Schisandra chinensiscombats pollution-induced stress

 A possible approach to attack ROS-mediated disorders for both preventive and treatment means is based on the use of substances, which can be found in plants as secondary metabolites, lignans being a promise candidate. The present study was aimed to better understand the cellular mechanisms beyond the oxidative changes induced by urban pollution (Urban dust 1649b, NIST) and the effect of Schisandra chinensis (S. chinensis)extract in reconstructed human epidermis, by a transcriptomic approach and secondly through the evaluation of Nrf2, AhR, NF-kB, and DJ-1pathways using an in vitromodel. Finally, we evaluated the effect of S. chinensison skin hydration, homogeneity, radiance and luminosity in Chengdu (China). Urban dust (80µg.mL-1) was able to activate the cytoplasmic expression of NF-kB and AhR when compared to control. S.chinensis extract attenuated the urban dust-induced oxidative stress, the protective mechanism being associated, at least in part, with the modulation of the Nrf2 and AhR pathways and the activation of DJ-1. S. chinensisextract, named Urbalys® protects from prolonged pollution aggression since it improves hydration, protects skin homogeneity, increases skin radiance and attenuates skin spot intensity after 21 days of pollution exposition.

Atmospheric pollution, which contains a quantity of microscopic suspended particulate matter (PM) carrying various toxic chemical molecules, including polycyclic aromatic hydrocarbons (PAHs), has to be considered nowadays as one of the main characteristics of areas where, worldwide, human population density is at a high level. It affects many rural, industrial, and urban sites1 and has been recognised as the most important environmental health issue in the world. However, few studies concern the impact of air pollution and PM on skin integrity, even if it has been shown that they are significantly associated with weakened barrier function, oxidative stress, skin diseases, and skin ageing.2 PM penetrate skin either through hair follicles or transdermally, and exert its detrimental effects through the generation of reactive oxygen species (ROS), which contributes to extrinsic skin ageing. ROS activate the mitogen-activated protein kinase (MAPK) signaling pathway inducing metalloproteinases (MMPs) production which are closely related to inflammatory skin diseases and skin ageing (Fig 1).1 

PAHs and PM are also well established to activate the aryl hydrocarbon receptor (AhR), a pollutant sensor that constitutes the starting point of the detoxification mechanism, by upregulating the transcription of responsive genes, such as cytochrome P450 superfamily. However, these activations generate ROS. Endogenous defense mechanisms including a fundamental biochemical pathway nuclear factor erythroid 2–related factor 2 (Nrf2) is activated in order to fight the deleterious effects of all pollutants on skin. It is able to help eliminate and inactivate exogenous toxic agents by fundamental biological pathways closely interconnected. Nrf2 is constitutively expressed in the cytoplasm, and its accumulation and activation in the nucleus are favoured in oxidative injury. Additionally, Nrf2 is stabilised by the Parkinson’s-associated protein, (DJ-1), a multifunctional protein expressed in almost all tissues involved in various physiological processes such as transcriptional regulation, anti-oxidative stress reaction, mitochondrial regulation, and signal transduction (Fig 1).3 More precisely, DJ-1 promotes Nrf2 binding to antioxidant response elements by which Nrf2 can regulate the expression of several endogenous antioxidative enzymes and reduce ROS production to protect mitochondria and can also respond to oxidative stress. Under oxidative stress, DJ-1 plays critical antioxidant defence roles by several molecular processes. Additionally, it protects mitochondria by directly maintaining mitochondrial complex I activity and translocating into mitochondria as an endogenous antioxidant.4