Objective To investigate the expressions of ubiquitin-proteasome markers，including E2-14K，MAFbx，MuRF-1，and nuclear factor-κB（NF- κB） p50，in diaphragm of COPD rats，and their relationship with IL-17 level in diaphragm and serum in order to elucidate the potential mechanism of diaphragm atrophy. Methods Thirty healthy adult male SD rats were randomly divided into a model group （n=18） and a normal control group （n=12）. The COPD rat model was established by instillation of lipopolysaccharide （LPS） and exposure to cigarette smoke for 28 days. The protein levels of E2-14K，MAFbx，MuRF-1，and NF-κB p50 in diaphragm were measured by Western blot. The concentration of IL-17 in serum and diaphragm was measured by ELISA. Results Western blot showed that the protein expressions of E2-14K，MAFbx，MuRF-1，and NF-κB p50 in diaphragm increased significantly in the COPD model group compared with the normal control group （0.96±0.12 vs. 0.53±0.09，0.99±0.10 vs. 0.53±0.08，0.95±0.08 vs. 0.51±0.16，1.11±0.10 vs. 0.64±0.50，respectively，Plt;0.01）. The IL-17 level in serum and diaphragm was significantly higher in the COPD group than the control group. The expression of NF-κB p50 was positively correlated with E2-14K，MAFbx，and MuRF-1 expressions （r=0.82，0.92，0.86，respectively，Plt;0.01）. Both in serum and diaphragm，IL-17 level was positively correlated with the percentage of neutrophils，levels of NF-κB p50，E2-14K，MAFbx，and MuRF-1 expressions（all Plt;0.01）. The IL-17 levels in serum and diaphragm were also positively correlated each other （r=0.84，Plt;0.01）. Conclusions The results show that the ubiquitin-proteasom pathway，the NF-κB pathway and IL-17 are up-regulated in diaphragm of COPD rats .These alterations may contribute to diaphragm atrophy in COPD.