Objective: This paper aims to investigate the mechanism by which epigenetic modifications play a role in the formation and maintenance of salt tolerance under long-term salt stress, and to clarify the regulatory network played by DNA methylation, histone modification, and non-coding RNA during long-term adaptation. Methods: A long-term salt stress treatment model was established, and the subjects were divided into a control group, a long-term salt stress group, and a recovery group. The recovery group was used to evaluate epigenetic memory. Salt tolerance phenotypes were evaluated by growth status, ionic homeostasis (Na⁺/K⁺), osmotic regulators, oxidative stress indicators, DNA methylation, histone modification, and non-coding RNA expression changes were detected by bisulfite sequencing, ChIP-qPCR, and transcriptome sequencing, and their causal effects were verified by epigenetic-related inhibitors or key enzyme interventions. Results: Long-term salt stress can improve the salt-tolerant phenotype, namely reduced growth inhibition, decreased Na⁺ accumulation, and enhanced antioxidant capacity. Remodeling of genome-wide methylation patterns, reduced methylation levels of salt-tolerant gene promoters and upregulated transcription; At the same time, there is an enhancement of active histone markers (H3K4me3, H3K9ac), which continuously activates salt-tolerant genes. The non-coding RNA network was also reconstructed, with some mirnas and lncrnas performing fine regulation by targeting genes related to ion transport and ABA signaling. Blocking DNA methylation or histone deacetylation weakens the salt-tolerant phenotype and reduces the expression of related genes. Conclusion: Long-term salt stress adaptation is a co-reprogramming of multiple levels of epigenetic modifications, where DNA methylation, histone modification, and non-coding RNA together continuously activate salt-tolerant genes and potentially form epigenetic memory, providing potential targets for salt tolerance improvement and salt-related injury intervention.