Atopic dermatitis (AD) is a chronic inflammatory skin disorder characterized by dysregulated immunity, skin barrier dysfunction, and cutaneous microbiome dysbiosis. While current therapies face limitations, Thuja sutchuenensis essential oil (TEO) shows promise due to its multi-target potential. We sought to explore the beneficial effects of TEO and delve into its mechanistic actions in a mouse model of AD. We combined network pharmacology with in vivo validation to evaluate the therapeutic efficacy and mechanisms of TEO in an AD model, and confirmed network-predicted targets in an in vitro inflammatory cell model. In AD mice, TEO alleviated pruritus and epidermal hyperplasia, suppressed systemic IL-4/TNF-α and IgE, and partially normalized serum ALB, LDL-C, and HDL-C. Microbial diversity increased after treatment, although potentially pathogenic taxa (Arthrobacter sp. and Corynebacterium mastitidis) remained enriched. Machine-learning analysis indicated the highest predicted metabolic activity in CK controls, whereas the AD and TEO groups showed elevated pathogenic phenotype scores. Network pharmacology prioritized active compounds [(E)-ligustilide, senkyunolide A, 3-butylisobenzofuran-1(3H)-one, butylated hydroxytoluene, Z-buthlidenephthalide, and β-Myrcene] and core targets (TNF, PTPRC, CCR5, JAK1), implicating T-cell receptor signaling, Staphylococcus aureus infection, and STAT3 pathways. Docking and molecular dynamics supported strong, stable binding of major constituents to JAK1, and Western blotting confirmed TEO-mediated inhibition of the JAK1/STAT3 axis. TEO effectively alleviates atopic dermatitis symptoms by modulating immune responses and enhancing microbial diversity. It targets key signaling pathways, such as JAK1/STAT3, highlighting its potential as a therapeutic option for AD.

Exogenous glutathione (GSH) can alleviate cadmium (Cd) stress, yet physiological improvement and changes in internal Cd burden may not occur in parallel. Salix variegata seedlings were exposed for 10 d to 0 or 100 μM Cd with 0–1500 μM GSH. Across the full dose series, GSH responses were non-monotonic: 10 μM GSH increased root length by 67.3% under Cd stress, 250 μM GSH increased chlorophyll a, chlorophyll b, and total chlorophyll by 21.4%, 39.0%, and 25.7%, respectively, whereas 1500 μM GSH inhibited several growth and pigment traits. A common 2 × 2 subset (0/250 μM GSH × 0/100 μM Cd) was used to integrate root/leaf physiology with root/shoot element status. At 250 μM GSH, H₂O₂ and MDA decreased in both roots and leaves, while antioxidant and osmotic responses differed between tissues. Root Cd concentration increased by 64.1%, root Cd accumulation by 165%, and total Cd accumulation by 117%, despite a 24.1% decrease in shoot Cd concentration. Root Fe concentration and total Fe accumulation increased by 173.2% and 170%, respectively. These results show that GSH responses in S. variegata are dose- and tissue-dependent and that improved physiological status can coexist with greater Cd burden and altered essential-metal homeostasis.