Particulate Matter 2.5 Mediates Cutaneous Cellular Injury by Inducing Mitochondria-Associated Endoplasmic Reticulum Stress: Protective Effects of Ginsenoside Rb1.

Mei Jing Piao,Ao Xuan Zhen,Mee Jung Ahn,Joo Mi Yi,Pincha Devage Sameera Madushan Fernando,Kyoung Ah Kang,Hee Kyoung Kang,Young Sang Koh,Yung Hyun Choi,Jin Won Hyun

doi:10.3390/antiox8090383

Abstract

The prevalence of fine particulate matter-induced harm to the human body is increasing daily. The aim of this study was to elucidate the mechanism by which particulate matter 2.5 (PM2.5) induces damage in human HaCaT keratinocytes and normal human dermal fibroblasts, and to evaluate the preventive capacity of the ginsenoside Rb1. PM2.5 induced oxidative stress by increasing the production of reactive oxygen species, leading to DNA damage, lipid peroxidation, and protein carbonylation; this effect was inhibited by ginsenoside Rb1. Through gene silencing of endoplasmic reticulum (ER) stress-related genes such as PERK, IRE1, ATF, and CHOP, and through the use of the ER stress inhibitor tauroursodeoxycholic acid (TUDCA), it was demonstrated that PM2.5-induced ER stress also causes apoptosis and ultimately leads to cell death; however, this phenomenon was reversed by ginsenoside Rb1. We also found that TUDCA partially restored the production of ATP that was inhibited by PM2.5, and its recovery ability was significantly higher than that of ginsenoside Rb1, indicating that the process of ER stress leading to cell damage may also occur via the mitochondrial pathway. We concluded that ER stress acts alone or via the mitochondrial pathway in the induction of cell damage by PM2.5, and that ginsenoside Rb1 blocks this process. Ginsenoside Rb1 shows potential for use in skin care products to protect the skin against damage by fine particles.

Highlights

Particulate matter 2.5 (PM2.5 ), a major cause of air pollution, is a particle with an aerodynamic size of 2.5 microns or less
Down-regulating several genes related to endoplasmic reticulum (ER) stress, such as PERK, IRE1, ATF6, and CHOP, we further by down-regulating several genes related to ER stress, such as PERK, IRE1, ATF6, and CHOP, we demonstrated that ER stress played an important role in the process of apoptosis induced by PM2.5
We have demonstrated that cell damage caused by PM2.5 is directly induced by ER stress, and by ER stress associated with the mitochondrial pathway (Figure 7c)

Summary

Introduction

Particulate matter 2.5 (PM2.5 ), a major cause of air pollution, is a particle with an aerodynamic size of 2.5 microns or less. Increasing studies have evaluated the effects of PM2.5 exposure on human health, most studies have focused on respiratory diseases such as respiratory inflammation, asthma, and cardiovascular diseases [1,2,3]. Owing to increasingly severe air pollution, the incidence of skin diseases has increased. Ambient air pollution is considered an important risk factor for skin diseases. Diesel exhaust components containing PM2.5 include black carbon, hydrocarbons (C14 –C35 ), heterocyclic polycyclic aromatic hydrocarbons (PAHs), and their derivatives [4].

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