Reduced muscle protein breakdown in septic rats following treatment with interleukin-1 receptor antagonist |
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| Institution: | 1. Department of Surgery, University of Cincinnati Medical Center, Cincinnati, OH 45267-0558 U.S.A.;2. Synergen, Inc., Boulder, Colorado, U.S.A.;1. Department of Animal Sciences, University of Florida, Gainesville 32611;2. DH Barron Reproductive and Perinatal Biology Research Program, University of Florida, Gainesville 32611;1. Department of Animal Sciences, University of Illinois, Urbana, IL 61801, USA;2. QualiTech Inc., Chaska, MN 55318, USA;1. National Center for PTSD at VA Boston Healthcare System, United States;2. Department of Psychiatry, Boston University School of Medicine, United States;3. Biomedical Genetics, Boston University School of Medicine, United States;4. Department of Biostatistics, Boston University School of Public Health, United States;5. Pathology and Laboratory Medicine, VA Boston Healthcare System, United States;6. Department of Neurology, Boston University School of Medicine, United States;7. Department of Pathology, Boston University School of Medicine, United States;2. Dairy and Swine Research and Development Centre, Agriculture and Agri-Food Canada, Sherbrooke, Québec, J1M 0C8 Canada;2. Research Institute for Bioscience Products and Fine Chemicals, Ajinomoto Co. Inc., Kanagawa, Japan, 210-8681;2. Animal Nutrition Group, Wageningen University and Research, Wageningen 6700 AH, the Netherlands |
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| Abstract: | - 1.1. The role ofinterleukin-1 (IL-1) in sepsis-induced muscle proteolysis was assessed by treating septic rats with recombinant IL-1 receptor antagonist (rIL-Ira).
- 2.2. In initial experiments, we tested the effectiveness of IL-Ira in preventing muscle proteolysis induced by administration of IL-1.
- 3.3. When normal rats were treated with rIL-α (three intraperitoneal doses of 100 μ g/kg body weight each over 16 hr), total and myofibrillar muscle protein breakdown rates, measured as release oftyrosine and 3-methylhistidine, respectively, by incubated extensor digitorum longus muscles, were significantly increased.
- 4.4. This metabolic response to IL-α was completely abolished by rIL-Ira, administered as three intraperitoneal doses of 3 mg/kg body weight each over 16hr.
- 5.5. In subsequent experiments, sepsis was induced in rats by cecal ligation and puncture (CLP); non-septic rats were sham-operated.
- 6.6. Treatment of septic rats over 16hr with a total dose of 25mg/kg body weight of rIL-Ira reduced, but did not normalize, the increased muscle protein breakdown rates seen during sepsis.
- 7.7. When the dose of rIL-Ira was more than doubled and given as a constant infusion at a rate of 4.2 mg/kg body weight/hr for 16 hr, the increased rate of muscle proteolysis in septic rats was normalized.
- 8.8. The present study offers the first direct evidence that IL-1 is involved in the regulation of muscle proteolysis during sepsis.
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