Nicotinamide mononucleotide ameliorates DNFB-induced atopic dermatitis-like symptoms in mice by blocking activation of ROS-mediated JAK2/STAT5 signaling pathway

• Published in: International immunopharmacology Vol. 109; p. 108812
• Main Authors: Gao, Jie-Fang, Tang, Liu, Luo, Fei, Zhang, Yi-Yuan, Chen, Lu, Ding, Hong, Meng, Zu-Dong
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier B.V 01.08.2022
• Subjects: Atopic dermatitis; Inflammatory cytokines; JAK2/STAT5 signaling pathway; Nicotinamide mononucleotide; Oxidative stress; Oxidative stress; Inflammatory cytokines; Atopic dermatitis; Nicotinamide mononucleotide; JAK2/STAT5 signaling pathway
• ISSN: 1567-5769; 1878-1705
• DOI: 10.1016/j.intimp.2022.108812

•Nicotinamide mononucleotide attenuated DNFB-induced AD-like symptoms.•Nicotinamide mononucleotide could reduce the epidermal thickness and recover epidermal barrier function.•Nicotinamide mononucleotide has an alleviatory effect on skin inflammation in DNFB-induced mice.•Nicotinamide mononucleotide could block activation of ROS-mediated JAK2/STAT5 signaling pathway. Atopic dermatitis (AD) is a chronic inflammatory skin disease, characterized by pruritus and impaired skin barrier function. The pathology of AD involves in immune dysfunction and epidermal barrier disruption. Reactive oxygen species (ROS) are found to be associated with AD, and play a role in the immunological abnormalities and dysfunctional skin barrier. Nicotinamide mononucleotide (NMN) plays an important role in oxidative stress related diseases, but its role in AD is unclear. KM mice were treated with DNFB to induce AD-like lesion and typical applied with NMN for two weeks. The dermatitis score, the degree of itching and TEWL were evaluated during modeling. Epidermal thickness of skin lesions and histopathological changes were detected. Further, inflammatory factors, epidermal differentiation-related genes, oxidative stress indicators and JAK2/STAT5 signaling pathway were evaluated. NHEK cells were stimulated by TNF-α/IFN-γ after pre-treatment with NMN, then ROS levels, inflammatory factors and JAK2/STAT5 signaling pathway were detected. NMN exhibited potent anti-atopic activities, shown by alleviated AD-like symptoms, inhibited the increased expression of inflammatory cytokines and restored proteins and mRNA level of skin barrier genes. In addition, NMN inhibited TNF-α/IFN-γ-stimulated elevation of inflammatory chemokines, which was associated with blocking the activation of ROS-mediated JAK2/STAT5 pathway. NMN may have a positive effect on relieving symptoms of AD.