaccharide (LPS) challenged mice was evaluated with the agonist of anti-inflammatory peptide, neurotensin (NTS), especially targeting the inflammation of the gut and liver. Swiss Albino Mice (Female, 8 weeks old) were maintained in eight groups: Group I as Control, Group II-Group V were exposed to intraperitoneal (i.p.
View Article and Find Full Text PDFLife Sci
December 2024
Department of Food Science and Biotechnology of Animal Resources, College of Sang-Huh Life Sciences, Konkuk University, 120 Neungdong-ro, Gwangjin-gu, Seoul 05029, Republic of Korea. Electronic address:
Neuroscience
September 2024
Department of Molecular and Cellular Physiology, Albany Medical College, United States; Department of Ophthalmology, Albany Medical College, United States. Electronic address:
Sepsis-associated encephalopathy (SAE) is associated with increased risk of long-term cognitive impairment. SAE is driven, at least in part, by brain endothelial dysfunction in response to systemic cytokine signaling. However, the mechanisms driving SAE and its consequences remain largely unknown.
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