Alpha-Linolenic Acid Alleviates Dextran Sulfate Sodium-Induced Ulcerative Colitis in Mice.

Ulcerative colitis (UC) is a type of inflammatory bowel disease characterized by inflammation of the large intestine, rectal bleeding, and abdominal pain. It can be alleviated by certain bioactive compounds, including α-linolenic acid (ALA), which is a bioactive component in fermented black radish (Raphanus sativus L. var. niger). The aim of this study was to evaluate the anti-inflammatory effects of ALA in dextran sulfate sodium (DSS)-induced UC in mice. UC was induced in C57BL/6 mice by allowing them to freely drink water containing 2.5% DSS for 7 days, followed by oral administration of ALA (30 and 60 mg/kg/day) or vehicle control for 7 days. DSS-induced colitis was evaluated using the Disease Activity Index (DAI) and by measuring colon length and performing a histopathological examination. Compared to the control group, the vehicle-treated group showed a higher DAI score, shorter colon, goblet cell loss, and crypt shortening. The ALA treatment mitigated clinical signs of UC and histopathological changes. Furthermore, it mitigated intestinal inflammation by reducing the expression of ionized calcium binding adaptor molecule 1-positive macrophages in the colon. These results show that ALA alleviates DSS-induced UC by suppressing colon damage, which includes goblet cell loss, crypt shortening, and a reduction of macrophages in the colon.

Inhibitory Effect of Black Radish (Raphanus sativus L. var. niger) Extracts on Lipopolysaccharide-Induced Inflammatory Response in the Mouse Monocyte/Macrophage-Like Cell Line RAW 264.7.

Black radish (Raphanus sativus L. var. niger), which is cultivated worldwide, is used in traditional medicine as it aids liver function, gastric secretion, gallbladder function, and gallstone mitigation. In this study, we examined the anti-inflammatory effects of black radish extract (BRE) on the lipopolysaccharide (LPS)- and interleukin (IL)-6-mediated inflammatory responses in the RAW 264.7 cell lines. Our findings show that BRE significantly ameliorated LPS-induced nitric oxide (NO) release and production of pro-inflammatory cytokines, such as IL-1ß, IL-6, tumor necrosis factor (TNF)-α, and prostaglandin E2. The levels of cyclooxygenase (COX)-2 and inducible NO synthase (iNOS) in LPS-stimulated RAW 264.7 cells were found to be suppressed by BRE. Further, BRE significantly suppressed the LPS-induced expression of mRNAs encoding COX-2, iNOS, IL-1ß, IL-6, and TNF-α in a concentration-dependent manner. BRE treatment significantly inhibited Janus kinase 2 (JAK2) and signal transducer and activator of transcription 3 (STAT3) phosphorylation in IL-6- and LPS-treated RAW 264.7 cells. In addition, BRE decreased the levels of phosphorylated extracellular signal-regulated protein kinases and c-Jun N-terminal kinase under the same conditions. Moreover, BRE induced high nuclear factor erythroid 2-related factor 2 (NRF2) levels and its target gene heme oxygenase 1 (HO-1) in the absence of LPS. These data demonstrate that BRE may be beneficial for treating inflammation through selective immunomodulatory effects, which may be mediated by inhibition of the STAT3/JAK2 and activation of the NRF2/HO-1 signal transduction pathways.

Atractyligenin, a terpenoid isolated from coffee silverskin, inhibits cutaneous photoaging.

Ultraviolet (UV) light exposure-induced photoaging of the skin is a multifactorial process involving both extrinsic and intrinsic cellular mechanisms. Several naturally occurring products are known to confer protection against UV light-induced skin damage. Our preliminary studies confirmed that the ethyl acetate fraction of coffee silverskin exhibits inhibitory effects on matrix metalloproteases (MMPs). Furthermore, we previously isolated and identified atractyligenin, which has MMP-inhibitory activity, from the silverskin ethyl acetate fraction. The aim of this study was to elucidate the anti-photoaging effects of atractyligenin on human dermal fibroblasts and the underlying mechanism. Human dermal fibroblasts were exposed to 8 J/cm2 UVA radiation, and cell viability was analyzed by MTT assay. The fluorescent dye 2', 7'-dichlorodihydrofluorescein diacetate (H2DCF-DA) was used to measure the intracellular reactive oxygen species (ROS) levels. Our study showed that atractyligenin significantly suppressed the expression of UVA-induced MMPs by inhibiting intracellular ROS production. Atractyligenin treatment reduced c-Jun phosphorylation and c-Fos expression by inhibiting the mitogen-activated protein kinase (MAPK) signaling pathway activated by UVA irradiation. Additionally, treatment with atractyligenin contributed to the homeostasis of collagen by restoring the loss of collagen absorption-related receptor Endo180 and altered fibroblast morphology induced by UVA irradiation. These results indicate that atractyligenin isolated from coffee silverskin inhibits multiple pathways in the human skin photoaging process and is thus a potential candidate for treatment or prevention of photoaging.

Black Radish (Raphanus sativus L. var. niger) Extract Mediates Its Hepatoprotective Effect on Carbon Tetrachloride-Induced Hepatic Injury by Attenuating Oxidative Stress.

Nonalcoholic fatty liver disease is a serious liver disorder associated with oxidative stress. Black radish (Raphanus sativus L. var. niger) extract (BRE) can lower the risk of this disease. The hepatoprotective effect of BRE containing 3-(E)-(methylthio)methylene-2-pyrrolidinethione was evaluated in human hepatocyte carcinoma (HepG2) cells and in rat livers with carbon tetrachloride (CCl4)-induced hepatic injury. BRE was administered at 125, 250, 500, and 1000 µg/mL to the oleic acid-induced HepG2 cells. Male Sprague-Dawley rats were randomly divided into seven groups: the control group, BRE group, CCl4 group, and BRE + CCl4 group. BRE was administered orally at 125, 250, 500, and 1000 mg/kg/day once daily for 7 consecutive days, followed by a single oral treatment of 1.5 mL/kg CCl4. Inhibition of lipid accumulation, serum markers of liver injury, histological evaluations, levels of oxidative stress related enzymatic and nonenzymatic antioxidants in HepG2 cells and liver tissue were investigated. The protein expression of main liver P450 isoenzymes such as cytochrome p450(CYP)2E1, the expression of nuclear factor erythroid 2-related factor-2(Nrf-2) and heme oxygenase-1(HO-1) were also studied. BRE has an inhibitory effect on lipid accumulation and caused acute hepatotoxicity manifested by increased levels of lipid peroxidation, serum alanine aminotransferase, and aspartate aminotransferase with corresponding histopathological changes and high levels of oxidative stress. BRE treatment significantly increased the level of CYP2E1, Nrf-2, and HO-1 in a dose-dependent manner. Besides, 3-(E)-(methylthio)methylene-2-pyrrolidinethione significantly increased radical-scavenging effects and the expression of Nrf-2 in oleic acid-treated HepG2 cells. These results suggest that BRE treatment reduces lipid accumulation in oleic acid-induced steatosis of HepG2 cells, and has a hepatoprotective effect against CCl4-induced liver injury in rats, possibly through Nrf-2/HO-1-mediated antioxidant effects.

Geraniin Promotes Recovery of Hematopoietic Cells after Radiation Injury.

Cells of the hematopoietic system are uniquely radiosensitive due to their rapid proliferation. Consequently, immune suppression readily and undesirably results from irradiation. Our previous studies demonstrated that geraniin isolated from Nymphaea tetragona var. angusta (water lily) had a protective effect on the splenocytes and intestinal tract of irradiated mice. This study was designed to assess the effectiveness of geraniin, an ellagitannin isolated from the water lily, in decreasing gamma ray irradiation-induced destruction of the hematopoietic system in mice. Geraniin treatment improved the survival time of bone marrow cells and maintained bone marrow integrity and also up-regulated the expression of stem cell receptors and the extent of cell mitosis. Geraniin also enhanced the proliferation and differentiation of immune cells that had been suppressed by irradiation. These results suggest geraniin is a promising agent for reconstituting hematopoietic cells after exposure to irradiation.

3-Hydroxy-4,7-megastigmadien-9-one, isolated from Ulva pertusa, attenuates TLR9-mediated inflammatory response by down-regulating mitogen-activated protein kinase and NF-κB pathways.

CONTEXT: Seaweeds are rich in bioactive compounds in the form of vitamins, phycobilins, polyphenols, carotenoids, phycocyanins and polysaccharides; many of these are known to have advantageous applications in human health. 3-Hydroxy-4,7-megastigmadien-9-one (comp) was isolated from Ulva pertusa (U. pertusa) Kjellman (Ulvaceae), which is a familiar edible green seaweed. OBJECTIVE: This study evaluates the anti-inflammatory activity of comp in CpG DNA-stimulated bone marrow-derived dendritic cells (BMDCs). MATERIALS AND METHODS: For evaluating the effect of comp on cytokines production, BMDCs were treated with doses of comp (0, 0.5, 1, 2, 5, 10, 25 and 50 µM) for 1 h before stimulation with CpG DNA (1 µM). Cytokine production was measured by ELISA. Western blotting was conducted for evaluating effect of comp (50 µM) on MAPKs and NF-κB pathways. Luciferase reporter gene assay was conducted for effect of comp (0, 5, 10 and 25 µM) on transcriptional activity of AP-1 and NF-κB. RESULTS: Comp exhibited strong inhibition of interleukin (IL)-12 p40, IL-6 and TNF-α cytokine production with IC50 values of 6.02 ± 0.35, 27.14 ± 0.73, and 7.56 ± 0.21 µM, respectively. It blocked MAPKs and NF-κB pathways by inhibiting the phosphorylation of ERK1/2, JNK1/2, p38 and IκBα. In addition, it strongly inhibited the transcriptional activity of AP-1 and NF-κB with IC50 values of 8.74 ± 0.31 and 12.08 ± 0.24 µM, respectively. DISCUSSION AND CONCLUSION: Taken together, these data suggest that comp has a significant anti-inflammatory property and warrants further studies concerning the potential of comp for medicinal use.

Beetroot (Beta vulgaris) rescues mice from γ-ray irradiation by accelerating hematopoiesis and curtailing immunosuppression.

CONTEXT: Beetroot [Beta vulgaris Linné (Chenopodiaceae)], a vegetable usually consumed as a food or a medicinal plant in Europe, has been reported to have antioxidant and anti-inflammatory properties. Since the lymphohematopoietic system is the most sensitive tissue to ionizing radiation, protecting it from radiation damage is one of the best ways to decrease detrimental effects from radiation exposure. OBJECTIVE: In this study, we evaluated the radio-protective effects of beetroot in hematopoietic stem cells (HSCs) and progenitor cells. MATERIALS AND METHODS: Beetroot extract was administered at a dose of 400 mg/mouse per os (p.o.) three times into C57BL/6 mice and, at day 10 after γ-ray irradiation, diverse molecular presentations were measured and compared against non-irradiated and irradiated mice with PBS treatments. Survival of beetroot-fed and unfed irradiated animal was also compared. RESULTS: Beetroot not only stimulated cell proliferation, but also minimized DNA damage of splenocytes. Beetroot also repopulated S-phase cells and increased Ki-67 or c-Kit positive cells in bone marrow. Moreover, beetroot-treated mice showed notable boosting of differentiation of HSCs into burst-forming units-erythroid along with increased production of IL-3. Also, beetroot-treated mice displayed enhancement in the level of hematocrit and hemoglobin as well as the number of red blood cell in peripheral blood. Beetroot diet improved survival rate of lethally exposed mice with a dose reduction factor (DRF) of 1.1. DISCUSSION AND CONCLUSION: These results suggest that beetroot has the potency to preserve bone marrow integrity and stimulate the differentiation of HSCs against ionizing radiation.

Anti-wrinkle effects of Sargassum muticum ethyl acetate fraction on ultraviolet B-irradiated hairless mouse skin and mechanistic evaluation in the human HaCaT keratinocyte cell line.

The present study investigated the photoprotective properties of the ethyl acetate fraction of Sargassum muticum (SME) against ultraviolet B (UVB)­induced skin damage and photoaging in a mouse model. HR­1 strain hairless male mice were divided into three groups: An untreated control group, a UVB­irradiated vehicle group and a UVB­irradiated SME group. The UVB­irradiated mice in the SME group were orally administered with SME (100 mg/kg body weight in 0.1 ml water per day) and then exposed to radiation at a dose of 60­120 mJ/cm2. Wrinkle formation and skin damage were evaluated by analysis of skin replicas, epidermal thickness and collagen fiber integrity in the dermal connective tissue. The mechanism underlying the action of SME was also investigated in the human HaCaT keratinocyte cell line following exposure of the cells to UVB at a dose of 30 mJ/cm2. The protein expression levels and activity of matrix metalloproteinase­1 (MMP­1), and the binding of activator protein­1 (AP­1) to the MMP­1 promoter were assessed in the HaCaT cells using western blot analysis, an MMP­1 fluorescent assay and a chromatin immune­precipitation assay, respectively. The results showed that the mean length and depth of the wrinkles in the UVB­exposed hairless mice were significantly improved by oral administration of SME, which also prevented the increase in epidermal thickness triggered by UVB irradiation. Furthermore, a marked increase in collagen bundle formation was observed in the UVB­treated mice with SME administration. SME pretreatment also significantly inhibited the UVB­induced upregulation in the expression and activity of MMP­1 in the cultured HaCaT keratinocytes, and the UVB­enhanced association of AP­1 with the MMP­1 promoter. These results suggested that SME may be useful as an anti-photoaging resource for the skin.

4-Hydroxy-2,3-Dimethyl-2-Nonen-4-Olide Has an Inhibitory Effect on Pro-Inflammatory Cytokine Production in CpG-Stimulated Bone Marrow-Derived Dendritic Cells.

This study was intended to assess the anti-inflammatory properties of 4-hydroxy-2,3-dimethyl-2-nonen-4-olide (Comp) isolated from Ulva pertusa Kjellman on production of pro-inflammatory cytokines. Comp revealed remarkable inhibitory effects on production of pro-inflammatory cytokines in bone marrow-derived dendritic cells (BMDCs). Comp pre-treatment in the CpG DNA-stimulated BMDCs exhibited strong inhibition of interleukin (IL)-12 p40 and IL-6 production with IC50 values ranging from 7.57 ± 0.2 to 10.83 ± 0.3, respectively. It revealed an inhibitory effect on the phosphorylation of ERK1/2, JNK1/2, and p38, and on activator protein (AP)-1 reporter activity. Comp displayed noteworthy inhibitory effects on phosphorylation and degradation of IκBα, and on NF-κB reporter activity. In summary, these data propose that Comp has substantial anti-inflammatory properties and warrants further study concerning its potential use as a therapeutic agent for inflammation-associated maladies.

Tangeretin triggers melanogenesis through the activation of melanogenic signaling proteins and sustained extracellular signal- regulated kinase in B16/F10 murine melanoma cells.

In order to test the effectiveness of tangeretin at ameliorating melanoma and melanoma-associated depigmentation, western blotting was used to assess the melanin content of treated melanoma cells. Tangeretin, a 4',5,6,7,8-pentamethoxyflavone, was found to trigger intracellular melanin production in a concentration-dependent manner in B16/F10 murine melanoma cells. Melanin content increased 1.74-fold in response to treatment with 25 µM of tangeretin, compared to that in non-treated cells. Examination of melanogenic protein expression showed that tyrosinase, tyrosinase-related protein (TRP)-1, and extracellular signal-regulated kinase (ERK) 1/2 levels increased in a dose-dependent manner. Furthermore, the expression of cyclic adenosine monophosphate response element binding protein (CREB) and microphthalmia transcription factor (MITF) was increased by tangeretin in 1 h and 4 h, respectively. Tangeretin- upregulated melanogenesis was suppressed by ERK 1/2 inhibitor and not by ERK1 inhibitor. These results suggest that tangeretin has therapeutic potential for melanoma and melanoma-associated depigmentation because it can induce hyperpigmentation through the activation of melanogenic signaling proteins and initiation of sustained ERK2 expression.

The ethyl acetate fraction of Sargassum muticum attenuates ultraviolet B radiation-induced apoptotic cell death via regulation of MAPK- and caspase-dependent signaling pathways in human HaCaT keratinocytes.

CONTEXT: Our previous work demonstrated that an ethyl acetate extract derived from Sargassum muticum (Yendo) Fenshol (SME) protected human HaCaT keratinocytes against ultraviolet B (UVB)-induced oxidative stress by increasing antioxidant activity in the cells, thereby inhibiting apoptosis. OBJECTIVE: The aim of the current study was to further elucidate the anti-apoptotic mechanism of SME against UVB-induced cell damage. MATERIALS AND METHODS: The expression levels of several apoptotic-associated and mitogen-activated kinase (MAPK) signaling proteins were determined by western blot analysis of UVB-irradiated HaCaT cells with or without prior SME treatment. In addition, the loss of mitochondrial membrane potential (Δψm) was detected using flow cytometry or confocal microscopy and the mitochondria membrane-permeate dye, JC-1. Apoptosis was assessed by quantifying DNA fragmentation and apoptotic body formation. Furthermore, cell viability was evaluated using the MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) assay. RESULTS: SME absorbed electromagnetic radiation in the UVB range (280-320 nm) of the UV/visible light spectrum. SME also increased Bcl-2 and Mcl-1 expression in UVB-irradiated cells and decreased the Bax expression. Moreover, SME inhibited the UVB-induced disruption of mitochondrial membrane potential and prevented UVB-mediated increases in activated caspase-9 and caspase-3 (an apoptotic initiator and executor, respectively) levels. Notably, treatment with a pan-caspase inhibitor enhanced the anti-apoptotic effects of SME in UVB-irradiated cells. Finally, SME reduced the UVB-mediated phosphorylation of p38 MAPK and JNK, and prevented the UVB-mediated dephosphorylation of Erk1/2 and Akt. DISCUSSION AND CONCLUSION: The present results indicate that SME safeguards HaCaT keratinocytes from UVB-mediated apoptosis by inhibiting a caspase-dependent signaling pathway.

Chemical constituents of Tilia taquetii leaves and their inhibition of MMP-1 expression and elastase activities.

The ethanol extract of Tilia taquetii Schneider leaves was investigated for its anti-wrinkle properties and for the relevant chemical constituents. Phytochemical studies led to the identification of five known compounds, viz. phytol (1), isoquercitrin (2), oleanderolide (3), arjunolic acid (4) and maslinic acid (5) from the extract. Of these, compounds 4 and 5 inhibited the expression of matrix metalloproteinase-1 (MMP-1), an enzyme responsible for the breakdown of collagen fiber. Moreover, compound 5 showed inhibition activity on elastase, a protease enzyme capable of degrading elastin. These results suggest that the extract of T. taquetii containing the triterpenes 4 and 5 could be applied as anti-wrinkle ingredients in cosmetic preparations.

Antioxidant and antiapoptotic effects of pine needle powder ingestion and endurance training in high cholesterol-fed rats.

PURPOSE: Pine needle is a kind of medicinal plant ingested traditionally for a variety of purposes. Therefore, we examined the antioxidant and antiapoptotic capacities of pine needle ingestion in high cholesterol-fed and endurance exercise-trained rats. METHODS: Animals were divided into six groups as; CON: normal diet control group; EX: normal diet and exercise training group; HC: high cholesterol diet group; HCE: high cholesterol diet and exercise training group; HCP: high cholesterol and pine needle group; HCPE: high-cholesterol and pine needle diet with exercise training group, respectively. Each group consisted of seven Sprague-Dawley male rats. The swim-training groups, EX, HCE, and HCPE swam in the swim pool 60 min/d and 5 d/week for 5 weeks. During the rearing periods, freeze-dried pine needle powder mix with 5% of the high cholesterol diet was supplied to the HCP and HCPE groups. Gastrocnemius muscle was used as the skeletal muscle. Malondialdehyde (MDA), Mn-containing superoxide dismutase (Mn-SOD), Cu, Zn containing superoxide dismutase (Cu,Zn-SOD), and glutathione peroxidase (GPx) were analyzed for their antioxidant capacities. Finally, p53, Bcl-2 (B-cell lymphoma 2), caspase-3 protein expression was analyzed to determine antiapoptotic ability. RESULTS: MDA showed low content in HCPE compared to the HC. Mn-SOD, Cu,Zn-SOD, and GPx protein expression was significantly increased by pine needle ingestion and/or exercise training. In addition, suppression of p53 protein expression resulted in Bcl-2 increase followed by caspase-3 decrease with/without pine needle ingestion and exercise training. CONCLUSION: When exercise training in addition to pine needle powder ingestion may be a helpful nutritional regimen to athletes and exercisers.

Acanthoic acid inhibits melanogenesis through tyrosinase downregulation and melanogenic gene expression in B16 melanoma cells.

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.

Apo-9'-fucoxanthinone, isolated from Sargassum muticum, inhibits CpG-induced inflammatory response by attenuating the mitogen-activated protein kinase pathway.

Sargassum muticum (S. muticum) is a brown edible alga and widely distributed in Korea. This report was designed to evaluate the anti-inflammatory properties of apo-9'-fucoxanthinone (APO-9') isolated from S. muticum on pro-inflammatory cytokine production. S. muticum extract (SME) exhibited significant inhibitory effects on pro-inflammatory cytokine production in bone marrow-derived macrophages (BMDMs) and dendritic cells (BMDCs). APO-9' pre-treatment in the CpG DNA-stimulated BMDMs and BMDCs showed a strong dose-dependent inhibitory effect on interleukin (IL)-12 p40, IL-6 and tumor necrosis factor (TNF)-α production with IC50 values ranging from 5.31 to 13.79. It exhibited a strong inhibitory effect on the phosphorylation of ERK1/2 and on activator protein (AP)-1 reporter activity. APO-9' pre-treatment exhibited significant inhibition of CpG DNA-induced production of inducible nitric oxide synthase. Taken together, these data suggest that SME and APO-9' have a significant anti-inflammatory property and warrant further studies concerning the potentials of SME and APO-9' for medicinal use.

Down-regulation of tyrosinase, TRP-1, TRP-2 and MITF expressions by citrus press-cakes in murine B16 F10 melanoma.

OBJECTIVE: To investigate the suitability of citrus-press cakes, by-products of the juice industry as a source for the whitening agents for cosmetic industry. METHODS: Ethylacetate extracts of citrus-press cakes (CCE) were examined for their anti-melanogenic potentials in terms of the inhibition of melanin production and mechanisim of melanogenesis by using Western Blot analysis with tyrosinese, tyrosinase-related protein-1 (TRP-1), TRP2, and microphthalmia-associated transcription factor (MITF) proteins. To apply the topical agents, citrus-press cakes was investigated the safety in human skin cell line. Finally flavonoid analysis of CCE was also determined by HPLC analysis. RESULTS: Results indicated that CCE were shown to down-regulate melanin content in a dose-dependent pattern. The CCE inhibited tyrosinase, TRP-2, and MITF expressions in a dose-dependent manner. To test the applicability of CCE to human skin, we used MTT assay to assess the cytotoxic effects of CCE on human keratinocyte HaCaT cells. The CCE exhibited low cytotoxicity at 50 µg/mL. Characterization of the citrus-press cakes for flavonoid contents using HPLC showed varied quantity of rutin, narirutin, and hesperidin. CONCLUSIONS: Considering the anti-melanogenic activity and human safety, CCE is considered as a potential anti-melanogenic agent and may be effective for topical application for treating hyperpigmentation disorders.

Anti-melanogenesis constituents from the seaweed Dictyota coriacea.

This study was conducted to identify the anti-melanogenesis constituents from a seaweed Dictyota coriacea (Holmes). Three known compounds, viz. 1,9-dihydroxycrenulide (1), epiloliolide (2) and D-mannitol (3), were isolated from the ethanol extract. The melanin synthesis inhibition activities were evaluated using B16F10 melanoma cells for the isolates. Compared with the positive control, arbutin, compounds 1 and 2 exhibited more potency, showing 27.8 and 22.6% inhibition activities at a substrate concentration of 30 microg/mL. Our studies also indicate that these compounds are not cytotoxic. Hence, they might prove to be useful therapeutic agents for treating hyperpigmentation and effective components of whitening cosmetics.

Chondracanthus tenellus (Harvey) hommersand extract protects the human keratinocyte cell line by blocking free radicals and UVB radiation-induced cell damage.

The aim of this study was to investigate the protective effects of the ethanol extract of the red algae Chondracanthus tenellus (Harvey) Hommersand (CTE) on cultured human keratinocyte cell line. The cellular protection conferred by CTE was evidenced by the ability of the extract to absorb ultraviolet B (UVB; 280-320 nm) and to scavenge the radical 1,1-diphenyl-2-picrylhydrazyl, as well as intracellular reactive oxygen species (ROS), induced by either hydrogen peroxide (H(2)O(2)) or UVB radiation. In addition, both superoxide anion generated by the xanthine/xanthine oxidase system and hydroxyl radical generated by the Fenton reaction (FeSO(4) + H(2)O(2)) were scavenged by CTE, as confirmed using electron spin resonance spectrometry. In the human keratinocyte cell line, CTE decreased the degree of injury resulting from UVB-induced oxidative stress to lipids, proteins, and DNA. CTE-treated cells also showed a reduction in UVB-induced apoptosis, as exemplified by fewer apoptotic bodies and less DNA fragmentation. Taken together, these results suggest that CTE confers protection on the human keratinocyte cell line against UVB-induced oxidative stress by absorbing UVB ray and scavenging ROS, thereby reducing injury to cellular constituents.

Acanthoic acid induces cell apoptosis through activation of the p38 MAPK pathway in HL-60 human promyelocytic leukaemia.

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.

Protective effect of the ethyl acetate fraction of Sargassum muticum against ultraviolet B-irradiated damage in human keratinocytes.

The aim of this study was to investigate the cytoprotective properties of the ethyl acetate fraction of Sargassum muticum (SME) against ultraviolet B (UVB)-induced cell damage in human keratinocytes (HaCaT cells). SME exhibited scavenging activity toward the 1,1-diphenyl-2-picrylhydrazyl radicals and hydrogen peroxide (H(2)O(2)) and UVB-induced intracellular reactive oxygen species (ROS). SME also scavenged the hydroxyl radicals generated by the Fenton reaction (FeSO(4) + H(2)O(2)), which was detected using electron spin resonance spectrometry. In addition, SME decreased the level of lipid peroxidation that was increased by UVB radiation, and restored the level of protein expression and the activities of antioxidant enzymes that were decreased by UVB radiation. Furthermore, SME reduced UVB-induced apoptosis as shown by decreased DNA fragmentation and numbers of apoptotic bodies. These results suggest that SME protects human keratinocytes against UVB-induced oxidative stress by enhancing antioxidant activity in cells, thereby inhibiting apoptosis.