Osteoarthritis is a degenerative joint disease and a leading cause of chronic pain affecting 10% of the global population. The ubiquitinated proteasome system (UPS) regulates majority of protein degradation. Voltage-gated potassium channels (VGKC) are involved in nerve impulses and pain signalling. The UPS plays a major role in OA and contributes to the symptom of chronic pain. The inhibition of the UPS by the MG132 inhibitor has been demonstrated to lead to a reduction in cartilage catabolism, inflammation and chronic pain. However, the specific mechanisms and downstream effects are yet to be fully understood. The aim of this study was to investigate how the inhibition of the UPS with MG132 affected the voltage-gated potassium channel. This was done by inducing OA with monosodium iodoacetate in 12 female Lewis rats. Half of the rats were then administered with MG132 dissolved in a vehicle and the other half with just the vehicle. The spinal cord of these rats was then removed and analysed using a quantitative mass spectrometer and 1583 proteins were identified. All UPS and VGKC proteins were statistically analysed. This resulted in a trend of UPS proteins being slightly downregulated in the MG132 group and VGKC proteins being upregulated in the MG132 group and the correlation between all UPS and VGKC proteins dropped significantly between each other with the introduction of MG132. This data demonstrates that the UPS have a significant influence on the VGKC which, however, needs further investigation.