Objective This study aims to explore the therapeutic effect of Morinda officinalis extract (MoE) on dexamethasone (Dex)-induced sarcopenia in mice and its possible mechanism of action.

Methods Firstly, the pharmacological components and important targets of Morinda officinalis were investigated using network pharmacology to predict the mechanism of action of MoE. In the animal experiment, 50 KM mice were randomly divided into 5 groups (control, sarcopenia, MoE-H, MoE-M, MoE-L). Except for the control group, the other groups were subcutaneously injected with Dex for 45 days to induce sarcopenia, and the three treatment groups were simultaneously orally administered different doses of MoE. During the experiment, the animals' body weight, exercise ability (treadmill and grip strength), and body composition were regularly measured. After euthanasia, the muscle coefficient of the hind limbs was calculated, and histological and related gene expression tests were performed.

Results The results of network pharmacology suggested that MoE may treat sarcopenia by upregulating the IGF-1/AKT/mTOR signaling pathway. The animal experiment results show that MoE significantly reverses the decrease in body weight and muscle coefficient caused by Dex, improved motor ability, improved histological lesions, upregulated the expression of genes such as IRS-1, mTOR, MFN2, OPA1, MYOD, and MYOG, and downregulated the expression of genes such as Atrogin-1, MuRF-1, and MSTN.

Conclusion MoE has a therapeutic effect on Dex-induced muscle atrophy, improving histological morphology, and its mechanism of action may involve the activation of the IGF-1/AKT/mTOR pathway.