Dieckol, an algae-derived phenolic compound, suppresses airborne particulate matter-induced skin aging by inhibiting the expressions of pro-inflammatory cytokines and matrix metalloproteinases through regulating NF-κB, AP-1, and MAPKs signaling pathways

2020 ◽  
Vol 146 ◽  
pp. 111823
Author(s):  
Lei Wang ◽  
WonWoo Lee ◽  
Thilina U. Jayawardena ◽  
Seon-Heui Cha ◽  
You-Jin Jeon
Antioxidants ◽  
2019 ◽  
Vol 8 (9) ◽  
pp. 379 ◽  
Author(s):  
Yong Chool Boo

The skin is directly exposed to the polluted atmospheric environment, and skin diseases, such as atopic dermatitis and acne vulgaris, can be induced or exacerbated by airborne particulate matter (PM). PM can also promote premature skin aging with its accompanying functional and morphological changes. PM-induced skin diseases and premature skin aging are largely mediated by reactive oxygen species (ROS), and the harmful effects of PM may be ameliorated by safe and effective natural antioxidants. Experimental studies have shown that the extracts and phenolic compounds derived from many plants, such as cocoa, green tea, grape, pomegranate, and some marine algae, have antioxidant and anti-inflammatory effects on PM-exposed cells. The phenolic compounds can decrease the levels of ROS in cells and/or enhance cellular antioxidant capacity and, thereby, can attenuate PM-induced oxidative damage to nucleic acids, proteins, and lipids. They also lower the levels of cytokines, chemokines, cell adhesion molecules, prostaglandins, and matrix metalloproteinases implicated in cellular inflammatory responses to PM. Although there is still much research to be done, current studies in this field suggest that plant-derived phenolic compounds may have a protective effect on skin exposed to high levels of air pollution.


2003 ◽  
Vol 70 ◽  
pp. 125-133 ◽  
Author(s):  
Tim E. Cawston ◽  
Jenny M. Milner ◽  
Jon B. Catterall ◽  
Andrew D. Rowan

We have investigated proteinases that degrade cartilage collagen. We show that pro-inflammatory cytokines act synergistically with oncastatin M to promote cartilage collagen resorption by the up-regulation and activation of matrix metalloproteinases (MMPs). The precise mechanisms are not known, but involve the up-regulation of c-fos, which binds to MMP promoters at a proximal activator protein-1 (AP-1) site. This markedly up-regulates transcription and leads to higher levels of active MMP proteins.


Animals ◽  
2021 ◽  
Vol 11 (3) ◽  
pp. 848
Author(s):  
Benjamin Eid ◽  
David Beggs ◽  
Peter Mansell

In 2019–2020, a particularly bad bushfire season in Australia resulted in cattle being exposed to prolonged periods of smoke haze and reduced air quality. Bushfire smoke contains many harmful pollutants, and impacts on regions far from the fire front, with smoke haze persisting for weeks. Particulate matter (PM) is one of the major components of bushfire smoke known to have a negative impact on human health. However, little has been reported about the potential effects that bushfire smoke has on cattle exposed to smoke haze for extended periods. We explored the current literature to investigate evidence for likely effects on cattle from prolonged exposure to smoke generated from bushfires in Australia. We conducted a search for papers related to the impacts of smoke on cattle. Initial searching returned no relevant articles through either CAB Direct or PubMed databases, whilst Google Scholar provided a small number of results. The search was then expanded to look at two sub-questions: the type of pollution that is found in bushfire smoke, and the reported effects of both humans and cattle being exposed to these types of pollutants. The primary mechanism for damage due to bushfire smoke is due to small airborne particulate matter (PM). Although evidence demonstrates that PM from bushfire smoke has a measurable impact on both human mortality and cardiorespiratory morbidities, there is little evidence regarding the impact of chronic bushfire smoke exposure in cattle. We hypothesize that cattle are not severely affected by chronic exposure to smoke haze, as evidenced by the lack of reports. This may be because cattle do not tend to suffer from the co-morbidities that, in the human population, seem to be made worse by smoke and pollution. Further, small changes to background mortality rates or transient morbidity may also go unreported.


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