Abstract

As fullerene-based compound applications have been rapidly increasing in the health industry, the need of biomedical research is urgently in demand. While shungite is regarded as a natural source of fullerene, it remains poorly documented. Here, we explored the in vivo effects of shungite against ultraviolet B- (UVB-) induced skin damage by investigating the physiological skin parameters, immune-redox profiling, and oxidative stress molecular signaling. Toward this, mice were UVB-irradiated with 0.75 mW/cm2 for two consecutive days. Consecutively, shungite was topically applied on the dorsal side of the mice for 7 days. First, we found significant improvements in the skin parameters of the shungite-treated groups revealed by the reduction in roughness, pigmentation, and wrinkle measurement. Second, the immunokine profiling in mouse serum and skin lysates showed a reduction in the proinflammatory response in the shungite-treated groups. Accordingly, the redox profile of shungite-treated groups showed counterbalance of ROS/RNS and superoxide levels in serum and skin lysates. Last, we have confirmed the involvement of Nrf2- and MAPK-mediated oxidative stress pathways in the antioxidant mechanism of shungite. Collectively, the results clearly show that shungite has an antioxidant and anti-inflammatory action against UVB-induced skin damage in hairless mice.

Highlights

  • Ultraviolet (UV) radiation often causes various skin diseases [1]

  • The mice were acclimatized for one week and randomly assigned into six groups: the non-ultraviolet B- (UVB-)irradiated normal control group (NC), and the five UVB-irradiated groups: no treatment group (UV), fullerenetreated group (PC), olive oil-treated group (OIL), mineralrich shungite-treated group (MRS), and mineral-less shungite-treated group (MLS)

  • This study aims to examine whether topical application of MRS and MLS could attenuate the related skin damage caused by UVB irradiation in hairless mice compared to the pure fullerene C60 positive control

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Summary

Introduction

Ultraviolet (UV) radiation often causes various skin diseases [1]. At short-term UV exposure, it could suppress immune function, and at chronic exposure, it could lead to photoaging and/or carcinoma [2, 3]. Skin damage induced by UV irradiation includes photosensitivity, erythema, and DNA damage resulting in invisible changes of cell and gene level [4,5,6]. These involve alterations in immune response such as increased mast cells, outburst of cytokines by keratinocytes, and suppressed levels of Langerhans cells [7,8,9]. The immune dysfunction and ROS would aggravate the skin barrier structure and function, leading to photoaging [15]. Convenient treatments or manipulations of UVinduced skin injury are still limited

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