Anemopsis californica Attenuates Photoaging by Regulating MAPK, NRF2, and NFATc1 Signaling Pathways

Abstract

Long-term exposure of the skin to solar radiation causes chronic inflammation and oxidative stress, which accelerates collagen degradation. This contributes to the formation of wrinkles and dark spots, skin fragility, and even skin cancer. In this study, Anemopsis californica (AC), a herb from North America that is well known for treating microorganism infection and promoting wound healing, was investigated for its photoprotective effects. The biological effects of AC were studied on two in vitro models, namely, lipopolysaccharide (LPS)-induced macrophages and ultraviolet B (UVB)-irradiated dermal fibroblasts, to characterize its underlying molecular mechanisms. The results showed that AC decreased the mRNA levels of inflammatory mediators in sensitized macrophages, including cytokines, inducible nitric oxide synthase (iNOS), and cyclooxygenase (COX-2). Moreover, AC alleviated UVB-induced photoaging in dermal fibroblasts by restoring procollagen synthesis. This resulted from the regulation of excessive reactive oxygen species (ROS) by AC, which was mediated by the activation of the antioxidative system nuclear factor erythroid 2-related factor 2 (NRF2). AC also alleviated oxidative stress and inflammatory responses by inhibiting the phosphorylation of mitogen-activated protein kinase (MAPK) and interfering with the nuclear translocation of the immune regulator nuclear factor of activated T-cells 1 (NFATc1). In conclusion, the protective effects of AC on skin cellular components suggested that it has the potential for use in the development of drugs and cosmetics that protect the skin from UVB-induced chronic inflammation and aging.

Heat-Killed Lacticaseibacillus paracasei Ameliorated UVB-Induced Oxidative Damage and Photoaging and Its Underlying Mechanisms

“…Oxidative damage and photoaging are the main features of skin injury exposed to UVB for a long period of time [ 5 , 6 ]. In recent years, several natural extracts and artificial compounds had been used to treat UVB-induced skin oxidative damage and photoaging [ 7 , 8 , 9 , 10 ].…”

“…Typically, UVB is the most threatening spectrum for skin health [ 3 , 4 ]. Prolonged exposure to UVB could cause skin oxidative damage and photoaging [ 5 , 6 ]. In recent years, some natural extracts and artificial compounds, such as xanthophyll, polyphenol, retinyl palmitate and hydroquinone, had been used as active ingredients in antioxidant and anti-photoaging products [ 7 , 8 , 9 , 10 ].…”

“…Skin oxidative damage could be induced by the increase in reactive oxygen species (ROS) generation upon repeated exposure to UVB irradiation [ 5 ]. A high level of ROS interacts with both lipid peroxidation and protein oxidation, whose biomarkers are malondialdehyde (MDA) and protein carbonyl (PC), respectively [ 27 ].…”

“…Skin photoaging is usually characterized by wrinkle formation and hyperpigmentation [ 5 ]. Type I collagen breakdown is a major cause of skin wrinkle formation [ 25 ].…”

“…It was reported that MMPs levels could be regulated by mitogen-activated protein kinase (MAPK, including ERK, JNK, and p38)/phosphorylating activator protein-1 (AP-1, including c-Jun and c-Fos) signaling pathways in skin photoaging process [ 25 ]. Moreover, skin hyperpigmentation disorder can result from the overproduction of melanin induced by UVB irradiation [ 5 ]. Melanogenesis is a physiological melanin-producing process and occurs through enzyme-catalyzed reactions involved in melanogenic enzymes, such as tyrosinase (TYR), tyrosinase-related protein 1 (TYRP-1) and tyrosinase-related protein 2 (TYRP-2) [ 36 ].…”