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BACKGROUND: From the pathological mechanism of Western medicine, ligamentum flavum hypertrophy is the key pathogenic factor of lumbar spinal stenosis, and there is a lack of biological information on lumbar spinal stenosis of the Qi deficiency and blood stasis type. OBJECTIVE: To analyze and compare differential protein expression between hypertrophic and normal ligamentum flavum in patients with lumbar spinal stenosis of the Qi deficiency and blood stasis type. METHODS: Ligamentum flavum tissue samples were collected from six lumbar spinal stenosis patients with Qi deficiency and blood stasis, including three cases of ligamentum flavum hypertrophy (experimental group) and three cases of normal ligamentum flavum (control group). 4D Label free quantitative proteomic detection was performed to screen differentially expressed proteins. Gene oncology and Kyoto Encyclopedia of Genes and Genomes were used for enrichment analysis. RESULTS AND CONCLUSION: There were 183 differentially expressed proteins between the two groups, including 87 up-regulated and 96 down-regulated. Gene oncology enrichment analysis showed that biological processes mainly focused on cell processes, biological regulation and response to stimuli. Cell composition was concentrated in cell, intracellular, and protein-complex species. The main molecular functions included linkage, catalytic activity and molecular function regulator. The up-regulated proteins were mainly enriched to lysosomal signaling pathway, rheumatoid arthritis signaling pathway, and Staphylococcus aureus infection signaling pathway, while the down-regulated proteins were enriched to eight signaling pathways, namely p53 signaling pathway, renal cell carcinoma signaling pathway, transforming growth factor β signaling pathway, ubiquitin-mediated protein hydrolysis signaling pathway, Ca signaling pathway, cGMP-PKG signaling pathway, hypoxia-inducible factor 1 signaling pathway, and proteoglycan signaling pathway in cancer. INHBA, MMP14, TNC, HTRA1, FGF2 were the important differentially expressed proteins in the experimental group. To conclude, there are differential protein expressions between hypertrophic and normal ligamentum flavum in patients with Qi-stagnation and blood-stasis type lumbar spinal stenosis. INHBA may be the determinant of this disease, and its mechanism may be the activation of transforming growth factor β/Smad related signaling pathway, causing ligamentum flavum hypertrophy and subsequently leading to lumbar spinal stenosis. [ABSTRACT FROM AUTHOR]