Journal
MEDIATORS OF INFLAMMATION
Volume 2008, Issue -, Pages -Publisher
HINDAWI LTD
DOI: 10.1155/2008/317851
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Funding
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [T32HL007734] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [T32DK007754, R01DK037908] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF NURSING RESEARCH [R01NR008545, R56NR008545] Funding Source: NIH RePORTER
- NHLBI NIH HHS [T32 HL007734] Funding Source: Medline
- NIDDK NIH HHS [R01 DK037908, T32 DK007754, R01 DK37908] Funding Source: Medline
- NINR NIH HHS [R01 NR008545, R01 NR08545, R56 NR008545] Funding Source: Medline
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We tested the hypothesis that treatment of rats with curcumin prevents sepsis-induced muscle protein degradation. In addition, we determined the influence of curcumin on different proteolytic pathways that are activated in septic muscle (i.e., ubiquitin proteasome-, calpain-, and cathepsin L-dependent proteolysis) and examined the role of NF-kappa B and p38/MAP kinase inactivation in curcumin-induced inhibition of muscle protein breakdown. Rats were made septic by cecal ligation and puncture or were sham-operated. Groups of rats were treated with three intraperitoneal doses (600 mg/kg) of curcumin or corresponding volumes of solvent. Protein breakdown rates were measured as release of tyrosine from incubated extensor digitorum longus muscles. Treatment with curcumin prevented sepsis-induced increase in muscle protein breakdown. Surprisingly, the upregulated expression of the ubiquitin ligases atrogin-1 and MuRF1 was not influenced by curcumin. When muscles from septic rats were treated with curcumin in vitro, proteasome-, calpain-, and cathepsin L-dependent protein breakdown rates were reduced, and nuclear NF-kappa B/p65 expression and activity as well as levels of phosphorylated (activated) p38 were decreased. Results suggest that sepsis-induced muscle proteolysis can be blocked by curcumin and that this effect may, at least in part, be caused by inhibited NF-kappa B and p38 activities. The results also suggest that there is not an absolute correlation between changes in muscle protein breakdown rates and changes in atrogin-1 and MuRF1 expression during treatment of muscle wasting. Copyright (C) 2008 Vitaliy Poylin et al.
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