Weon-Jong Yoon

Evaluation of anti-inflammatory effect of fucoxanthin isolated from brown algae in lipopolysaccharide-stimulated RAW 264.7 macrophages.

In this study, potential anti-inflammatory effect of fucoxanthin isolated from brown algae was assessed via inhibitory effect of nitric oxide (NO) production in lipopolysaccharide (LPS) induced RAW 264.7 macrophage cells. The Myagropsis myagroides was selected for further experiments due to its profound NO inhibitory effect, and was partitioned with different organic solvents. Highest NO inhibitory effect was detected in the chloroform fraction, and the active compound was identified as fucoxanthin, a kind of carotenoid available in brown algae evidenced high correlation with the inhibitory effect of NO production (r(2)=0.9511). Though, fucoxanthin significantly inhibited the NO production, it slightly reduced the prostaglandin E(2) (PGE(2)) production. The inducible nitric oxide synthase (iNOS) and cyclooxygenase 2 (COX-2) protein expressions were inhibited by fucoxanthin. Further, RT-PCR analysis indicated that the iNOS and COX-2 mRNA expressions were suppressed by fucoxanthin. Moreover, the release of tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta), and interleukin-6 (IL-6), and the mRNA expression levels of those cytokines were reduced by the addition of fucoxanthin in a dose-dependent manner. Hence, these results suggest that the use of fucoxanthin may be a useful therapeutic approach for the various inflammatory diseases.

Fucoxanthin inhibits the inflammatory response by suppressing the activation of NF-κB and MAPKs in lipopolysaccharide-induced RAW 264.7 macrophages

It has been previously determined that pro-inflammatory mediators including nitric oxide (NO), prostaglandin E₂ (PGE₂), tumor necrosis factor (TNF)-α, and interleukin (IL)-1β and IL-6 contribute to the courses of a variety of inflammatory diseases. In this study, we evaluated the anti-inflammatory effects of fucoxanthin (FX), a natural biologically active substance isolated from Ishige okamurae, by determining its inhibitory effects on pro-inflammatory mediators in lipopolysaccharide (LPS)-stimulated murine macrophage RAW 264.7 cells. FX induced dose-dependent reductions in the levels of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) proteins and concomitant reductions in the production of NO and PGE₂. Additionally, FX was shown to suppress the production of inflammatory cytokines including IL-1β, TNF-α, and IL-6. Furthermore, FX inhibited the cytoplasmic degradation of inhibitors of B (IκB)-α and the nuclear translocation of p50 and p65 proteins, resulting in lower levels of nuclear factor (NF)-κB transactivation. Additionally, FX was shown to induce a dose-dependent inhibition of the phosphorylation of mitogen-activated protein kinases (MAPKs; JNK, ERK and p38). Collectively, the results of this study demonstrate that FX reduces the levels of pro-inflammatory mediators including NO, PGE₂, IL-1β, TNF-α, and IL-6 via the inhibition of NF-κB activation and the suppression of MAPK phosphorylation in RAW 264.7 cells. These findings reveal, in part, the molecular basis underlying the anti-inflammatory properties of FX.

Artemisia fukudo essential oil attenuates LPS-induced inflammation by suppressing NF-κB and MAPK activation in RAW 264.7 macrophages

In the present study, the chemical constituents of Artemisia fukudo essential oil (AFE) were investigated using GC-MS. The major constituents were alpha-thujone (48.28%), beta-thujone (12.69%), camphor (6.95%) and caryophyllene (6.01%). We also examined the effects of AFE on the production of nitric oxide (NO), prostaglandin E(2) (PGE(2)), tumour necrosis factor (TNF)-alpha, interleukin (IL)-1beta, and IL-6, in lipopolysaccharide (LPS)-activated RAW 264.7 macrophages. Western blotting and RT-PCR tests indicated that AFE has potent dose-dependent inhibitory effects on pro-inflammatory cytokines and mediators. We investigated the mechanism by which AFE inhibits NO and PGE(2) by examining the level of nuclear factor-kappaB (NF-kappaB) activation within the mitogen-activated protein kinase (MAPK) pathway, which is an inflammation-induced signal pathway in RAW 264.7 cells. AFE inhibited LPS-induced ERK, JNK, and p38 phosphorylation. Furthermore, AFE inhibited the LPS-induced phosphorylation and degradation of Ikappa-B-alpha, which is required for the nuclear translocations of the p50 and p65 NF-kappaB subunits in RAW 264.7 cells. Our results suggest that AFE might exert an anti-inflammatory effect by inhibiting the expression of pro-inflammatory cytokines. Such an effect is mediated by a blocking of NF-kappaB activation which consequently inhibits the generation of inflammatory mediators in RAW264.7 cells. AFE may be useful for treating inflammatory diseases.

Abies koreana Essential Oil Inhibits Drug-Resistant Skin Pathogen Growth and LPS-Induced Inflammatory Effects of Murine Macrophage

Since acne vulgaris is the combined result of a bacterial infection and the inflammatory response to that infection, we examined whether Abies koreana essential oil (AKE) possessed anti-inflammatory and antibacterial activities against skin pathogens. In this study, AKE showed excellent antibacterial activities against drug-susceptible and -resistant Propionibacterium acnes and Staphylococcus epidermidis, which are acne-causing bacteria. In addition, AKE reduced the LPS-induced secretion of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), IL-6, NO and PGE2 in RAW 264.7 cells, indicating that it has anti-inflammatory effects. Therefore, we suggest that AKE may be an attractive candidate for promoting skin health.

Oenothera laciniata inhibits lipopolysaccharide induced production of nitric oxide, prostaglandin E2, and proinflammatory cytokines in RAW264.7 macrophages.

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.

Biological Activities of Korean Citrus obovoides and Citrus natsudaidai Essential Oils against Acne-Inducing Bacteria

This study was designed to analyze the chemical composition of Citrus obovoides (Geumgamja) and Citrus natsudaidai (Cheonyahagyul) oils and to test their biological activities. These citrus essential oils were obtained by steam distillation of fruits collected from Jeju Island, Korea, and were analyzed using gas chromatograph (GC)-flame ionization detectors (FID) and GC-MS. Limonene and γ-terpinene were the major components of the two citrus species. To evaluate in vitro anti-acne activity, they were tested against Propionibacterium acnes and Staphylococcus epidermidis, which are involved in acne. The Geumgamja and Cheonyahagyul oils exhibited antibacterial activity against both P. acnes and S. epidermidis. Their effects on DPPH radical scavenging, superoxide anion radical scavenging, and nitric oxide radical were also assessed. Cheonyahagyul and Geumgamja exhibited only superoxide anion radical-scavenging activity. To assess their potential usefulness in future cosmetic product applications, the cytotoxic effects of the two oils were determined by colorimetric MTT assays using two animal cell lines: normal human fibroblasts and HaCaT cells. They exhibited low cytotoxicity at 0.1 μl/ml in both cell lines. In addition, they reduced P. acnes-induced secretion of interleukin-8 (IL-8) and tumor necrosis factor alpha (TNF-α) in THP-1 cells, an indication of anti-inflammatory effects. Therefore, based on these results, we suggest that Geumgamja and Cheonyahagyul essential oils are attractive acne-mitigating candidates for topical application.

Anti-inflammatory effect of essential oil and its constituents from fingered citron (Citrus medica L. var. sarcodactylis) through blocking JNK, ERK and NF-κB signaling pathways in LPS-activated RAW 264.7 cells

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.

Chromene induces apoptosis via caspase-3 activation in human leukemia HL-60 cells

In this study, the potent anti-tumor effects of brown algae on human leukemia HL-60 cells were investigated. The Sargassum siliquastrum extract among the 14 species of brown algae exhibited profound growth inhibitory effect on HL-60 cells in the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, therefore, S. siliquastrum was selected for use in further experiments. The highest inhibitory activity of S. siliquastrum on HL-60 cells was detected in the chloroform fraction, and the active compound was identified as a kind of chromene, sargachromanol E (SE). SE treatment showed significant growth inhibitory effects on HL-60 cells in a dose-dependent manner by inducing apoptosis, as evidenced by the formation of apoptotic bodies, fragmented DNA ladder, and the accumulation of DNA in the sub-G(1) phase of cell cycle. SE induced apoptosis was accompanied by downregulation of Bcl-xL, upregulation of Bax, activation of caspase-3, and cleavage of poly (ADP-ribose) polymerase (PARP). Moreover, z-DEVD-fmk, a caspase-3 inhibitor, significantly inhibited cell cytotoxicity, apoptotic characteristics such as apoptotic bodies, sub-G(1) DNA content, and cleavage of PARP induced by SE. These results suggest that SE exerts its growth inhibitory effects on HL-60 cells through caspase-3-mediated induction of apoptosis. Therefore, SE offers promising chemotherapeuric potential to prevent cancers such as human leukemia.

Anti-inflammatory effect of sargachromanol G isolated from Sargassum siliquastrum in RAW 264.7 cells

A study on the anti-inflammatory activity of brown alga Sargassum siliquastrum led to the isolation of sargachromanol G (SG). In this study, the anti-inflammatory effect and the action mechanism of SG have been investigated in murine macrophage cell line RAW 264.7. SG dosedependently inhibited the production of inflammatory markers [nitric oxide (NO), inducible nitric oxide synthase (iNOS), prostaglandin E2 (PGE2), and cyclooxygenase-2 (COX-2)] and pro-inflammatory cytokines [tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, and IL-6] induced by LPS treatment. To further elucidate the mechanism of this inhibitory effect of SG, we studied LPS-induced nuclear factor-κB (NF-κB) activation and mitogen-activated protein kinases (MAPKs) phosphorylation. SG inhibited the phosphorylation IκB-α and NF-κB (p65 and p50) and MAPK (ERK1/2, JNK, and p38) in a dose dependent manner. These results suggest that the anti-inflammatory activity of SG results from its modulation of pro-inflammatory cytokines and mediators via the suppression of NF-κB activation and MAPK phosphorylation.

Quercitrin protects against ultraviolet B-induced cell death in vitro and in an in vivo zebrafish model

Chronic exposure of skin to ultraviolet (UV) B radiation induces oxidative stress, which in turn, plays a crucial role in the induction of skin aging. The search for strategies to reverse skin aging is being constantly pursued. Here, the cytoprotective effect of quercitrin (QR) on UVB-induced cell injury in HaCaT human keratinocytes and in the zebrafish was investigated. Intracellular reactive oxygen species (ROS) generated by the exposure of HaCaT cells to UVB radiation were significantly decreased after treatment with QR, and significantly so with QR at 50 μM. As a result, QR reduced UVB-induced cell death and apoptosis in HaCaT cells. QR similarly reduced UVB-induced ROS generation and cell death in live zebrafish.