Erianin Targets PINK1/Parkin-Mediated Mitophagy and Apoptosis to Ameliorate Atopic Dermatitis

Atopic dermatitis (AD) is a chronic inflammatory skin lesions. Mitochondrial dysregulation is associated with various pathologic conditions, including inflammation in the skin. Prior research has indicated that Erianin, a naturally occurring compound derived from Dendrobium plants, has antioxidant and anti-inflammatory effects. Generally, Erianin has been demonstrated to be effective in cutaneous melanoma and ulcerative colitis. However, there is limited knowledge regarding its biological components and the mechanisms by which it prevents and treats AD. To investigate the protective effects of Erianin against AD and to elucidate the potential mechanism of inflammation in AD, with a particular focus on the role of mitochondrial impairment pathways. Combined with vivo and vitro models of inflammation was employed to assess skin conditions, oxidative stress, and mitochondrial dysfunction. The mitochondrial homeostasis was analyzed, and the effects of Erianin treatment on these processes were evaluated using histological analysis, biochemical assays, molecular techniques, and targeting inflammatory cytokines, oxidative stress, mitophagy, and apoptosis. Erianin effectively alleviated AD, and computational simulations suggested a potential interaction with PINK1. Treatment with Erianin significantly reversed these dysfunctional states by promoting mitophagy activity, thereby alleviating mitochondrial dysfunction and reducing ROS levels, which ultimately suppressed apoptosis. These findings demonstrate that Erianin exerts therapeutic potential in AD by targeting mitophagy, with PINK1/Parkin-mediated mitophagy playing a crucial role in the pathogenesis of AD.