Objective To study the effect of tumor necrosis factor-α( TNF-α) onhypermetabolism of skeletal muscle protein in rats with chronic obstructive pulmonary disease ( COPD) and explore its underlying mechanism. Methods Forty-five SD rats were randomly divided into a normal control group, a COPD group and a COPD + TNF-α group, with 15 rats in each group. COPD model was established by passive cigarette smoking in COPD group and COPD + TNF-αgroup. Then the extensor digitorium longus muscles ( EDL) were dissected and incubated in vitro muscle incubation system with adequate oxygen supply. The EDL were either cultured with or without recombinant rat TNF-α( 10 μg/L) . The mRNA and protein expressions of proteasome subunit C2 in EDL were quantified by real-time quantitative PCR and Western blot analysis, respectively. Results The mRNA and protein expressions of proteasome subunit C2 were both significant higher in the COPD group and COPD + TNF-αgroup than those in the normal control group( P lt;0. 01 or 0. 05) . The COPD+TNF-αgroup had higher expression of proteasome subunit C2 mRNA than that in the COPD group( P lt; 0. 01) , whereas the protein expression was not significantly different( P gt; 0. 05) . Conclusion Incresed proteolytic metabolism in skeletal muscle in COPD might be regulated by TNF-αactivated ubiquitin-dependent pathway.
