Purpose: 6-Shogaol is one of the spicy flavor ingredients of ginger and hydrolysis product of gingerols. The purpose of this study is to investigate the potential of 6-shogaol as a natural cosmetic raw material by examining cell protection and inflammation inhibitory activity in human dermal fibroblasts (HDFs). Methods: To verify the cytoprotective effects of 6-shogaol, cell viability was measured by watersoluble tetrazolium salt (WST-1) assay. To verify the anti-inflammatory effects of 6-shogaol, we performed nuclear factor kappa-light-chain-enhancer of activated B cells (NFΚB) promoter luciferase assay to check the expression of NFΚB. Additionally, the expression of inflammation related gene such as cyclooxygenase 2 (COX2), receptor for advanced glycation end product (RAGE), tumor necrosis factor alpha (TNFΑ), interleukin 6 (IL6), and interleukin 8 (IL8) mRNA was measured by quantitative real-time polymerase chain reaction (qRT-PCR). Results: 6-Shogaol showed no toxicity in HDFs at concentrations of 5, 10, 20, and 40 μM, respectively and the cell viability was increased in a dose dependent manner. qRT-PCR analysis showed 6-shogaol treatment downregulated the expression of NFΚB, COX2, RAGE, TNFΑ, IL6, and IL8 in a dose dependent manner, resulting that 6-shogaol leads to protective activities against inflammatory responses in HDFs. Conclusion: As mentioned above, 6-shogaol restored cell viability and decreased the expression of inflammatory factors in a dose dependent manner. Consequently, these results suggest the possibility of 6-shogaol as cosmetic material preventing skin aging, through identified functions on cytoprotection and anti-inflammation.
Background: Paclitaxel well known as anti-cancer drug has been shown to cause alopecia in chemotherapy. The paclitaxel chemotherapy-mediated alopecia is induced by apoptotic damage in human dermal papilla (HDP) cells. Epigallocatechin-3-gallate (EGCG) inhibits apoptosis against anti-cancer drug such as cisplatin. EGCG, one of the green tea extract ingredients, has been reported to enhance cell viability and to inhibit apoptosis. However, it is unclear that EGCG enhances cell viability and inhibits apoptosis against paclitaxel-induced apoptotic damage in HDP cells. Methods: We show cell viability, cell cycle, and microRNA (miRNA) expression in EGCG-mediated rescue cell to paclitaxel-mediated cell death and growth arrest. Results: EGCG promotes cell survival and cell death inhibitory effects and alteration of miRNA expression in paclitaxelexposed HDP cells were investigated. Firstly, paclitaxel increases apoptosis and EGCG promotes cell survival and represses paclitaxel-induced apoptosis in a dose-dependent manner. Fluorescence-activated cell sorting (FACS) analysis showed that EGCG protects apoptosis in paclitaxel-exposed HDP cells. miRNA microarray analysis was performed and 48 miRNAs changed by EGCG in paclitaxel-exposed HDP cells were identified. In gene ontology analysis in silico, miRNAs regulate apoptosis and cell proliferation-regulated genes, such as BCL2L1, BCL2L2, BBC3, and MDM2. In Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis, miRNAs are related to mitogen-activated protein kinase (MAPK) signaling pathway and Wnt signaling pathway, which regulate apoptosis and cell proliferation. Conclusions: EGCG inhibits apoptosis through regulating miRNA expression related to apoptosis and cell proliferation in paclitaxel-treated HDP cells.
Background: Annona muricata (A. muricata) L. (also known as graviola) contains various antioxidants that have beneficial effects on headaches, hypertension, coughs and asthma. A. muricata L. also has various other physiological effects, such as antispasmodic effects for the treatment of heart conditions, and sedative and nervine effects. In the present study, the effect of A. muricata L. extracts on melanogenesis was investigated and the ensuing inhibitory mechanisms were determined. Methods: The inhibitory effects of A. muricata L. extracts on melanogenesis were initially investigated by measuring melanin contents. Subsequently, the ensuing mechanisms were characterized by determining changes in the activity of tyrosinase, which is the rate-limiting step of melanogenesis. Finally, mRNA and protein expression levels of tyrosinase and the melanogenesis-associated transcription factor (MITF) were determined.
Background: Among various extra stimuli of humans, ultraviolet (UV) has been the most studied factor because it arouses not only internal but also external irritation in the body. UVA, one type of UV rays, has a wavelength between 320 and 400 nm and capacity to penetrate the skin dermal layer. Therefore, studies on how to reduce UVA-induced maleficence have been investigated vibrantly. Angelic acid has been demonstrated to aid in wound healing and exhibited sedative and psychotropic properties. But there have not been sufficient reports whether angelic acid has potential properties in the cosmeceutical aspect. Methods: To investigate protective effects of angelic acid on UVA-induced oxidative stress and disruption of extracellular matrix, researchers analyzed cell proliferation rate, intracellular reactive oxygen species (ROS) scavenging capacity, cellular senescence, transcriptional activity of activating protein-1 (AP-1) transcription factor, and gene expression of antioxidant enzymes and connective tissue-related proteins.
Purpose: The purpose of the present study was to explore the possibility of using sinapic acid as a skin anti-aging cosmetic by demonstrating its antioxidant and anti-inflammatory effects in keratinocytes damaged by ultraviolet (UV) irradiation. Methods: The effects of sinapic acid against oxidative stress were examined in a UVB-induced aging model of human keratinocyte HaCaT cells. The water-soluble tetrazolium salt (WST-1) assay was employed to examine protective effects against UVB. Changes in the concentration of reactive oxygen species (ROS) produced by UVB were measured using 2',7'-dichlorofluorescin diacetate (DCF-DA). Expression of genes associated with anti-oxidant and anti-inflammatory effects were confirmed using quantitative real-time polymerase chain reaction (qRT-PCR). Results: Sinapic acid protected cells from UVB-induced cytotoxicity and reduced ROS produced by UVB irradiation. Expression of genes associated with antioxidant effects including, superoxide dismutase 1 (SOD1), catalase (CAT), glutathione peroxidase 1 (GPX1), nuclear factor (erythroid-derived 2)-like 2 (NRF2), and heme oxygenase 1 (HO1), increased and lipid peroxidation decreased in a dose-dependent manner. The expression of cyclooxygenase 2 (COX2), interleukin 6 (IL6), and interleukin 8 (IL8) genes, which are associated with inflammation, also decreased in a dose-dependent manner. Conclusion: These results suggest that sinapic acid has potential as an anti-aging cosmetic ingredient with anti-oxidant, anti-inflammatory properties against UVB irradiation.
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