In this experiment, Escherichia coli and Listeria innocua were selected as the representative G- and G+ bacteria to explore the antibacterial mechanism of LAE towards bacterial membranes. The antibacterial mechanism was examined via investigating LAE’s antibacterial curve, the ability of neutralizing endotoxin, and bacterial surface characteristics, and constructing liposomes to simulate the interaction between LAE and phospholipid bilayers and evaluate the ion leakage and the permeability of LAE through G- bacterial outer membrane and cytoplasmic membrane. The experimental results showed that LAE had significant bactericidal activities against both G- and G+ bacteria with the minimum inhibitory concentration as 8 μg/mL. LAE could neutralize up to 96.56%endotoxin through binding to lipopolysaccharide, reduce the zeta potential on the cell surface, enhance hydrophobicity of bacterial surface, and exert a greater impact on G- bacteria. LAE could cause the leakage of a liposome-encapsulated fluorescein, calcein, in a concentration-dependent manner, but LAE didn’t collapse completely the liposome membrane. LAE was able to increase the permeability of the outer membrane of G- bacteria, which made E. coli more sensitive to the antibiotic probes, rifampicin and erythromycin, while disturbed greatly the cytoplasmic membrane, causing the leakage of intracellular contents, thereby inhibiting the growth of bacteria. The results of this study indicate that LAE exerts bacteriostatic effects mainly through changing the cell wall membrane permeability and consequently leading to the leakage of intracellular substances.