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Dietary Supplementation of Curcumin Alleviates NF-ΚB-dependent Skeletal Muscle Wasting in Rat

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Background: Activation of the nuclear factor-kappa β (NF-ΚB) signaling results in releasing of a variety of inflammatory cytokines that can induce skeletal muscle wasting (MW) in mammals. Curcumin is a natural product from spice turmeric that can block biological events in which NF-ΚB plays a critical role.

Objective: The present study was conducted to evaluate the beneficial effects of curcumin on the NF-ΚB-dependent MW in rats.

Methods: The MW rats were induced by lipopolysaccharide (LPS) injection and rats were fed 15 g curcumin per kg diet for 16 d.

Results: LPS not only decreased the growth performance of rat, but significantly elevated its serum IL-1 concentration and muscle proteolysis rate. Interestingly, curcumin significantly prevented the muscle proteolysis rate and down-regulated expression levels of two critical muscle-specific ubiquitin ligases (Atrogin-1 and MuRF-1). When muscles from MW rats were incubated with curcumin in vitro, the calpain-, cathepsin L-, and proteasome-dependent muscle proteolysis were significantly decreased. Moreover, the nuclear NF-ΚB/p65 protein abundance were also decreased by curcumin.

Conclusion: The results not only suggest a molecular mechanism by which curcumin modulates the inflammatory responses, but also offer a feasible avenue to ameliorate the NF-ΚB-dependent muscle proteolysis.
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Keywords: Curcumin; inflammation; muscle wasting; nutrition; rat; regulation

Document Type: Research Article

Publication date: June 1, 2016

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  • This journal is devoted to timely reviews of experimental and clinical studies in the field of endocrine, metabolic, and immune disorders. Specific emphasis is placed on humoral and cellular targets for natural, synthetic, and genetically engineered drugs that enhance or impair endocrine, metabolic, and immune parameters and functions. Topics related to the neuroendocrine-immune axis are given special emphasis in view of the growing interest in stress-related, inflammatory, autoimmune, and degenerative disorders.
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