Abstract: This study explored the therapeutic effect of Cistanche deserticola extract (CdE) on dexamethasone (Dex)-induced sarcopenia in mice and the possible mechanism of action.Firstly, the pharmacodynamic components and important targets of Cistanche were studied by network pharmacology, and the pathways were enriched to predict the mechanism of action of CdE. In animal experiments, 50 KM mice were randomly divided into 5 groups (control group, Dex model group, CdEhigh-dose group, CdE medium-dose group, and CdE low-dose group). Except for the control group, the other groups were injected subcutaneously to induce sarcopenia after 42 days, and the three treatment groups were given different doses of CdE orally at the same time. During the experiment, the animal weight, exercise capacity and body composition were regularly tested. After the animals were sacrificed, the muscle coefficient of hind limbs was calculated, and histology and related gene expression tests were performed. Network pharmacology results show that CdE may treat sarcopenia by upregulating IGF-1-re-lated signaling pathways. The results of animal experiments show that CdE significantly reverse the decrease of lean meat content and muscle coefficient caused by Dex, improve exercise capacity, reduce fat content,improve the histological status of the muscles, up-regulated IGF-1, MyoD and MyoG, and down-regulated the expression of Atrogin-1 and MuRF-1. CdE has a therapeutic effect on Dex-induced muscle atrophy and can improve muscle histological morphology, and its mechanism of action may be the activation of IGF-1 signaling pathway.