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In this study, the safety and functionality of using citrus juice processing waste (CJPW) was confirmed. Large quantities of CJPW are generated on Jeju Island and cause environmental problems. CJPW extract (2,000 mg/kg) was administered intragastrically to male and female Sprague-Dawley (SD) rats for 14 days and the rats were analyzed. No general signs of toxicity were observed in SD rats administered CJPW extract. Feed intake did not differ between experimental and control animals. However, male and female rats administered CJPW extract had greater weight gain (102.9±5.53% and 114.15±6.89%, respectively) compared with the control animals. Higher weight gain was found in male and female experimental animals, but the difference was only significant in female animals. Serum analyses indicated that total protein and albumin, indicators of nutritional status, were significantly increased in animals administered CJPW. Further, serum glucose values were lower in male and female rats treated with CJPW (91.6±9.02% and 69.9±4.11%, respectively) compared with the controls; again, the difference was significant only for female animals. From the results of this study, CJPW can be considered as a safe material that does not induce toxicity in experimental animals. Therefore, CJPW is a potential raw material that can be used as a supplement in animal feed to help improve weight gain and achieve serum glucose con-trol.

This study investigated the safety and functionality of a functional additive for humans and animals from Sargassum horneri (SH) and Ulva australis (UA) waste for recycling marine refuse generated in large quantities in Jeju. Sprague-Dawley rats were orally administered functional additives at 2,000 mg/kg to assess 14-day repeated dose toxicity of the two extracts. For female rats, weight gain after administration of SH was 66.2±18.8% vs. controls. Male rats administered UA showed weight gain of 92.3±8.0% vs. controls. SH and UA significantly decreased serum glucose levels in male rats compared with controls (79.8±11.10% and 76.1±9.67%, respectively). Similarly, significant decrease in serum glucose levels were shown for female rats after administration of SH and UA (79.2±1.58% and 82.8±3.21%, respectively). Furthermore, rats showed significant differences vs. controls in several serological parameters after receiving extracts, however results remained within the normal range. Thus, the SH and UA extracts were considered safe substances that may be used as functional additives to help reduce body weight and serum glucose.

Ecklonia maxima is a brown seaweed, which is abundantly distributed in South Africa. This study investigated an efficient approach using high-performance centrifugal partition chromatography (HPCPC), which has been successfully developed for the isolation and purification of phlorotannins, eckmaxol, and dieckol from the ethyl acetate fraction of E. maxima (EEM). We evaluated EEM for its inhibitory effect against lipopolysaccharide (LPS)-induced inflammatory responses in zebrafish embryos. The separation of eckmaxol and dieckol from samples of EEM using HPCPC was found to be of high purity and yield under an optimal solvent system composed of n-hexane:ethyl acetate:methanol:water (2:7:3:7, v/v/v/v). To evaluate the anti-inflammatory efficacy of EEM containing active compounds, zebrafish embryos exposed to LPS were compared with and without EEM treatment for nitric oxide (NO) production, reactive oxygen species (ROS) generation, and cell death two days after fertilization. These evaluations indicate that EEM alleviated inflammation by inhibiting cell death, ROS, and NO generation induced by LPS treatment. According to these results, eckmaxol and dieckol isolated from brown seaweed E. maxima could be considered effective anti-inflammatory agents as pharmaceutical and functional food ingredients.

Background/aim Lapathoside A, a phenylpropanoid ester, was isolated from the roots of buckwheat by searching for bioactive compounds against human pancreatic cancer cells. Materials and methods Buckwheat root extracts, prepared by 70% ethanol, were separated into n-hexane, methylene chloride, ethyl acetate, n-butanol, and water fraction by solvent partitioning. Seven fractions were obtained from the ethyl acetate fraction by liquid chromatography, and fraction No. 6 contained lapathoside A. The effects of lapathoside A on Panc-1 and SNU-213 human pancreatic cancer cell lines were examined. Results The structure of lapathoside A was determined by liquid chromatography-mass spectrometry, liquid chromatography-tandem mass spectrometry, and nuclear magnetic resonance analysis. Next, we investigated whether lapathoside A has anticancer activity in human pancreatic cancer cell lines (PANC-1 and SNU-213). After treatment with 25 μM lapathoside A, viability of PANC-1 and SNU-213 cells decreased to about 40 and 27%, respectively. In addition, lapathoside A treatment also increased apoptosis while affecting the expression levels of apoptotic proteins. Conclusion The effect of lapathoside A on apoptosis was confirmed in pancreatic cancer cell lines, supporting the application of lapathoside A in the treatment of pancreatic cancer.

Green mandarins are widely consumed unripe as mandarin oranges (Citrus unshiu Marcov.), which exhibit anti-inflammatory and anti-wrinkle effects by inhibiting the production of inflammatory cytokines and matrix metalloproteinase. A randomized, double-blind, placebo-controlled clinical study was performed to verify the skin improvement efficacy and safety of green mandarin extract (PTE). For the standardization of PTE, narirutin was set as a marker compound, and PTE with a constant narirutin content was prepared for the study. After randomizing subjects with periorbital wrinkles, they were orally administered PTE (300 mg/day) or a placebo for 12 weeks. Periorbital wrinkles were measured using PRIMOSCR SF. Skin elasticity, moisture content, transepidermal water loss, and gloss were also measured. In the study results, the depth, volume, and skin roughness of the periorbital wrinkles were significantly improved compared to the control group (p = 0.011, 0.009, and 0.004, respectively). The survey confirmed that the skin condition improved after PTE consumption for 12 weeks. No adverse reactions associated with PTE were observed during the study period. Thus, the results demonstrate that PTE effectively improves UV-induced skin wrinkles. Therefore, it is considered that PTE has sufficient value as a functional food ingredient that can prevent skin aging.

The complete mitochondrial (mt) genome of Stereolepis doederleini was sequenced from a specimen collected in a commercial aquarium in Jeju Island. The sequence was 16,513 base pairs in length and, similar to other vertebrate mt genomes, included 37 mt genes and a noncoding control region; the gene order was identical to that of typical vertebrate mt genome. Mitochondrial genome sequences of 17 species from 12 families were used to reconstruct phylogenetic relationships within the order Pempheriformes. The phylogenetic trees were constructed with three methods (neighbor joining [NJ], maximum likelihood [ML], and Bayesian method) using 12 protein coding genes, but not ND6. In all phylogenetic trees, Pempheriformes were clustered into three strongly supported clades. Two Acropomatidae species (Synagrops japonicus in clade-Ⅰ and Doederleinia berycoides in clade-Ⅲ) were polyphyletic; S. japonicus was close to Lateolabracidae and was the sister of Glaucosomatidae + (Pempheridae/(Percophidae+Creediidae)), and D. berycoides was sister to Howellidae + Epigonidae. All phylogenetic trees supported a sister relationship between Creediidae and Percophidae in clade-Ⅰ. Glaucosomatidae formed a sister clade with Pempheridae. The relationships within clade-Ⅱ, which was composed of four families (Pentacerotidae, Polyprionidae, Banjosidae, and Bathyclupeidae), slightly differed between NJ/ML and BI tree topologies. In clade-Ⅲ, the relationships among Howellidae, Epigonidae, and Acropomatidae were strongly supported.

Lapathoside A, a phenylpropanoid ester, was isolated from the roots of buckwheat by searching for bioactive compounds against human pancreatic cancer cells.Buckwheat root extracts, prepared by 70% ethanol, were separated into n-hexane, methylene chloride, ethyl acetate, n-butanol, and water fraction by solvent partitioning. Seven fractions were obtained from the ethyl acetate fraction by liquid chromatography, and fraction No. 6 contained lapathoside A. The effects of lapathoside A on Panc-1 and SNU-213 human pancreatic cancer cell lines were examined.The structure of lapathoside A was determined by liquid chromatography-mass spectrometry, liquid chromatography-tandem mass spectrometry, and nuclear magnetic resonance analysis. Next, we investigated whether lapathoside A has anticancer activity in human pancreatic cancer cell lines (PANC-1 and SNU-213). After treatment with 25 μM lapathoside A, viability of PANC-1 and SNU-213 cells decreased to about 40 and 27%, respectively. In addition, lapathoside A treatment also increased apoptosis while affecting the expression levels of apoptotic proteins.The effect of lapathoside A on apoptosis was confirmed in pancreatic cancer cell lines, supporting the application of lapathoside A in the treatment of pancreatic cancer.

A phytochemical application of leaves from Ficus erecta var. sieboldii (Miq.) King has not been widely investigated. We determined an anti-inflammatory effect of F. erecta extracts on lipopolysaccharide (LPS)-mediated production through modulation of several pro-inflammatory mediators and prostaglandin E2 (PGE2). Among the F. erecta extracts, the CH2Cl2 fraction (CFE) most effectively suppressed the LPS-mediated production of nitric oxide (NO) in Raw264.7 cells. As determined by immunoblotting and PCR, CFE was shown to have an inhibitory effect on LPS-induced mRNA and protein expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2). In addition, CFE showed significant inhibitory effects on LPS-mediated production of tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6, and PGE2 (P2 production were syringaresinol (C1) and 6,7-furano-5-methoxy hydrocoumaric acid (C2). In conclusion, CFE showed an inhibitory effect on LPS-mediated inflammatory responses by suppressing iNOS, COX-2, TNF-α, IL-1β, and IL-6 production. The compounds C1 and C2 showed strong inhibitory effects on LPS-mediated production of PGE2 and may be applicable as starter compounds for developing anti-inflammatory and anti-nociceptive drugs.

We evaluated the effects of Cynanchum wilfordii (CW) ethanolic extract on blood cholesterol levels in adults with high low-density lipoprotein cholesterol (LDL-C) levels. In a double-blind, randomized, placebo-controlled, parallel trial, 84 subjects were recruited. Participants were randomly divided into two groups with a low-dose (300 mg/d) or high-dose (600 mg/d) of CW. Levels of very low-density lipoprotein (p = 0.022) and triglycerides (p = 0.022) were significantly lower in the low-dose CW group than in the placebo group after 8 weeks. In a subgroup of participants with LDL-C&ge, 150 mg/dL (n = 33), there was a significant decrease in total cholesterol (low-dose, p = 0.012, high-dose, p = 0.021), apolipoprotein B (low-dose, p = 0.022, high-dose, p = 0.016), and cholesteryl ester transfer protein (low-dose, p = 0.037, high-dose, p = 0.016) after 8 weeks of CW. The correlation between changes in total cholesterol and baseline LDL-C levels was significant in the groups that received both doses of CW (low-dose, p = 0.010, high-dose, p = 0.015). These results show that the CW ethanolic extract can regulate blood cholesterol in subjects with LDL-C&ge, 150 mg/dL.

The anti-inflammatory activities of the products of supercritical fluid extraction of Litsea japonica fruit (SFELJF) using supercritical carbon dioxide were investigated. The SFELJF extract dose-dependently inhibited the production of inflammatory markers [nitric oxide (NO), inducible nitric oxide synthase (iNOS), prostaglandin E2 (PGE2), and cyclooxygenase-2 (COX-2)] and proinflammatory cytokines [tumour necrosis factor-α (TNF-α), interleukin (IL)-1β, and IL-6] induced by lipopolysaccharide (LPS) treatment. To further elucidate the mechanisms underlying these inhibitory effects, LPS-induced nuclear factor-κB (NF-κB) activation and mitogen-activated protein kinase (MAPK) phosphorylation were studied. The SFELJF extract inhibited NF-κB (p65 and p50) activation and MAPK [extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK), and p38] phosphorylation in a dose-dependent manner. These results suggest that the anti-inflammatory activities of SFELJF extracts are due to proinflammatory cytokines and mediators via suppression of NF-κB activation and MAPK phosphorylation.

Atherosclerosis is a major cause of coronary heart disease. As a result of the development of atherosclerotic lesions, the walls of blood vessels become thicker and inhibit blood circulation. Atherosclerosis is caused by a high-fat diet and vascular injury. Chronic arterial inflammation plays an important role in the pathogenesis of atherosclerosis. In particular, secretion of the pro-atherogenic cytokine tumor necrosis factor-α induces expression of endothelial adhesion molecules including P-selectin, vascular cell adhesion molecule 1 (VCAM-1), and intercellular adhesion molecule 1 (ICAM-1), which mediate attachment of circulating monocytes and lymphocytes. In this study, we examined the anti-atherosclerotic effect of sorghum, which is known to have anti-oxidant and anti-inflammatory activity. A 50% ethanol extract of Sorghum bicolor L. Moench fermented with Aspergillus oryzae NK (fSBE) was used for experiments. In vitro expression of endothelial adhesion molecules VCAM-1 and ICAM-1 and pro-inflammatory factor cyclooxygenase-2 was significantly decreased and that of the anti-atherogenic factor heme oxygenase-1 significantly increased by fSBE (P

The anti-inflammatory effects of compounds isolated from the Litsea japonica fruit were investigated in LPS-stimulated murine macrophage (RAW 264.7) cells. The results indicated that litsenolide (LN)B2 significantly inhibited the LPS-induced release of pro-inflammatory mediators, such as NO and PGE 2 . LNC2, and, on the other hand, exhibited cytotoxicity at the same concentrations at which it exhibited an inhibitory property. Therefore, only LNB2 was used for further experimentation. LNB2 reduced the LPS-induced production of pro-inflammatory cytokines. We further investigated the mechanism by which LNB2 inhibits pro-inflammatory mediators and cytokines by examining the level of NF-κB and MAPKs phosphorylation, which all serve as key components in inflammation-induced signaling pathways in RAW 264.7 cells. LNB2 inhibited the LPS-induced phosphorylation of NF-κB and MAPKs. These results suggest that LNB2 has an anti-inflammatory effect, inhibiting the production of pro-inflammatory mediators and cytokines via inhibition of NF-κB and MAPK signaling in LPS-stimulated RAW 264.7 cells.

The root of Cynanchum wilfordii (C. wilfordii) contains several biologically active compounds which have been used as traditional medicines in Asia. In the present study, we evaluated the anti-inflammatory effects of an ethanol root extract of C. wilfordii (CWE) on tumor necrosis factor (TNF)-α-stimulated human aortic smooth muscle cells (HASMCs). The inhibitory effects of CWE on vascular cell adhesion molecule (VCAM)-1 expression under an optimum extraction condition were examined. CWE suppressed the expression of VCAM-1 and ICAM-1 and the adhesion of THP-1 monocytes to the TNF-α-stimulated HASMCs. Consistent with the in vitro observations, CWE inhibited the aortic expression of ICAM-1 and VCAM-1 in atherogenic diet-fed mice. CWE also downregulated the expression of nuclear factor-κB (NF-κB p65) and its uclear translocation in the stimulated HASMCs. In order to identify the active components in CWE, we re-extracted CWE using several solvents, and found that the ethyl acetate fraction was the most effective in suppressing the expression of VCAM-1 and ICAM-1. Four major acetophenones were purified from the ethyl acetate fraction, and two components, p-hydroxyacetophenone and cynandione A, potently inhibited the expression of ICAM-1 and VCAM-1 in the stimulated HASMCs. We assessed and determined the amounts of these two active components from CWE, and our results suggested that the root of C. wilfordii and its two bioactive acetophenones may be used for the prevention and treatment of atherosclerosis and vascular inflammatory diseases.

The aim of this study was to investigate the chemical constituents of Lindera erythrocarpa essential oil (LEO) by gas chromatography-mass spectrometry and evaluate their inhibitory effect on the expression of pro-inflammatory mediators in lipopolysaccharide (LPS)-stimulated RAW264.7 cells. Fifteen compounds, accounting for 63.7 % of the composition of LEO, were identified. The main compounds were nerolidol (18.73 %), caryophyllene (14.41 %), α-humulene (7.73 %), germacrene-D (4.82 %), and α-pinene (4.47 %). LEO significantly inhibited the expression of inducible nitric oxide (NO) synthase and cyclooxygenase-2, and subsequent production of NO and prostaglandin E2. In addition, it reduced the release of pro-inflammatory cytokines in LPS-activated RAW264.7 cells. The molecular mechanism underlying the effect of LEO was associated with inhibition of the phosphorylation of mitogen-activated protein kinase (MAPK). Furthermore, LEO inhibited LPS-induced phosphorylation and degradation of inhibitor of kappa B-α, which is required for the activation of the p50 and p65 nuclear factor (NF)-κB subunits in RAW264.7 cells. Taken together, these data suggest that LEO exerted its anti-inflammatory effect by downregulating LPS-induced production of pro-inflammatory mediators through the inhibition of NF-κB and MAPK signaling in RAW264.7 cells.

Fruits of the Litsea family of trees and shrubs contain biologically active compounds, some of which have been used as natural nutrients and flavoring agents in food. In this study, we identified novel anti-nociceptive effects of the 30% ethanol extract, the CH(2)Cl(2) fraction and the associated active components (Hamabiwalactone A and B) from Litsea japonica fruit by using in vivo peripheral and central nervous pain models. In addition, we compared the anti-inflammatory effects of several fractions from L. japonica fruit extracts using lipopolysaccharide (LPS)-stimulated Raw264.7 cells. The CH(2)Cl(2) fraction of L. japonica fruit (LJM) had an optimal combination of anti-inflammatory effects and low cytotoxicity. Dose response studies were performed to determine the inhibitory effects of LJM on the pro-inflammatory enzymes, COX-2/PGE(2) and NO/iNOS, and pro-inflammatory cytokines, IL-1β, IL-6, and TNF-α. Molecular profiling revealed that LJM exerts anti-inflammatory effects through inhibition of NF-κB and JNK/p38 MAPK signaling in LPS-induced macrophages. This study suggests that CH2Cl2 fraction of L. japonica fruit and its bioactive components are potential candidates as anti-inflammatory and analgesic agents (painkillers) for the treatment of inflammatory diseases.

Background Adonis amurensis Regel & Radde, commonly found in East Asia, has been traditionally used to treat cardiac insufficiency and edema. Although this plant extract has been shown to regulate cell growth and neovascularization, the anti-cancer mechanism of A. amurensis has not been fully investigated. Purpose In this study, we aimed to examine the anti-cancer activity of A. amurensis and identify its underlying mechanism. Methods The growth of cancer cells was evaluated by MTT and hollow fiber assays. A cancer xenograft nude mouse model was used to assess the anti-cancer activities in vivo. Autophagic activity was measured by the detection of autophagosome formation and by performing a monodansylcadaverine (MDC) assay. Result A. amurensis extract showed potent anti-cancer activity both in vitro and in vivo. Importantly, the treatment of cancer cells with A. amurensis extract dramatically increased the formation of autophagosomes and was involved in the activation of multiple signaling components including AKT, ERK, and MAPK. Furthermore, we isolated an active ingredient, Multioside, which exhibited strong anti-cancer activity through autophagy. Conclusion A. amurensis displays anti-cancer activity that is mediated by the activation of autophagy, suggesting that A. amurensis could be a useful therapeutic anti-cancer agent.

The hepatoprotective activity of Acanthopanax koreanum Nakai extract (AE) was investigated against D-Galactosamine/Lipopolysaccharide (D-GalN/LPS)-induced liver failure rats compared with that of acanthoic acid (AA) isolated from AE. Although D-GalN/LPS (250 mg/kg body weight/10 μg/kg body weight, i.p.) induced hepatic damage, pretreatments with AE (1 and 3% AE/g day) and AA (0.037% AA, equivalent to 3% AE/g day) alleviated the hepatic damage. This effect was the result of a significant decrease in the activity of alanine transaminase. Concomitantly, both the nitric oxide and IL-6 levels in the plasma were significantly decreased by high-dose AE (AE3) treatment compared to the GalN/LPS control (AE0). This response resulted from the regulation of pro-inflammatory signaling via a decrease in TLR4 and CD14 mRNA levels in the liver. While a high degree of necrosis and hemorrhage were observed in the AE0, pretreatment with AE3 and AA reduced the extent of hepatocyte degeneration, necrosis, hemorrhage and inflammatory cell infiltrates compared to the AE0. In conclusion, these results suggest that especially high-dose AE are capable of alleviating D-GalN/LPS-induced hepatic injury by decreasing hepatic toxicity, thereby mitigating the TLR 4-dependent cytokine release. The anti-inflammatory effect of AE could be contributing to that of AA and AE is better than AA.

We investigated the composition of essential oil from fingered citron (Citrus medica L. var. sarcodactylis) (FCEO) peels by GC–MS and its anti-inflammatory effects on lipopolysaccharide (LPS) – stimulated mouse macrophage (RAW 264.7) cells. Fifteen compounds, representing 98.97% of the essential oil, were tentatively identified; the main constituents were limonene (52.44%) and γ-terpinene (28.41%). FCEO significantly inhibited nitric oxide (NO) and prostaglandin E2 (PGE2) by suppressing the protein expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase (COX)-2, respectively. Additionally, FCEO suppressed the production of tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, and IL-6. FCEO attenuated LPS-induced nuclear factor-κB (NF-κB) activation via inhibition of inhibitor κB-α phosphorylation. Furthermore, FCEO blocked activation of c-Jun N-terminal kinase (JNK) and extracellular signal-regulated kinase (ERK) but not that of p38 mitogen-activated protein kinase. These results indicate that FCEO inhibits LPS-stimulated inflammation by blocking the NF-κB, JNK, and ERK pathways in macrophages, and demonstrate that FCEO possesses anti-inflammatory properties.

The present study was designed to evaluate the molecular mechanisms of the action of acanthoic acid (ACAN) from Acanthopanax koreanum (Araliaceae) against HL-60 human promyelocytic leukaemia cells. ACAN reduced the proliferation of HL-60 cells in a dose- and time-dependent manner accompanied by the induction of apoptosis. Possible mechanisms of ACAN-induced apoptosis were also examined. The results showed that ACAN-induced the phosphorylation of members of the mitogen-activated protein kinase (MAPK) family, c-Jun N-terminal kinase (JNK), p38 MAPK (p38), and extracellular signal-regulated kinase (ERK). A specific p38 MAPK inhibitor (SB203580) significantly blocked ACAN-induced apoptosis and cell viability, whereas an ERK inhibitor (PD98059) and JNK inhibitor (SP600125) had no effect. Moreover, ACAN induced the cleavage of caspase-3 and poly-ADP-ribose polymerase (PARP), and decreased the level of Bcl-xL, but these effects were inhibited by SB203580 pre-treatment. These results strongly suggest that ACAN may have cancer chemopreventive and therapeutic potential, due to its ability to activate the p38 MAPK-mediated signalling pathways.

In this study, we investigate a plant commonly used in herbal medicines, Lycopodium serratum , which is believed to have anti-cancer properties. An alcoholic extract of L. serratum (LSE) was investigated for its ability to induce apoptosis in cultured human promyelocytic leukemia HL-60 cells. Treatment of HL-60 cells with various concentrations of LSE (6–100 μg/mL) resulted in a sequence of events characteristic of apoptosis, including loss of cell viability, morphological changes, and increased sub-G 1 DNA content. Serratenediol (SE), a known biologically active agent, was isolated from MC fraction of LSE and was able to demonstrate significant and dose-dependent growth inhibitory effects on HL-60 cells. Similar to the effects observed with the crude LSE, the SE-related effects included the formation of apoptotic bodies and fragmented DNA, as well as the accumulation of DNA in the sub-G 1 phase of the cell cycle. Analysis of the mechanism of these events indicated that SE treated cells had an increased ratio of Bax/Bcl-xL, released the cytochrome c , activated caspase-9, -3, and cleaved poly-ADP-ribose polymerase (PARP); these observations are hallmarks of apoptotic events. Thus, the results suggest that SE can induce apoptosis via regulating the ratio of Bax/Bcl-xL in HL-60 cell lines.

As part of our ongoing alternative medicine program, we have directed our attention toward the identification of edible seaweeds in Korea. Here we report on the anti-inflammatory activities of Ecklonia stolonifera. The present study was undertaken to elucidate the pharmacological and biological effects of E. stolonifera extracts on the production of inflammatory mediators in macrophages. The results indicate that the hexane fraction of E. stolonifera extract (ESH) is an effective inhibitor of lipopolysccharide (LPS)-induced NO, prostaglandin E2, and proinflammatory cytokine production in RAW 264.7 cells. These inhibitory effects of ESH were accompanied by decreases in the expression of inducible nitric oxide synthase and cyclooxygenase-2 proteins. Furthermore, ESH inhibited the LPS-induced phosphorylation and degradation of IκB-α, which is required for the nuclear translocations of the p50 and p65 nuclear transcription factor kappa-B (NF-κB) subunits in RAW 264.7 cells. Our results suggest that ESH might exert an anti-inflammatory effect by inhibiting the expression of pro-inflammatory cytokines. Such an effect is mediated by a blocking of NF-κB activation, which consequently inhibits the generation of inflammatory mediators in RAW264.7 cells. Through HPLC fingerprinting of the E. stolonifera extract, the phloroglucinol was also identified and quantified as standard substance. Moreover, we tested the potential application of E. stolonifera extract as a cosmetic material by performing human skin primary irritation tests. In these assays, E. stolonifera extracts did not induce any adverse reactions. Based on these results, we suggest that E. stolonifera extracts be considered possible anti-inflammatory candidates for topical application.

Despite its beneficial role in host defense mechanisms, excessive nitric oxide (NO) production by activated macrophages has been implicated in several inflammatory diseases. To clarify the mechanisms of the anti-inflammatory activities of Sargassum micracanthum, we evaluated whether extracts of S. micracanthum could modulate the production of NO by activated macrophages. S. micracanthum were extracted with 80% EtOH. The extract was then successively partitioned with hexane, CH 2 Cl 2 , EtOAc, BuOH, and water. The results indicate that the hexane and CH2Cl2 fractions of S. micracanthum extract were effective inhibitors of LPS-induced NO and prostaglandin E2 (PGE2) production in RAW 264.7 cells. The inhibitory effects of the hexane and CH2Cl2 fractions of S. micracanthum were accompanied by dosedependent decreases in the production of iNOS and COX-2 proteins and iNOS and COX-2 mRNA expression. To test the inhibitory effects of S. micracanthum fractions on other cytokines, we also performed ELISA and RT-PCR assays for TNF- , IL-1s, and IL-6 in LPSstimulated RAW 264.7 macrophage cells. In these assays, the hexane and CH2Cl2 fractions of S. micracanthum produced dose-dependent decreases in the production and mRNA expression of TNF- , IL-1s, and IL-6. To test the potential application of S. micracanthum extract as a cosmetic material, we also performed MTT assays on human dermal fibroblast cells, as well as primary skin irritation tests. In these assays, S. micracanthum extracts did not induce any adverse reactions. Based on these results, we suggest that S. micracanthum extracts may be considered potential anti-inflammatory candidates for topical application.

We elucidated the pharmacological and biological effects of Oenothera laciniata extracts on the production of inflammatory mediators in macrophages. The CH(2)Cl(2) fraction of O. laciniata extract effectively inhibited LPS-induced NO, PGE(2), and proinflammatory cytokine production in RAW264.7 cells. These inhibitory effects of the CH(2)Cl(2) fraction of O. laciniata were accompanied by decreases in the expression of iNOS and COX-2 proteins and iNOS, COX-2, TNF-alpha, IL-1beta, and IL-6 mRNA. Asiatic acid and quercetin were present in the HPLC fingerprint of the O. laciniata extract. We tested the potential application of O. laciniata extract as a cosmetic material by performing primary skin irritation tests. In New Zealand white rabbits, primary irritation tests revealed that application of O. laciniata extracts (1%) did not induce erythema or edema formation. Human skin primary irritation tests were performed on the normal skin (upper back) of 30 volunteers to determine if any material in O. laciniata extracts had irritation or sensitization potential. In these assays, O. laciniata extracts did not induce any adverse reactions. Based on these results, we suggest that O. laciniata extracts be considered possible anti-inflammatory candidates for topical application.

Osteoarthritis (OA) is a degenerative chronic disease that affects various tissues surrounding the joints, such as the subchondral bone and articular cartilage. The onset of OA is associated with uncontrolled catabolic and anabolic remodeling processes of the joints, including the cartilage and subchondral bone, to adapt to local biological and biochemical signals. In this study, we determined whether 70% ethanolic (EtOH) extract of Litsea japonica fruit (LJFE) had beneficial effects on the articular cartilage, including structural changes in the tibial subchondral bone, matrix degradation, and inflammatory responses, in OA by using a rat model of monosodium iodoacetate-induced OA. Our results showed that administration of LJFE increased the bone volume and cross-section thickness, but the mean number of objects per slice in this group was lower than that in the OA control (OAC) group. In addition, the LJFE decreased the expression of inflammatory cytokines. Compared to the OAC group, the group treated with high doses of LJFE (100 and 200 mg/kg) showed a more than 80% inhibition of the expression of matrix metalloproteinases and tissue inhibitors of metalloproteinases. Our results suggest that LJFE can be used as a potential anti-osteoarthritic agent.

During our on-going screening program designed to isolate natural compounds from marine environments, we isolated isoketochabrolic acid (IKCA) from Sargassum micracanthum, an important brown algae distributed in Jeju Island, Korea. Furthermore, we evaluated the inhibitory effects of IKCA on nitric oxide (NO) production in lipopolysaccharide (LPS)-triggered macrophages. IKCA strongly inhibited NO production, with an IC50 value of 58.31 μM. Subsequent studies demonstrated that IKCA potently and concentration-dependently reduced prostaglandin E2 (PGE2), tumor necrosis factor-alpha (TNF-α), interleukin (IL)-1β, and IL-6 cytokine production. In conclusion, to the best of our knowledge, this is the first study to show that IKCA isolated from S. micracanthum has a potent anti-inflammatory activity. Therefore, IKCA might be useful as an anti-inflammatory health supplement or functional cosmetics., EXCLI Journal;Vol. 14, 2015

Ultraviolet (UV) radiation stimulates the expression of matrix metalloproteinases (MMPs) and inflammatory cytokines. These signaling pathways participate in the degradation of the extracellular matrix and induce inflammatory responses that lead to photoaging. This study evaluated the antioxidant activity and the effect on MMPs and procollagen of putgyul extract in vitro. The anti-photoaging activity of putgyul extracts was estimated in vivo using hairless mice (HR-1). The putgyul extracts reduced MMP-1 production and increased the content of procollagen type I carboxy-terminal peptide in human dermal fibroblasts. Ultravilot-B (UVB)-induced expression of inflammatory cytokines and MMPs was detected in mice, and putgyul extracts suppressed the expression. These results suggest that putgyul extract inhibits photoaging by inhibiting the expression of MMPs that degrade collagen and inhibiting cytokines that induce inflammatory responses. The mouse model also demonstrated that oral administration of putgyul extracts decreased wrinkle depth, epidermal thickness, collagen degradation, and trans-epidermal water loss, and increased β-glucosidase activity on UVB exposed skin. Putgyul extract protects against UVB-induced damage of skin and could be valuable in the prevention of photoaging.

powder (4.0 kg) was extracted using 80% MeOH toprovide the oily material (1.0 kg). The extract was partition-ed between water and ethyl acetate. The obtained ethylacetate fraction was successively column chromatographedusing celite and then sephadex LH-20 to give 11 fractions.The eighth fraction was further purified by using Prep-LC(LC-9104, JAI) system, yielded compound

The aim of this study was to investigate the in vitro inhibitory effects of acanthoic acid (ACAN), isolated from Acanthopanax koreanum, on melanogenesis and its related enzymes such as tyrosinase, tyrosinase-related protein (TRP)-1, and TRP-2 in B16 melanoma cells. We found that ACAN significantly attenuates melanin synthesis and reduces the activity of intracellular tyrosinase, the rate-limiting melanogenic enzyme. Western blot analysis showed that ACAN also decreases tyrosinase, TRP-1, and TRP-2 protein expression. In addition, ACAN significantly decreased the expression of microphthalmia-associated transcription factor (MITF), a key regulator of melanogenesis. These results indicate that ACAN effectively inhibits melanin biosynthesis through down-regulation of MITF and thus could be useful as a new skin-whitening agent.

During our ongoing screening program designed to determine the anti-inflammatory potential of natural compounds, we isolated sargachromenol fromSargassum micracanthum. In the present study, we investigated the anti-inflammatory effects of sargachromenol on lipopolysaccharide (LPS)-induced inflammation in murine RAW 264.7 macrophage cells and the underlying mechanisms. Sargachromenol significantly inhibited the LPS-induced production of nitric oxide (NO) and prostaglandin E2(PGE2) in a dose-dependent manner. It also significantly inhibited the protein expression of inducible NO synthase (iNOS) and cyclooxygenase-2 (COX-2) in a dose-dependent manner in LPS-stimulated macrophage cells. Further analyses showed that sargachromenol decreased the cytoplasmic loss of inhibitorκBα(IκBα) protein. These results suggest that sargachromenol may exert its anti-inflammatory effects on LPS-stimulated macrophage cells by inhibiting the activation of the NF-κB signaling pathway. In conclusion, to our knowledge, this is the first study to show that sargachromenol isolated fromS. micracanthumhas an effective anti-inflammatory activity. Therefore, sargachromenol might be useful for cosmetic, food, or medical applications requiring anti-inflammatory properties.

powder (4.0 kg) was extracted using 80% MeOH toprovide the oily material (1.0 kg). The extract was partition-ed between water and ethyl acetate. The obtained ethylacetate fraction was successively column chromatographedusing celite and then sephadex LH-20 to give 11 fractions.The eighth fraction was further purified by using Prep-LC(LC-9104, JAI) system, yielded compound

We investigated the cytoprotective effect of phloroglucinol, which was isolated from Ecklonia cava (brown alga), against oxidative stress induced cell damage in Chinese hamster lung fibroblast (V79-4) cells. Phloroglucinol was found to scavenge 1,1-diphenyl-2-picrylhydrazyl (DPPH) radical, hydrogen peroxide (H(2)O(2)), hydroxy radical, intracellular reactive oxygen species (ROS), and thus prevented lipid peroxidation. As a result, phloroglucinol reduced H(2)O(2) induced apoptotic cells formation in V79-4 cells. In addition, phloroglucinol inhibited cell damage induced by serum starvation and radiation through scavenging ROS. Phloroglucinol increased the catalase activity and its protein expression. In addition, catalase inhibitor abolished the protective effect of phloroglucinol from H(2)O(2) induced cell damage. Furthermore, phloroglucinol increased phosphorylation of extracellular signal regulated kinase (ERK). Taken together, the results suggest that phloroglucinol protects V79-4 cells against oxidative damage by enhancing the cellular catalase activity and modulating ERK signal pathway.

In the present study, triphlorethol-A, a phlorotannin, was isolated from Ecklonia cava and its antioxidant properties were investigated. Triphlorethol-A was found to scavenge intracellular reactive oxygen species (ROS) and 1,1-diphenyl-2-picrylhydrazyl (DPPH) radical, and thus prevented lipid peroxidation. The radical scavenging activity of triphlorethol-A protected the Chinese hamster lung fibroblast (V79-4) cells exposed to hydrogen peroxide (H2O2) against cell death, via the activation of ERK protein. Furthermore, triphlorethol-A reduced the apoptotic cells formation induced by H2O2. Triphlorethol-A increased the activities of cellular antioxidant enzymes like, superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx). Hence, from the present study, it is suggestive that triphlorethol-A protects V79-4 cells against H2O2 damage by enhancing the cellular antioxidative activity.