Helicobacter pylori (H. pylori) causes gastritis and gastric cancers. Oxidative stress is involved in the pathological mechanism of H. pylori-induced gastritis and gastric cancer induction. Therefore, reducing oxidative stress may be beneficial for preventing the development of H. pylori-associated gastric diseases. Nuclear factor erythroid-2-related factor 2 (Nrf2) is a crucial regulator for the expression of antioxidant enzyme heme oxygenase-1 (HO-1), which protects cells from oxidative injury. α-Lipoic acid (α-LA), a naturally occurring dithiol, shows antioxidant and anti-inflammatory effects in various cells. In the present study, we examined the mechanism by which α-LA activates the Nrf2/HO-1 pathway, suppresses the production of pro-inflammatory cytokine interleukine-8 (IL-8), and reduces reactive oxygen species (ROS) in H. pylori-infected AGS cells. α-LA increased the level of phosphorylated and nuclear-translocated Nrf2 by decreasing the amount of Nrf2 sequestered in the cytoplasm by complex formation with Kelch-like ECH1-associated protein 1 (KEAP 1). By using exogenous inhibitors targeting Nrf2 and HO-1, we showed that up-regulation of activated Nrf2 and of HO-1 results in the α-LA-induced suppression of interleukin 8 (IL-8) and ROS. Consumption of α-LA-rich foods may prevent the development of H. pylori-associated gastric diseases by decreasing ROS-mediated IL-8 expression in gastric epithelial cells.
Rice koji, used as a starter for maximizing fermentation benefits, produces versatile end products depending on the inoculum microbes used. Here, we performed metabolite profiling to compare rice koji fermented with two important filamentous fungus, Aspergillus oryzae and A. cristatus, during 8 days. The multivariate analyses showed distinct patterns of primary and secondary metabolites in the two kojis. The rice koji fermented with A. oryzae (RAO) showed increased α-glucosidase activity and higher contents of sugar derivatives than the one fermented with A. cristatus (RAC). RAC showed enhanced β-glucosidase activity and increased contents of flavonoids and lysophospholipids, compared to RAO. Overall, at the final fermentation stage (8 days), the antioxidant activities and anti-aging effects were higher in RAC than in RAO, corresponding to the increased metabolites such as flavonoids and auroglaucin derivatives in RAC. This comparative metabolomic approach can be applied in production optimization and quality control analyses of koji products.
A metabolomics approach was used to profile metabolites of Panax notoginseng fermented with Aspergillus cristatus in two ways, liquid-state fermentation (LF-P) and solid-state fermentation (SSF-P) and examine metabolite markers representing antioxidant activity and skin anti-aging. Protopanaxadiol (PPD) and protopanaxatriol (PPT) contents were higher in SSF-P than in LF-P and showed a multiplicative increase over the fermentation period of four days. PPD and PPT levels also correlated with antioxidant and anti-aging effects in skin, based on the mRNA expression of dermal extracellular matrix components. In the bioactivity validation assays, PPD and PPT significantly improved the expression of type-I collagen, fibrillin-1, and elastin in human dermal fibroblasts from both young and old subjects; these were comparable with the effects of the SSF-P extracts. Overall, our results suggest that changes in the metabolites of P. notoginseng fermented with A. cristatus enhance the quality and availability of bioactive compounds associated with skin anti-aging.
Aspergillus cristatus is a beneficial fungus of microbial fermented teas such as China’s Fuzhuan brick tea and Pu-erh tea, and is commonly called golden flower fungus (GFF) because its cleistothecium has a yellow millet or sand grain shape. Since natural materials fermented with GFF exhibit various physiological activities, a new active cosmeceutical ingredient was developed by solid-state fermentation of ginseng, a famous active material for healthy skin, with GFF. The extract of solid-state fermented ginseng with GFF (GFFG) exhibited potent anti-aging efficacy on the skin such as the increase of hyaluronic acid synthesis, aquaporin expression, and mRNA level of filaggrin in HaCaT keratinocyte. GFFG also inhibited the expression of MMP-1 increased by TNF-α in human dermal fibroblast. Sophisticated chromatographic and spectroscopic studies have elucidated isodihydroauroglaucin and flavoglaucin as the metabolites which were not present in ginseng extract nor GFF extract alone. Bioassay of these metabolites revealed that these compounds were part of active principles of GFFG. These results suggest that GFFG would be a potential active ingredient in anti-aging cosmeceutical products.
In recent years, a number of active materials have been developed to provide anti-aging benefits for skin and, among them, peptides have been considered the most promising candidate due to their remarkable and long-lasting anti-wrinkle activity. Recent studies have begun to elucidate the relationship between the secretion of emotion-related hormones and skin aging. Kisspeptin, a neuropeptide encoded by the KISS1 gene, has gained attention in reproductive endocrinology since it stimulates the reproductive axis in the hypothalamus; however, the effects of Kisspeptin on skin have not been studied yet. In this study, we synthesized Kisspeptin-10 and Kisspeptin-E, which are biologically active fragments, to mimic the action of Kisspeptin. Next, we demonstrated the anti-aging effects of the Kisspeptin-mimicking fragments using UV-induced skin aging models, such as UV-induced human dermal fibroblasts (Hs68) and human skin explants. Kisspeptin-E suppressed UV-induced 11 beta-hydroxysteroid dehydrogenase type 1 (11β-HSD1) stimulation leading to a regulation of skin aging related genes, including type I procollagen, matrix metalloproteinases-1 (MMP-1), interleukin-6 (IL-6), and IL-8, and rescued the skin integrity. Taken together, these results suggest that Kisspeptin-E could be useful to improve UV-induced skin aging by modulating expression of stress related genes, such as 11β-HSD1.
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