Eupafolin nanoparticles protect HaCaT keratinocytes from particulate matter-induced inflammation and oxidative stress

Abstract

Exposure to particulate matter (PM), a major form of air pollution, can induce oxidative stress and inflammation and may lead to many diseases in various organ systems including the skin. Eupafolin, a flavonoid compound derived from Phyla nodiflora , has been previously shown to exhibit various pharmacological activities, including antioxidant and anti-inflammatory effects. Unfortunately, eupafolin is characterized by poor water solubility and skin penetration, which limits its clinical applications. To address these issues, we successfully synthesized a eupafolin nanoparticle delivery system (ENDS). Our findings showed that ENDS could overcome the physicochemical drawbacks of raw eupafolin with respect to water solubility and skin penetration, through reduction of particle size and formation of an amorphous state with hydrogen bonding. Moreover, ENDS was superior to raw eupafolin in attenuating PM-induced oxidative stress and inflammation in HaCaT keratinocytes, by mediating the antioxidant pathway (decreased reactive oxygen species production and nicotinamide adenine dinucleotide phosphate oxidase activity) and anti-inflammation pathway (decreased cyclooxygenase-2 expression and prostaglandin E2 production through downregulation of mitogen-activated protein kinase and nuclear factor-κB signaling). In summary, ENDS shows better antioxidant and anti-inflammatory activities than raw eupafolin through improvement of water solubility and skin penetration. Therefore, ENDS may potentially be used as a medicinal drug and/or cosmeceutical product to prevent PM-induced skin inflammation.

Inhibitory effects of Euphorbia supina on Propionibacterium acnes-induced skin inflammation in vitro and in vivo

“…The fact that IL-1β is secreted in acne skin condition has proposed valuable effects of IL-1β-targeted therapy in patients suffering from anti-inflammatory acne-lesions [ 24 , 26 ]. P. acnes is able to induce the secretion of chemokine CXCL8 in monocytes and keratinocyte [ 25 , 26 ]. We also observed that the mRNA expression levels of cytokines in P. acnes -induced THP-1 cells were decreased by ES treatment.…”

“…Based on our in vivo results, we observed the anti-inflammatory effects of ES in P. acnes -treated animal model. Several studies have described that injection of live P. acnes can lead to the development of inflammatory skin disease in ear-inflammation model [ 26 ]. These studies have demonstrated that live P. acnes treated group has roughly 2 fold increase in ear thickness compared to PBS treated ear [ 26 ].…”

“…Several studies have described that injection of live P. acnes can lead to the development of inflammatory skin disease in ear-inflammation model [ 26 ]. These studies have demonstrated that live P. acnes treated group has roughly 2 fold increase in ear thickness compared to PBS treated ear [ 26 ]. P.acnes can lead to accumulate immune cells such as neutrophil, monocyte, and eosinophil.…”

Glycofullerenes Inhibit Particulate Matter Induced Inflammation and Loss of Barrier Proteins in HaCaT Human Keratinocytes

“…al. [23] and it can be a reliable differentiation model to estimate the inflammatory and repair response, as well as a cell platform for the development of novel treatments and the investigation of disease mechanisms [5,[24][25][26][27][28]. In our The HaCaT cell line was first generated by Boukamp et.…”

“…[23] and it can be a reliable differentiation model to estimate the inflammatory and repair response, as well as a cell platform for the development of novel treatments and the investigation of disease mechanisms [5,[24][25][26][27][28]. In our previous study [27,29], we prepared water-soluble 7, 3 , 4 -trihydroxyisoflavone NPs by using the planetary ball mill method [27] and eupafolin NP delivery system [25,29] to investigate their individual antioxidant and anti-inflammatory activities in PM-induced skin inflammation [5,24,25,29]. The results of our previous study suggested that PM-induced skin cell inflammation regulated the AhR/p47 phox/NADPH oxidase pathway, and subsequently increased ERK1/2, p38/nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), and c-Jun N-terminal kinase (JNK)/Activator protein 1 (AP-1) levels [5].…”