A Torilis Japonica Extract–GHK-Cu Complex Attenuates Th2 Cytokines and Promotes Keratinocyte Recovery: A Potential Antioxidant Strategy for Atopic Dermatitis

Atopic dermatitis (AD) is a chronic skin disorder driven by Th2 immune dysregulation, persistent inflammation, and epidermal barrier defects. Oxidative stress acts as a major upstream factor in this process, amplifying inflammatory signals and worsening disease severity. While current treatments relieve acute symptoms, long-term application is often constrained by side effects and poor barrier restoration, pointing to a need for safer, multifaceted alternatives. Here, we formulated a complex of Torilis japonica extract (TJE) and GHK-Cu (Glycyl-L-histidyl-L-lysine copper(II)) complex and examined its anti-atopic and skin-regenerative properties using a TNF-α (Tumor necrosis factor-α)/IFN-γ (Interferon-γ)-stimulated HaCaT cell model. TJE decreased the expression of AD-related chemokines (TARC(Thymus and activation-regulated chemokine (CCL17)) and CTACK(Cutaneous T-cell-attracting chemokine (CCL27)) as well as IgE production, confirming the suppression of Th2-driven inflammation. An optimized 6:4 ratio (TJE:GHK-Cu) yielded the highest efficacy compared to individual treatments, indicating a synergistic interaction. TJE–GHK-Cu complex suppressed the transcription of key Th2 cytokines (IL-4, IL-5, IL-10, and IL-13) and promoted keratinocyte migration during wound healing assays. The formulation also displayed strong radical scavenging activity without compromising cell viability. These results demonstrate that the TJE–GHK-Cu complex provides simultaneous anti-inflammatory, antioxidant, and regenerative benefits, presenting a formulation warranting further investigation for managing AD.