Monobenzone 40% in Cetomacrogol cream (Formula A)

Vitiligo is a complex skin disorder that involves oxidative stress and inflammatory responses and currently lacks a definitive cure. Transcutaneous auricular vagus nerve stimulation (taVNS) is a noninvasive method for targeting the auricular branch of the vagus nerve and has gained widespread attention for potential intervention in the autonomic nervous system. Although previous research has suggested that vagus nerve stimulation can potentially inhibit inflammatory responses, its specific role and mechanisms in vitiligo treatment remain unknown. This study aimed to explore the therapeutic effects of taVNS in a mouse model of vitiligo induced by monobenzone. Initially, a quantitative assessment of the treatment effects on vitiligo mice was conducted using a scoring system, revealing that taVNS significantly alleviated symptoms, particularly by reducing the depigmented areas. Subsequent immunohistochemical analysis revealed the impact of taVNS treatment on melanocyte granules, mitigating pigment loss in the skin of monobenzone-induced vitiligo mice. Further analysis indicated that taVNS exerted its therapeutic effects through multiple mechanisms, including the regulation of oxidative stress, enhancement of antioxidant capacity, promotion of tyrosine synthesis, and suppression of inflammatory responses. The conclusions of this study not only emphasize the potential value of taVNS in vitiligo therapy, but also lay a foundation for future research into the mechanisms and clinical applications of taVNS.

Abstract licence: CC BY 4.0

Vitiligo is a common primary, limited or generalized skin depigmentation disorder. Its pathogenesis is complex, multifactorial and unclear. For this reason, few animal models can simulate the onset of vitiligo, and studies of drug interventions are limited. Studies have found that there may be a pathophysiological connection between mental factors and the development of vitiligo. At present, the construction methods of the vitiligo model mainly include chemical induction and autoimmune induction against melanocytes. Mental factors are not taken into account in existing models. Therefore, in this study, mental inducement was added to the monobenzone (MBEH)-induced vitiligo model. We determined that chronic unpredictable mild stress (CUMS) inhibited the melanogenesis of skin. MBEH inhibited melanin production without affecting the behavioral state of mice, but mice in the MBEH combined with CUMS (MC) group were depressed and demonstrated increased depigmentation of the skin. Further analysis of metabolic differences showed that all three models altered the metabolic profile of the skin. In summary, we successfully constructed a vitiligo mouse model induced by MBEH combined with CUMS, which may be better used in the evaluation and study of vitiligo drugs.

Abstract licence: CC BY 4.0

Monobenzyl ether hydroquinone (MEBHQ) is a cream that promotes the spread and evenness of skin patches in vitiligo. Our aim was to investigate the oxidative and inflammatory effects of this cream on vitiligo patients consuming MEBHQ.

Abstract licence: CC BY 4.0

Purpose: Vitiligo is an autoimmune disease that results in the loss of epidermal melanocytes. The treatments for patients with vitiligo remain lacking. Erzhiwan (EZW), a traditional Chinese Medicine composed of Ligustri Lucidi Fructus and Ecliptae Herba , was used to ameliorate depigmentation since ancient China. This study aims to investigate the effect of EZW on vitiligo-related depigmentation. Methods: A vitiligo-related depigmentation mouse model was induced by monobenzone and restraint stress. The experimental depigmentation mice were treated with EZW. Histological observation of skin was conducted. Cutaneous oxidative damage and inflammation were determined. A network pharmacology analysis was carried out. Results: EZW reduced depigmentation score ( p < 0.01), cutaneous inflammatory infiltration ( p < 0.01), and CD8α-positive expression ( p < 0.01), and increased cutaneous melanin content in experimental depigmentation mice. EZW reduced stress reaction in experimental depigmentation mice ( p < 0.01). EZW inhibited 8-hydroxy-2-deoxyguanosine (8-OHdG)-related DNA oxidative damage in the skin ( p < 0.05, p < 0.01). In addition, EZW reduced cutaneous macrophage migration inhibitory factor (MIF)-CD74-NF-κB signaling ( p < 0.01). The network pharmacology analysis demonstrated that EZW regulated necroptosis, apoptosis, and FoxO signaling pathways in vitiligo. An in vitro experiment showed that the main ingredient of EZW, specnuezhenide, protected against monobenzone and MIF-induced cell death in HaCaT cells ( p < 0.01). Conclusion: EZW ameliorates restraint stress- and monobenzone-induced depigmentation via the inhibition of MIF and 8-OHdG signaling. The findings provide a data basis of an utilization of EZW in vitiligo. Keywords: vitiligo, 8-hydroxy-2-deoxyguanosine, Ligustri Lucidi Fructus , Ecliptae Herba , specnuezhenide

Abstract licence: CC BY-NC 3.0

Background Pityriasis lichenoides (PL), comprising acute (PLEVA) and chronic (PLC) subtypes, represents a spectrum of inflammatory skin conditions with overlapping clinical and histopathological features. Standard treatments include oral antibiotics, phototherapy, and immunosuppressive agents. Dupilumab, an IL-4Rα antagonist, is approved for atopic dermatitis and used off-label for other inflammatory skin conditions but has limited documentation in PL treatment. Objective To report a novel case of successful PLC management with dupilumab and an unexpected reemergence of skin pigmentation following prior monobenzone depigmentation therapy for vitiligo. Methods A 40-year-old female with a history of extensive vitiligo and monobenzone depigmentation therapy presented with scaly, erythematous plaques and severe pruritus. Skin biopsy confirmed PLC. Conventional treatments were declined due to concerns about pigmentation changes. Dupilumab was initiated at a loading dose of 600 mg, followed by 300 mg biweekly. Results After three months of dupilumab therapy, significant improvement in PLC lesions and pruritus was observed, with only residual erythematous plaques. Remarkably, skin repigmentation occurred spontaneously, contrasting with previously reported cases of vitiligo exacerbation following dupilumab use. Depigmentation therapy with monobenzone was resumed without exacerbating PLC or pruritus. Conclusion: This case highlights dupilumab's potential as an effective treatment for PLC and its intriguing role in promoting skin repigmentation in a patient with prior vitiligo. These findings suggest a possible link between type 2 inflammation and PLC pathogenesis, warranting further investigation. Dupilumab could serve as a promising therapeutic alternative for refractory PLC. Keywords: Biologics - Case report - Depigmentation - Dupilumab - Pityriasis Lichenoides Chronica - Pityriasis Lichenoides et Varioliformis Acuta - PLC - Vitiligo

Abstract licence: CC BY-NC 4.0

Vitiligo is a depigmenting autoimmune disease driven by oxidative stress and immune-mediated melanocyte destruction. Current therapies are limited by poor drug permeability, systemic side effects, and insufficient efficacy. Herein, we developed a novel carbomer-based hydroxypropyl-β-cyclodextrin-encapsulated crisaborole/curcumin hydrogel (Cri/Cur@CD-Gel) for combinational transdermal intervention of vitiligo via dual antioxidant and anti-inflammatory pathways. Hydroxypropyl-β-cyclodextrin (HP-β-CD) inclusion complexation overcame the inherent hydrophobicity of crisaborole (Cri) and curcumin (Cur), significantly enhancing their aqueous solubility, stability, and transdermal permeability. Leveraging its skin-adhesive properties, the carbomer hydrogel matrix enhanced drug retention and enabled sustained release at lesion sites, thereby improving drug bioavailability. In vitro, Cri/Cur@CD, leveraging the solubilizing power of HP-β-CD, restored melanocyte viability under oxidative stress, scavenged ROS, normalized mitochondrial membrane potential, and elevated cAMP levels to enhance melanogenesis and tyrosinase activity. In vivo, Cri/Cur@CD-Gel achieved significant repigmentation in monobenzone-induced vitiligo mice, markedly reducing epidermal ROS, CD8+ T-cell infiltration, and inflammatory cytokines (TNF-α, IL-1β, and IL-6). This study demonstrates that the combination of HP-β-CD-based encapsulation and carbomer hydrogel delivery serves as a potential topical administration platform for co-delivering hydrophobic crisaborole and curcumin, and establishes a promising strategy to alleviate vitiligo, that concurrently addresses oxidative damage, inflammatory responses, and melanocyte regeneration.

Abstract licence: CC BY-NC-ND