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.

We have investigated the cytoprotective effect of eckol, which was isolated from Ecklonia cava, against oxidative stress induced cell damage in Chinese hamster lung fibroblast (V79-4) cells. Eckol was found to scavenge 1,1-diphenyl-2-picrylhydrazyl radical, hydrogen peroxide (H 2 O 2 ), hydroxy radical, intracellular reactive oxygen species (ROS), and thus prevented lipid peroxidation. As a result, eckol reduced H 2 O 2 induced cell death in V79-4 cells. In addition, eckol inhibited cell damage induced by serum starvation and radiation by scavenging ROS. Eckol was found to increase the activity of catalase and its protein expression. Further, molecular mechanistic study revealed that eckol increased phosphorylation of extracellular signal-regulated kinase and activity of nuclear factor j B. Taken together, the results suggest that eckol protects V79-4 cells against oxidative damage by enhancing the cellular antioxidant activity and modulating cellular signal pathway.

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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 CH 2 Cl 2 fractions of S. micracanthum extract were effective inhibitors of LPS-induced NO and prostaglandin E 2 (PGE 2 ) production in RAW 264.7 cells. The inhibitory effects of the hexane and CH 2 Cl 2 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-1ß, and IL-6 in LPSstimulated RAW 264.7 macrophage cells. In these assays, the hexane and CH 2 Cl 2 fractions of S. micracanthum produced dose-dependent decreases in the production and mRNA expression of TNF-, IL-1ß, 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.

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.

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BackgroundThe marine environment is a unique source of bioactive natural products, of which Sargassum muticum (Yendo) Fensholt is an important brown algae distributed in Jeju Island, Korea. S. muticum is a traditional Korean food stuff and has pharmacological functions including anti-inflammatory effects. However, the active ingredients from S. muticum have not been characterized.MethodsBioguided fractionation of the ethanolic extract of S. muticum, collected from Jeju island, led to the isolation of a norisoprenoid. Its structure was determined by analysis of the spectroscopic data. In vitro anti-inflammatory activity and mechanisms of action of this compound were examined using lipopolysaccharide (LPS)-stimulated RAW 264.7 cells through ELISA assays and Western blot analysis.ResultsApo-9′-fucoxanthinone, belonging to the norisoprenoid family were identified. Apo-9′-fucoxanthinone effectively suppressed LPS-induced nitric oxide (NO) and prostaglandin E2 (PGE2) production. This compound also exerted their anti-inflammatory actions by down-regulating of NF-κB activation via suppression of IκB-α in macrophages.ConclusionsThis is the first report describing effective anti-inflammatory activity for apo-9’-fucoxanthinone′-fucoxanthnone isolated from S. muticum. Apo-9′-fucoxanthinone may be a good candidate for delaying the progression of human inflammatory diseases and warrants further studies.