Exogenous salicylic acid (SA) enhances plant tolerance to cadmium (Cd) stress by preserving chlorophyll, stabilizing osmoprotectants, and upregulating antioxidant activity alongside the ASA-GSH system. However, the role of endogenous SA in plant tolerance to Cd stress remains poorly understood. Therefore, we cultivated Monochoria korsakowii hydroponically and sprayed the SA biosynthesis inhibitors (2-aminoindane-2-phosphonic acid and 1-aminobenzotriazole) in an attempt to explore the correlation between endogenous SA and other Cd tolerance mechanisms. Compared with control, 0.3 mM Cd treatment induced reductions of net photosynthetic rate (Pn), total chlorophyll (T Chl), catalase (CAT), and soluble protein (SP), while malondialdehyde increased. To mitigate Cd toxicity, M. korsakowii upregulated peroxidase (POD), superoxide dismutase (SOD), glutathione reductase (GR), ascorbic acid (ASA), nonprotein thiols (NPT), phytochelatin (PC), and proline. High concentrations of SA inhibitors exacerbated Cd-induced oxidative damage and suppressed these tolerance mechanisms. Compared with T4, T6 plants exhibited marked reductions in Pn, T Chl, CAT, POD, SOD, GSH, GR, ASA, ascorbate peroxidase, NPT, PCs, SP, and translocation factors. Concurrently, T6 plants sprayed with SA inhibitors exhibited suppressed SA, methyl salicylate, and zeatin accumulation, contrasting with heightened jasmonic acid and abscisic acid concentrations. We propose that endogenous SA is crucial for preserving the photosynthetic apparatus, activating the antioxidant system, and promoting the accumulation of chelators and SP in M. korsakowii under Cd stress. Furthermore, endogenous SA may function synergistically with methyl salicylate and zeatin to regulate plant physiological responses to Cd. This study provides valuable insights into the Cd tolerance mechanisms in M. korsakowii.