(-)-α-Bisabolol (BIS) is a sesquiterpene alcohol derived mostly from Matricaria recutita L., which is a traditional herb and exhibits multiple biologic activities. BIS has been reported for treatment of skin disorders, but the effect of BIS on anti-atopic dermatitis (AD) remains unclear. Therefore, we investigated the effects of BIS on 2,4-dinitrochlorobenzene (DNCB)-induced AD in BALB/c mice and the underlying mechanism in Bone Marrow-Derived Mast Cells (BMMCs). Topical BIS treatment reduced AD-like symptoms and the release of interleukin (IL)-4 without immunoglobulin (Ig)-E production in DNCB-induced BALB/c mice. Histopathological examination revealed that BIS reduced epidermal thickness and inhibited mast cells in the AD-like lesions skin. Oral administration of BIS effectively and dose-dependently suppressed mast-cell-mediated passive cutaneous anaphylaxis. In IgE-mediated BMMCs, the levels of β-hexosaminidase (β-hex), histamine, and tumor necrosis factor (TNF)-α were reduced by blocking the activation of nuclear factor-қB (NF-қB) and c-Jun N-terminal kinase (JNK) without P38 mitogen activated protein (P38) and extracellular regulated protein kinases (Erk1/2). Taken together, our experimental results indicated BIS suppresses AD by inhibiting the activation of JNK and NF-κB in mast cells. BIS may be a promising therapeutic agent for atopic dermatitis and other mast-cell-related diseases.

Background. Scrophularia dentata is an important medicinal plant and used for the treatment of exanthema and fever in Traditional Tibetan Medicine. Scrodentoids H and I (SHI), a pair of epimerides of C₁₉‐norditerpenoids isolated from Scrophularia dentata, could transfer to each other in room temperature and were firstly reported in our previous work. Here, we first reported the anti‐inflammatory effects of SHI on LPS‐induced inflammation. Purpose. To evaluate the anti‐inflammatory property of SHI, we investigated the effects of SHI on LPS‐activated THP‐1 cells. Methods. THP‐1 human macrophages were pretreated with SHI and stimulated with LPS. Proinflammatory cytokines IL‐1β and IL‐6 were measured by RT‐PCR and enzyme‐linked immunosorbent assays (ELISA). The mechanism of action involving phosphorylation of ERK, JNK, P38, and STAT3 was measured by western Blot. The NF‐κB promoter activity was evaluated by Dual‐Luciferase Reporter Assay System in TNF‐α stimulated 293T cells. Results. SHI dose‐dependently reduced the production of proinflammatory cytokines IL‐1β and IL‐6. The ability of SHI to reduce production of cytokines is associated with phosphorylation depress of JNK and STAT3 rather than p38, ERK, and NF‐κB promoter. Conclusions. Our experimental results indicated that anti‐inflammatory effects of SHI exhibit attenuation of LPS‐induced inflammation and inhibit activation through JNK/STAT3 pathway in macrophages. These results suggest that SHI might have a potential in treating inflammatory disease.