Abstract
Gardeniae Fructus (GF) is the fruit of Gardenia jasminoides Ellis and is traditionally prescribed to treat pyogenic infections and skin ulcers. This study investigated the protective effects of GF and the underlying mechanism responsible for these effects on diesel exhaust particulate matter- (DEP-) induced skin damage. The protective effects of an ethanolic extract of GF (GFE) and its constituents (geniposidic acid, gardenoside, geniposide, chlorogenic acid, and genipin) were examined by analyzing reactive oxygen species (ROS) production, apoptosis, and tight junction (TJ) protein expression in HaCaT cells. Treatment with GFE dose-dependently inhibited intracellular ROS production and apoptosis by regulating the protein expressions of Bax, Bcl-2, and cytochrome C in DEP-stimulated (100 μg/ml) HaCaT cells. Mechanistic studies revealed that the protective effects of GFE were related to its activation of Nrf2 and HO-1 signaling in HaCaT cells. Geniposide, a main constituent of GFE, enhanced the expression of occludin in DEP-stimulated HaCaT cells. Furthermore, topical application of geniposide reduced the expressions of 8-OHdG and Bax and increased the expression of occludin in the dorsal skin lesions of DEP-stimulated mice. Gardeniae Fructus and its main component geniposide are potential candidates for the repair of DEP-induced skin damage due to their antioxidant and antiapoptotic activities.
Highlights
Air pollution is cited as a major risk factor of skin aging as it promotes pigmentation and wrinkle formation [1, 2]
Gardeniae Fructus (GF) is the fruit of Gardenia jasminoides Ellis and is traditionally prescribed to treat pyogenic infections and skin ulcers [9]. e GF has been included in a traditional herbal formula which is commonly used for the treatment of eczema [10]. e antiallergic effects of GF and its constituent, geniposide, in a mouse model of Dermatophagoides farinae extract-induced atopic dermatitis have been recently reported [11]
Oxidative stress caused by the excessive generation of reactive oxygen species (ROS) is a critical event in tissues exposed to Diesel Exhaust Particulate (DEP) and damages DNA and proteins, which can lead to apoptosis and tissue destruction [15]. e present study shows DEP dose-dependently increased intracellular ROS synthesis in HaCaT keratinocytes and that GF obtained (GFE) inhibited this diesel exhaust particulate matter- (DEP-)induced ROS generation and increased nuclear localization of Nrf2 and upregulated the expressions of antioxidant enzymes like HO-1
Summary
Air pollution is cited as a major risk factor of skin aging as it promotes pigmentation and wrinkle formation [1, 2]. Air pollution causes or aggravates inflammatory skin conditions such as atopic dermatitis, acne, and psoriasis [3], and as a result, antipollution cosmetics are being actively developed. It has been established that these types of products protect the skin from oxidative stress and inflammation-induced damage [4, 5]. According to a recent study, airborne PM with diameters
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