The acute and sub-chronic toxicity and hepatoprotective activity of aloe liquor was studied in mice with alcohol-induced liver injury. The difference between health risks of aloe liquor and base liquor were evaluated by a one-time acute oral toxicity test. A mouse model of alcohol-induced liver injury was established to measure serum and liver biochemical indices, observe histopathological changes in the liver, and determine the hepatoprotective effect of aloe liquor on mice with alcohol-induced liver injury. Both the median lethal dose (LD50) and 95% (or 99%) confidence interval of aloe liquor were higher than the values of base liquor, indicating that the former is safer and has a low level of toxicity. Compared with base liquor, aloe liquor could significantly reduce the levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), total cholesterol (TC), and total triglyceride (TG), while increase superoxide dismutase (SOD), glutathione (GSH), and glutathione peroxidase (GSH-PX) activities, and reduce the contents of AST, ALT, and malondialdehyde (MDA) in liver tissue. The optimal efficacy for alleviating liver injury were seen in mice treated with low- and medium-dose aloe liquor. The liver histological observations demonstrated that optimal amounts of aloe liquor exhibited hepatoprotective effects in mice with alcohol-induced liver injury, and the protective mechanism is related to the inhibition of lipid peroxidation and enhancement of liver antioxidant capacity.