Amelioration of Atopic Dermatitis by Frankincense Oil Extract Is Associated with TRPV3 Regulation and Cutaneous Inflammation Suppression
Gang-Ning Tan, Wen-Sheng Zhang, Yu-Sang Li, He-Bin TangIn traditional Chinese medicine, frankincense is widely recognized for its anti-inflammatory and immunomodulatory capacities and has been conventionally applied to manage multiple chronic inflammatory skin disorders. Nevertheless, its therapeutic potency and molecular mechanisms against atopic dermatitis (AD) remain poorly clarified. This study aimed to explore the protective efficacy of frankincense oil extract (FOE) and its active constituents in AD mouse models, thereby clarifying underlying regulatory mechanisms. Two classic AD models induced by 2,4-dinitrochlorobenzene (DNCB) and carvacrol were established to evaluate the therapeutic performance of FOE and its bioactive components. Hematoxylin–eosin and toluidine blue staining were applied to characterize lesional histopathological alterations, immunohistochemistry was used to detect expression profiles of TRPV3, β-catenin, and COX-2 in skin lesions, and calcium fluorescence imaging was applied to monitor TRPV3-mediated intracellular calcium dynamics. The results showed that FOE markedly alleviated typical AD-like manifestations, reducing inflammatory injury, ear edema and splenomegaly in DNCB- and carvacrol-challenged mice. Histological evaluation confirmed that FOE improved pathological lesions, mitigated epidermal hyperplasia, and reduced mast cell infiltration. Meanwhile, FOE remodeled the abnormal expression patterns of TRPV3, β-catenin, and COX-2 triggered by AD stimulation. Additionally, FOE effectively regulated carvacrol-evoked calcium influx mediated by TRPV3 activation. Collectively, FOE and its active components exert anti-inflammatory effects, restraining epidermal over-proliferation and ameliorating epidermal structural disorders, thereby supporting the restoration of epidermal tissue morphology. Such benefits are attributed to modulating TRPV3 activity and remodeling the cutaneous inflammatory microenvironment. This work highlights FOE as a promising novel candidate for atopic dermatitis intervention.