Ultraviolet (UV) irradiation induces detrimental changes in human skin which result in photoaging. UV-induced intracellular changes cause degradation of extracellular matrix (ECM). UV-stimulated cleavage of collagen in ECM occurs via matrix metalloproteinases (MMPs). (±)-syringaresinol (SYR), a phytochemical which belongs to the lignan group of polyphenols, was investigated for its ability to reverse the UVA-induced changes in human HaCaT keratinocytes and dermal fibroblasts (HDFs) in vitro. Effect of SYR on UVA-induced changes was investigated by production and activation of MMPs and its transcriptional upstream effectors; mitogen-activated protein kinases (MAPKs) and pro-inflammatory mediators. Levels of expression were determined using ELISA, RT-PCR and immunoblotting. UVA irradiation stimulated the production of MMP-1 and inhibited collagen production. SYR treatment suppressed MMP-1 and enhanced collagen production in UVA-irradiated HaCaT keratinocytes and HDFs. SYR repressed the UV-induced phosphorylation of p38, ERK and JNK MAPKs in HaCaT keratinocytes while only suppressing JNK phosphorylation in HDFs. In addition, SYR was able to inhibit UVA-induced production of inflammatory cytokines; TNF-α, COX-2, IL-1β and IL-6. Moreover, SYR suppressed the activator protein-1 (AP-1), a heterodimer of phosphorylated transcription factors c-Jun and c-Fos. SYR-treatment decreased nuclear levels of activated c-Fos and c-Jun as a mechanism to inhibit UVA-induced transcriptional activities leading to MMP-1 production. In conclusion, current results demonstrated that SYR could inhibit UVA-induced upregulation of MMP-1 by suppressing MAPK/AP-1 signaling in HaCaT keratinocytes and HDFs. Therefore, SYR was suggested as a potential compound with antiphotoaging properties against UVA-induced skin aging.
Artemisia princeps, the Korean mugwort, is an edible plant that has various beneficial effects on health, and which has been used as a part of traditional folk medicine. The current study investigated the possible effects of solvent (H2O, n-BuOH, 85% aq. MeOH, and n-hexane) partitioned fractions of A. princeps crude extract (APE) on adipogenic differentiation of 3T3-L1 mouse pre-adipocytes. Characteristics of the differentiated adipocytes were evaluated by Oil red O staining of intracellular lipid droplets, analyzing mRNA and protein levels of peroxisome proliferator-activated receptor (PPAR) γ, CCAAT/enhancer-binding protein (C/EBP) α, and sterol regulatory element-binding protein (SREBP)-1c, and immunoblotting of phosphorylated mitogen-activated protein kinase (MAPK) pathway proteins such as p38, extracellular-signal-regulated kinase (ERK), and c-Jun N-terminal kinase (JNK). Introduction of APE fractions to differentiating adipocytes resulted in lowered lipid accumulation and downregulation of the PPARγ pathway. APE fractions significantly decreased mRNA and protein expression of PPARγ, C/EBPα, and SREBP-1c. Analysis of MAPK pathway activation showed similar results since treatment with the APE fraction treatment decreased levels of phosphorylated p38, ERK, and JNK. Overall, the n-BuOH and n-hexane fractions were observed to be the most active fractions to suppress adipogenesis-related signaling in 3T3-L1 cells. The promising ability of APE fractions to inhibit adipocyte differentiation of 3T3-L1 cells suggest that A. princeps has potential to be utilized as a source of anti-obesity compounds.
Preserved scleral graft with AMT was simple, fast, and effective. It was particularly advantageous when large scleral defects or conjunctival scarring was present. With these therapeutic results, preserved scleral graft with AMT qualifies as a new treatment alternative for scleromalacia.
Limonium tetragonum has been well-known for its antioxidative properties as a halophyte. This study investigated the antimetastasis effect of solvent-partitioned L. tetragonum extracts (LTEs) and isolated compounds on HT1080 mouse melanoma cell model with a focus on matrix metalloproteinase (MMP) activity and TIMP and MAPK pathways. Upregulation and stimulation of MMPs result in elevated degradation of extracellular matrix which is part of several complications such as metastasis, cirrhosis, and arthritis. The anti-MMP capacity of LTEs was confirmed by their MMP-inhibitory effects, regulation of MMP and TIMP expression, and suppression of MAPK pathway. Among all tested LTEs, 85% aq. MeOH and n-BuOH were found to be most active fractions which later yielded two known flavonoid glycosides, myricetin 3-galactoside and quercetin 3-o-beta-galactopyranoside. Anti-MMP potential of the compounds was confirmed by their ability to regulate MMP expression through inhibited MAPK pathway activation. These results suggested that L. tetragonum might serve as a potential source of bioactive substances with effective anti-MMP properties.
Natural products, especially phenols, are promising therapeutic agents with beneficial effects against aging-related complications such as osteoporosis. This study aimed to investigate the effect of quercetin 3-O-β-D-galactopyranoside (Q3G), a glycoside of a common bioactive phytochemical quercetin, on osteogenic and adipogenic differentiation of human bone marrow-derived mesenchymal stromal cells (hBM-MSCs). hBM-MSCs were induced to differentiate into osteoblasts and adipocytes in the presence or absence of Q3G and the differentiation markers were analyzed to observe the effect. Q3G treatment stimulated the osteoblastogenesis markers: cell proliferation, alkaline phosphatase (ALP) activity and extracellular mineralization. In addition, it upregulated the expression of RUNX2 and osteocalcin protein as osteoblastogenesis regulating transcription factors. Moreover, Q3G treatment increased the activation of osteoblastogenesis-related Wnt and bone morphogenetic protein (BMP) signaling displayed as elevated levels of phosphorylated β-catenin and Smad1/5 in nuclear fractions of osteo-induced hBM-MSCs. The presence of quercetin in adipo-induced hBM-MSC culture inhibited the adipogenic differentiation depicted as suppressed lipid accumulation and expression of adipogenesis markers such as PPARγ, SREBP1c and C/EBPα. In conclusion, Q3G supplementation stimulated osteoblast differentiation and inhibited adipocyte differentiation in hBM-MSCs via Wnt/BMP and PPARγ pathways, respectively. This study provided useful information of the therapeutic potential of Q3G against osteoporosis mediated via regulation of MSC differentiation.
derivatives of caffeoylquinic acid (cQa) have been studied and reported as potent bioactive molecules possessing various health benefits including antioxidant and anti-inflammatory activities. In the present study, the protective effect of 3,5-dicaffeoyl-epi-quinic acid (dceQa) isolated from Atriplex gmelinii on uVB-induced damages was investigated in human HaCaT keratinocytes. The effect of DCEQA against UVB-induced oxidative stress-mediated damages was determined measuring its ability to alleviate uVB-induced elevation of oxidative stress, proinflammatory response and antioxidant enzyme suppression through nuclear factor-like 2 (Nrf2). Treatment with DCEQA hindered the generation of intracellular reactive oxygen species. Increased levels of proinflammatory cytokines TNF-α, coX-2, il-6 and il-1β following UVB exposure were suppressed by the introduction of DCEQA. Additionally, DCEQA upregulated the mRNA and protein expression of antioxidant enzymes superoxide dismutase-1 and heme oxygenase-1 which were inhibited under UVB irradiation. Antioxidant enzyme regulation transcription factor Nrf2 was also upregulated in the presence of DCEQA. These results suggest that dceQa prevents photoaging via protection of keratinocytes from uVB irradiation by ameliorating the oxidative stress and pro-inflammatory response.
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