In this study, to assess the feasibility of phlorotannins isolated from Ecklonia cava as an inhibitor of melanin formation, we evaluated its inhibitory effects on mushroom tyrosinase and 3-isobutyl-1-methylxanthine (IBMX)-induced melanin formation inhibitory effects in B16F10 melanoma cell. The ethanolic (EtOH) extract and ethyl acetate (EtOAc) soluble fraction obtained from E. cava evidenced a marked inhibitory effect on mushroom tyrosinase at a concentration of 50 μg/mL. Repeated column chromatography of the active EtOAc fraction resulted in the isolation of three phlorotannins. Their structures were elucidated on the basis of spectroscopic techniques [1D and 2D nuclear magnetic resonance (NMR)] and characterized as phloroglucinol (1), dioxinodehydroeckol (2), and 7-phloroeckol (3), respectively. Among the compounds, 7-phloroeckol (3) evidenced more potent tyrosinase inhibitory effect with an IC(50) value of 0.85 μM than arbutin (IC(50) = 243.16 μM) and kojic acid (IC(50) = 40.28 μM), which were used as positive controls. Lineweaver-Burk plots suggest that 7-phloroeckol plays as a noncompetitive inhibitor against tyrosinase. Furthermore, these compounds were evaluated for their inhibitory effects on IBMX-induced melanin formation in B16F10 melanoma cells. Treatment with 7-phloroeckol (6.25-100 μM) resulted in a significant inhibition of melanin production in the melanoma cells. In this study, we suggest that 7-phloroeckol might prove useful as a novel inhibitor of melanin formation in cosmetic applications.

Inflammatory bowel disease (IBD) is a result of chronic inflammation caused, in some part, by dysbiosis of intestinal microbiota, mainly commensal bacteria. Gut dysbiosis can be caused by multiple factors, including abnormal immune responses which might be related to genetic susceptibility, infection, western dietary habits, and administration of antibiotics. Consequently, the disease itself is characterized as having multiple causes, etiologies, and severities. Recent studies have identified >200 IBD risk loci in the host. It has been postulated that gut microbiota interact with these risk loci resulting in dysbiosis, and this subsequently leads to the development of IBD. Typical gut microbiota in IBD patients are characterized with decrease in species richness and many of the commensal, and beneficial, fecal bacteria such as Firmicutes and Bacteroidetes and an increase or bloom of Proteobacteria. However, at this time, cause and effect relationships have not been rigorously established. While treatments of IBD usually includes medications such as corticosteroids, 5-aminosalicylates, antibiotics, immunomodulators, and anti-TNF agents, restoration of gut dysbiosis seems to be a safer and more sustainable approach. Bacteriotherapies (now called microbiota therapies) and dietary interventions are effective way to modulate gut microbiota. In this review, we summarize factors involved in IBD and studies attempted to treat IBD with probiotics. We also discuss the potential use of microbiota therapies as one promising approach in treating IBD. As therapies based on the modulation of gut microbiota becomes more common, future studies should include individual gut microbiota differences to develop personalized therapy for IBD.

No abstract

Unbalanced dietary habits and gut dysmotility are causative factors in metabolic and functional gut disorders, including obesity, diabetes, and constipation. Reduction in luminal butyrate synthesis is known to be associated with gut dysbioses, and studies have suggested that restoring butyrate formation in the colon may improve gut health. In contrast, shifts in different types of gut microbiota may inhibit luminal butyrate synthesis, requiring different treatments to restore colonic bacterial butyrate synthesis. We investigated the influence of high-fat diets (HFD) and low-fiber diets (LFD), and loperamide (LPM) administration, on key bacteria and genes involved in reduction of butyrate synthesis in mice. MiSeq-based microbiota analysis and HiSeq-based differential gene analysis indicated that different types of bacteria and genes were involved in butyrate metabolism in each treatment. Dietary modulation depleted butyrate kinase and phosphate butyryl transferase by decreasing members of the Bacteroidales and Parabacteroides. The HFD also depleted genes involved in succinate synthesis by decreasing Lactobacillus. The LFD and LPM treatments depleted genes involved in crotonoyl-CoA synthesis by decreasing Roseburia and Oscilllibacter. Taken together, our results suggest that different types of bacteria and genes were involved in gut dysbiosis, and that selected treatments may be needed depending on the cause of gut dysfunction.

Rumex crispus is a perennial plant that grows in humid environments across Korea. Its roots are used in traditional Korean medicine to treat several diseases, including diseases of the spleen and skin and several inflammatory pathologies. In this study, different solvent fractions (n-hexane, dichloromethane, ethyl acetate, n-butanol, and aqueous fractions) from an ethanol extract of R. crispus roots were evaluated for the presence and composition of anthraquinone compounds and antioxidants by checking for such things as free radical scavenging activity, and electron and proton atom donating ability. In addition, anti-inflammatory activity was measured by NO scavenging activity and inflammatory cytokine production; furthermore, anti-cancer activity was measured by apoptosis-inducing ability. Polyphenolic and flavonoid compounds were shown to be abundant in the dichloromethane and ethyl acetate fractions, which also exhibited strong antioxidant activity, including free radical scavenging and positive results in FRAP, TEAC, and ORAC assays. HPLC analysis revealed that the dichloromethane fractions had higher anthraquinone contents than the other fractions; the major anthraquinone compounds included chrysophanol, emodin, and physcione. In addition, results of the anti-inflammatory assays showed that the ethyl acetate fraction showed appreciable reductions in the levels of nitric oxide and inflammatory cytokines (TNF-α, IL-1β, and IL-6) in Raw 264.7 cells. Furthermore, the anthraquinone-rich dichloromethane fraction displayed the highest anticancer activity when evaluated in a human hepatoma cancer cell line (HepG2), in which it induced increased apoptosis mediated by p53 and caspase activation.

No abstract

Eight kinds of phenolic acid conjugated chitooligosaccharides (COSs) were synthesized using hydroxyl benzoic acid and hydroxyl cinnamic acid. These phenolic acid conjugated-COSs with different substitution groups, including p-hydroxyl, 3,4-dihydroxyl, 3-methoxyl-4-hydroxyl and 3,5-dimethoxyl-4-hydroxy groups, were evaluated for their inhibitory activities against β-site amyloid precursor protein (APP)-cleaving enzyme (BACE) and inhibited BACE with a ratio of 50.8%, 74.8%, 62.1%, 64.8% and 42.6%, respectively at the concentration of 1,000 μg/mL. BACE is a critical component to reduce the levels of Aβ amyloid peptide in Alzheimer's disease (AD) which is based on the amyloid cascade theory in the brain, as this protease initiates the first step in Aβ production. Among them, Caffeic acid conjugated-COS (CFA-COS) was further analysed to determine mode of inhibition of BACE and it showed non-competitive inhibition. Hence in this study, we suggest that CFA-COS derivatives have potential to be used as novel BACE inhibitors to reduce the risk of AD.

Glycyrrhiza glabra has been used in medicine for thousands of years. Our previous study revealed that the methanolic extract of Glycyrrhiza glabra L. (EGGR) exhibits significant nitric oxide (NO) inhibitory effect on lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophages among 100 other extracts. Accordingly, the aim of the present study was to investigate the potential anti-inflammatory effect of EGGR. The anti-inflammatory effect of EGGR on LPS-stimulated RAW 264.7 macrophages was measured by MTT assay, NO content analysis, reactive oxygen species (ROS) level analysis, RT-PCR, Western blot analysis, and ELISA assay. Low doses of EGGR were non-toxic to macrophages and imparted protective effect against LPS induced cell death. Incubation of LPS-treated macrophages with 100 μg/mL EGGR led to an increase in cell viability from 66.6 to 99%. Moreover, EGGR led to down regulation of NO (NO2+NO3) and ROS productions in a dose-dependent manner. In particular, 100 μg/mL EGGR led to a reduction in NO2+NO3 level from 336.2 to 24.1 pM/mL, and ROS level from 483.5 to 128.4%. Consistent with the result related to NO production, EGGR suppressed the ability of LPS to induce mRNA and protein expressions of nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2) cytokines, tumor necrosis factor-α (TNF-α), interleukin 1β (IL-1β), and IL-6 productions which were analyzed by an ELISA assay. These results provide a comprehensive approach into the anti-inflammatory effect of EGGR on LPS-stimulated macrophages; however, efforts are underway on gaining detailed insight into anti-inflammatory signaling pathways.