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Objective: Food accumulation fever (FAF), a common clinical disease in children, is generally induced by the excessive intake of high-calorie or high-fat foods. Methods: Network pharmacological analyses of ZQCLD and FAF were conducted. Animal experiments lasted for 14 days. Rats in the model, positive control, and low-, medium-, and high-dose groups were fed a high-calorie diet. On days 11-14, the positive group was given a domperidone solution. The low-, medium-, and high-dose groups were administered different concentrations of ZQCLD. The body temperature, gastric emptying rate, and intestinal propulsion rate were measured. Relevant indicators were determined by ELISA. Results: The main target proteins included IL-1β, C-C motif chemokine 2 (CCL2), prostaglandin G/H synthase 2 (PTGS2), transcription factor AP-1 (JUN), haem oxygenase 1 (HMOX1), interferon-gamma (IFN-γ), peroxisome proliferator-activated receptor-gamma (PPAR-γ), and inducible nitric oxide synthase (NOS2/iNOS). Compared with those in the control group, body weight, gastric emptying rate, intestinal propulsion rate, and neuronal nitric oxide synthase (NOS1/nNOS) levels were significantly lower in the model group, whereas body temperature and endotoxin, interleukin-1β (IL-1β), PGE2, and iNOS levels were increased. In each treatment group, body temperature and PGE2 levels returned to normal levels. Compared with those in the model group, the gastric emptying rates in the positive group and the low- and medium-dose groups increased; the intestinal propulsion rates were higher in the medium- and high-dose groups, whereas the endotoxin and IL-1β levels were lower; and the nNOS level was higher in the high-dose group, whereas the iNOS level was lower. Conclusions: ZQCLD may treat FAF by regulating jejunal IL-1β and nNOS, serum endotoxin, and hypothalamic PGE2 and iNOS levels.