No abstract

Kaempferol, a bioflavonoid present in fruits and vegetables, has a variety of antioxidant and anti-inflammatory capacities, but the functional role of kaempferol in oxidative skin dermal damage has yet to be well studied. In this study, we examine the role of kaempferol during the inflammation and cell death caused by 12-O-tetradecanoylphorbol-13-acetate (TPA) in normal human dermal fibroblasts (NHDF). TPA (5 μM) significantly induced cytotoxicity of NHDF, where a robust increase in the interleukin (IL)-1β mRNA among the various pro-inflammatory cytokines. The skin fibroblastic cytotoxicity and IL-1β expression induced by TPA were significantly ameliorated by a treatment with 100 nM of kaempferol. Kaempferol blocked the production of the intracellular reactive oxygen species (ROS) responsible for the phosphorylation of c-jun N-terminal kinase (JNK) induced by TPA. Interestingly, we found that kaempferol inhibited the phosphorylation of nuclear factor-kappa B (NF-κB) and the inhibitor NF-κB (IκBα), which are necessary for the expression of cleaved caspase-3 and the IL-1β secretion in TPA-treated NHDF. These results suggest that kaempferol is a functional agent that blocks the signaling cascade of the skin fibroblastic inflammatory response and cytotoxicity triggered by TPA.

Astaxanthin, a natural antioxidant carotenoid, is a nutrient with diverse health benefits, given that it decreases the risk of oxidative stress-related diseases. In the present study, we investigate the functional role of astaxanthin during autophagic cell death induced by the estrogenic endocrine-disrupting chemical bisphenol A (BPA) in normal human dermal fibroblasts (NHDF). BPA significantly induced apoptotic cell death and autophagy in NHDF. Autophagic cell death evoked by BPA was significantly restored upon a treatment with astaxanthin (10 μM) via the inhibition of intracellular reactive oxygen species (ROS) production. Astaxanthin inhibited the phosphorylation of extracellular signal-regulated kinases (ERK) stimulated by ROS production, but it did not influence the activation of c-Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (MAPK) in BPA-treated NHDF. Astaxanthin abrogated the ERK-mediated activation of nuclear factor-kappa B (NF-κB), which is responsible for the mRNA expression of LC3-II, Beclin-1, Atg12, and Atg14 during apoptotic cell death induced by BPA. These results indicate that astaxanthin is a pharmacological and nutritional agent that blocks the skin fibroblastic autophagic cell death induced by BPA in human dermal fibroblasts.

Tart cherry (Prunus cerasus L.), a medicinal food containing high concentrations of phytochemicals, has a variety of antioxidant activities and health benefits. Here, we investigate the functional effect of tart cherry during apoptotic cell death elicited by airborne particulate matter with a diameter of <10 μm (PM10) in human epidermal keratinocyte HaCaT cells. The PM10 particles significantly induced cytotoxicity in the HaCaT cells. The decrease in cell viability was restored upon treatment with tart cherry extract (200 μg/mL) containing chlorogenic acid, quercetin, and kaempferol. Tart cherry inhibited the intracellular reactive oxygen species (ROS) responsible for the distinctive activations of the extracellular signal-regulated kinase (ERK) and p38 mitogen-activated protein kinase (MAPK) in PM10-treated HaCaT cells. Interestingly, tart cherry significantly inhibited the expression of apoptosis-related genes (B-Cell Lymphoma 2 (Bcl-2), Bcl-2 associated X protein (Bax), and caspase-3) as regulated by the activation of transcription factor nuclear factor-kappa B (NF-κB). These results demonstrate that tart cherry is a medicinal food that blocks the mitochondrial pathway of apoptosis induced by PM10 in human epidermal keratinocytes.

The Republic of Korea (ROK) has officially declared its national vision of green growth, and actively develops and implements policies related to education for sustainable development (ESD)

Grifola frondosa (GF), a species of Basidiomycotina, is widely distributed across Asia and has been used as an immunomodulatory, anti-bacterial, and anti-cancer agent. In the present study, the pharmacological activity of the GF extract against an ecotoxicological industrial chemical, bisphenol A (BPA) in normal human dermal fibroblasts (NHDFs), was investigated. GF extract containing naringin, hesperidin, chlorogenic acid, and kaempferol showed an inhibitory effect on cell death and inflammation induced by BPA in the NHDFs. For the cell death caused by BPA, GF extract inhibited the production of reactive oxygen species responsible for the unique activation of the extracellular signal-regulated kinase. In addition, GF extract attenuated the expression of apoptosis-related proteins (Bax, Bcl-2, and cleaved caspase-3) and the pro-inflammatory cytokine IL-1β by the suppression of the redox-sensitive transcription factor, nuclear factor-kappa B (NF-κB) in BPA-treated NHDFs. For the inflammation triggered by BPA, GF extract blocked the inflammasome-mediated caspase-1 activation that leads to the secretion of IL-1β protein. These results indicate that the GF extract is a functional antioxidant that prevents skin fibroblastic pyroptosis induced by BPA.

Sphingomonas yanoikuyae strain B1 is able to degrade a wider range of aromatic hydrocarbons than S. paucimobilis strain TNE12 can degrade. Various culture techniques were used to corroborate that B1 used m-xylene, biphenyl, toluene, naphthalene, and phenanthrene as sole carbon and energy sources. In contrast, TNE12 could not mineralize m-xylene, biphenyl, toluene, or naphthalene. However, fluoranthene served as carbon and energy source for TNE12 but not B1. Southern blots were performed using the cloned genomic region (approximately 23 kb) containing the degradative genes for the upstream pathways for biphenyl and m-xylene and a TOL plasmid-type meta operon from B1 as a probe against the KpnI restriction-digested total DNA of TNE12. This 23 kb probe hybridized to three KpnI-digested fragments of TNE12 DNA; thus significant homology existed between the aromatic hydrocarbon-degrading genes of B1 and TNE12. Further work with smaller probes revealed, however, that TNE12 DNA fragments did not hybridize with the probe containing the genes encoding for xylene monooxygenase and part of an aromatic dioxygenase. A recombinant plasmid, which contains only the genes for xylene monooxygenase, is able to complement TNE12 on m-xylene. These genes are, therefore, probably missing from TNE12. Hence, TNE12 cannot use monocyclic aromatics whereas B1 can. Pulsed field gel electrophoresis coupled with Southern blotting revealed that the aromatic degradative genes were on an approximately 240 kb plasmid of TNE12; the same genes in B1 are known to be chromosomal.

No abstract