Abstract

Particulate matter (PM), a widespread air pollutant, consists of a complex mixture of solid and liquid particles suspended in air. Many diseases have been linked to PM exposure, which induces an imbalance in reactive oxygen species (ROS) generated in cells, and might result in skin diseases (such as aging and atopic dermatitis). New techniques involving nanomedicine and nano-delivery systems are being rapidly developed in the medicinal field. Fullerene, a kind of nanomaterial, acts as a super radical scavenger. Lower water solubility levels limit the bio-applications of fullerene. Hence, to improve the water solubility of fullerene, while retaining its radical scavenger functions, a fullerene derivative, fullerenol C60(OH)36, was synthesized, to examine its biofunctions in PM-exposed human keratinocyte (HaCaT) cells. The PM-induced increase in ROS levels and expression of phosphorylated mitogen-activated protein kinase and Akt could be inhibited via fullerenol pre-treatment. Furthermore, the expression of inflammation-related proteins, cyclooxygenase-2, heme oxygenase-1, and prostaglandin E2 was also suppressed. Fullerenol could preserve the impaired state of skin barrier proteins (filaggrin, involucrin, repetin, and loricrin), which was attributable to PM exposure. These results suggest that fullerenol could act against PM-induced cytotoxicity via ROS scavenging and anti-inflammatory mechanisms, and the maintenance of expression of barrier proteins, and is a potential candidate compound for the treatment of skin diseases.

Highlights

  • Exposure to air particulate matter (PMs) through inhalation is correlated with pulmonary dysfunction, cardiovascular disease, atherosclerosis, and hepatic fibrogenesis, and with a higher level of morbidity and mortality [1,2]

  • Fullerene can be obtained in skin whitening, sunscreen, or antiaging products

  • This study focuses on the synthesis of water-soluble fullerenes C60(OH)36 and investigates the levels of inflammation and oxidative stress induced by them in response to Particulate matter (PM) exposure

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Summary

Introduction

Exposure to air particulate matter (PMs) through inhalation is correlated with pulmonary dysfunction, cardiovascular disease, atherosclerosis, and hepatic fibrogenesis, and with a higher level of morbidity and mortality [1,2]. Cumulative data from epidemiological studies have shown that exposure to air pollutants could lead to an increase in cardiovascular ischemic events (out-of-hospital cardiac arrests and ischemic heart disease) and enhance atherosclerosis; their possible pathogeneses were investigated [2,3,4,5]. The possible pathological mechanisms for PM-induced skin diseases are linked to an increase in reactive oxygen species (ROS) level and inflammatory activity, and a loss of barrier proteins [7]. PMs can be grouped into four classes based on their size, as ultrafine particles (PM < 0.1 μm), fine particles (PM < 2.5 μm), coarse particles (PM 2.5–10 μm), and thoracic particles (PM >10 μm) [4] Among these air pollutant particles, the fine particles (PM2.5) have the longest atmospheric half-life of a few days to weeks [4]. We had studied PM-induced toxic effects that were attributable to inflammatory and oxidative stress mechanisms in vitro and in vivo [10]

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