intervertebral disc degeneration (idd) is a major cause of a number of spinal diseases, resulting in serious public health problems. evodiamine (evo) is an indole quinazoline alkaloid extracted from Evodia rutaecarpa, which has antioxidant, anti-apoptosis and anti-inflammatory effects. The purpose of the present study was to investigate lipopolysaccharide (LPS)-induced IDD progression in human nucleus pulposus cells (nPcs) and its potential mechanism. The viability and apoptosis of NPCs were detected by Cell Counting Kit-8 (CCK-8) and TUNEL staining, respectively. Western blotting was used to detect the expression levels of proteins, cell transfection was performed to knockdown Sirtuin 1 (SirT1) and the expression of tumor necrosis factor-alpha (TnF-α) and interleukin 6 (il-6) was detected by enzyme-linked immunosorbent assay kits. The results showed that Evo effectively alleviated LPS-induced NPCs apoptosis and caspase-3 activation and evo treatment reversed the upregulation of matrix metalloproteinase-13, as well as the downregulation of collagen type II (collagen II), Sry-type high-mobility-group box 9 and aggrecan and reduced the production of pro-inflammatory factors TNF-α and il-6 in lPS-stimulated nPcs. in addition, treatment with evo upregulated SirT1 and activated the Pi3K/Akt pathway, knockdown of SIRT1 inhibited the phosphorylation of Akt and PI3K in lPS-stimulated nPcs. in general, evo upregulated SirT1 and inhibited lPS-induced nPcs apoptosis, extracellular matrix degradation and inflammation by activating the PI3K/akt pathway.