Alhagi camelorum is a dominant leguminous shrub distributed in the Taklamakan Desert, an area characterized by extreme drought and high soil salinization, which can complete its life cycle normally in salt-affected soils. However, the underlying molecular regulatory mechanism of its salt tolerance remains largely unclear. The AcABI5 gene was successfully cloned and characterized, and it encodes a typical nuclear-localized bZIP transcription factor. Functional characterization demonstrated that overexpression of AcABI5 markedly improved the salt stress tolerance of A. camelorum calli, whereas silencing of AcABI5 via virus-induced gene silencing (VIGS) rendered the plant more sensitive to salt stress. Further mechanistic investigations revealed that AcABI5 enhanced salt tolerance by regulating the expression of superoxide dismutase (SOD)- and peroxidase (POD)-related antioxidant genes. Compared with the wild type, AcABI5-overexpressing calli exhibited significantly increased SOD and POD activities and remarkably reduced malondialdehyde (MDA) content under salt treatment, whereas AcABI5-silenced lines exhibited the opposite physiological phenotypes. Furthermore, heterologous silencing of AcABI5 in Nicotiana benthamiana via virus-induced gene silencing (VIGS) produced comparable salt-sensitive phenotypes, similar to those observed in A. camelorum AcABI5-silenced lines. Collectively, these results provide insights into the molecular mechanism by which AcABI5 enhances salt tolerance in A. camelorum, and lay a solid theoretical foundation for the optimization of the A. camelorum genetic transformation system and the expansion of related salt-tolerant crop research.