Senescence represents a developmentally orchestrated and precisely regulated cascade of events, culminating in the abscission of plant organs and ultimately leading to the demise of the plant or its constituent parts. In this study, we observed that senescence in cut Lilium tigrinum flowers is induced by elevated ABA levels and the hyperactivation of lipoxygenase (LOX) activity. This cascade increased ROS concentrations, heightened oxidative damage, and disrupted cellular redox equilibrium. This was evidenced by elevated lipid peroxidation, attenuated antioxidant machinery, and reduced membrane stability index (MSI). Despite its known role in delaying flower senescence, the specific biochemical and molecular mechanisms by which nitric oxide (NO) regulates senescence in cut L. tigrinum flowers are not fully elucidated. Specifically, the interactions between NO signaling and ABA metabolism, the regulation of protease activity, and the influence of NO-mediated ROS scavenging, senescence-associated gene expression requires further exploration. Exogenous application of sodium nitroprusside (SNP), a source of NO, mitigated senescence in L. tigrinum cut flowers by upregulating the activity of superoxide dismutase (SOD), catalase (CAT), ascorbate peroxidase (APX) and reducing the LOX activity, an indicator of lipid peroxidation. SNP treatment also downregulated the relative expression of senescence-associated gene (SAG12),lipoxygenase 1 (LOX1), and abscisic aldehyde oxidase 3 (AAO3). NO also upregulated defender against apoptotic death 1 (DAD1) expression correlated with minimized protease activity and reduced α-amino acid content in SNP-treated tepals. This regulation was accompanied by increased contents of sugars, proteins and phenols and reduced abscisic acid content, which collectively delayed the senesecence and enhanced the longevity of L. tigrinum cut flowers. This study demonstrates that exogenous SNP application can effectively mitigate senescence in cut L. tigrinum flowers by modulating antioxidant enzyme activities, reducing oxidative stress, and regulating the expression of key senescence-associated genes. This study unravels the complex molecular networks involved in NO-mediated senescence delay, which may lead to the development of innovative approaches for improving flower longevity.