Abstract
The World Health Organization estimates that 7 million people die every year due to pollution exposure. Among the different pollutants to which living organism are exposed, ozone (O3) represents one of the most toxic, because its location which is the skin is one of the direct tissues exposed to the outdoor environment. Chronic exposure to outdoor stressors can alter cutaneous redox state resulting in the activation of inflammatory pathways. Recently, a new player in the inflammation mechanism was discovered: the multiprotein complex NLRP1 inflammasome, which has been shown to be also expressed in the skin. The topical application of natural compounds has been studied for the last 40 years as a possible approach to prevent and eventually cure skin conditions. Recently, the possibility to use blueberry (BB) extract to prevent pollution-induced skin toxicity has been of great interest in the cosmeceutical industry. In the present study, we analyzed the cutaneous protective effect of BB extract in several skin models (2D, 3D, and human skin explants). Specifically, we observed that in the different skin models used, BB extracts were able to enhance keratinocyte wound closure and normalize proliferation and migration responses previously altered by O3. In addition, pretreatment with BB extracts was able to prevent ozone-induced ROS production and inflammasome activation measured as NRLP1-ASC scaffold formation and also prevent the transcripts of key inflammasome players such as CASP1 and IL-18, suggesting that this approach as a possible new technology to prevent cutaneous pollution damage. Our data support the hypothesis that BB extracts can effectively reduce skin inflammation and be a possible new technology against cutaneous pollution-induced damage.
Highlights
Human keratinocytes and skin 3D models (RHE) were pretreated for 24 hours with different doses of BB extracts (0.1, 0.5, 1, 5, and 10 μg/ml for the HaCaT and 10, 50, and 100 μg/ml for the RHE), and cytosolic Lactate Dehydrogenase (LDH) released was evaluated in the supernatant
Our results showed that BB treatment did not affect cellular viability at all the doses tested in both the models
It should be mentioned that the O3 derived from the stratospheric–tropospheric exchanges accounts for 20% of its tropospheric level
Summary
The last estimates of the World Health Organization (WHO) state that 9 out of 10 people living in urban areas are exposed to pollution levels above the healthy recommendations, leading to around 7 million deaths per year [1]. O3 is a secondary pollutant because its formation is due to the interaction between the hydrocarbons and oxides of nitrogen released from car exhaust and sunlight (UV), leading to photochemical smog [2]. The effects of O3 exposure on target organs such as the respiratory tract have been investigated over the last 3 decades, and a strong correlation was Oxidative Medicine and Cellular Longevity clearly revealed between the development of respiratory conditions and ozone exposure. O3 is not a radical per se, it is very reactive and its ability to induce tissue damage is mainly associated with its interaction with the cutaneous lipids present in the stratum corneum (SC), generating molecules such as hydrogen peroxide (H2O2) and lipid peroxidation products (4 hydroxynonenal (4HNE)) that can trigger an inflammatory response [12,13,14,15,16]
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