Sargassum fulvellumProtects HaCaT Cells and BALB/c Mice from UVB-Induced Proinflammatory Responses

Abstract

Ultraviolet (UV) radiation has been reported to induce cutaneous inflammation such as erythema and edema via induction of proinflammatory enzymes and mediators. Sargassum fulvellum is a brown alga of Sargassaceae family which has been demonstrated to exhibit antipyretic, analgesic, antiedema, antioxidant, antitumor, fibrinolytic, and hepatoprotective activities. The purpose of this study is to investigate anti-inflammatory effects of ethylacetate fraction of ethanol extract of Sargassum fulvellum (SFE-EtOAc) in HaCaT keratinocytes and BALB/c mice. In HaCaT cells, SFE-EtOAc effectively inhibited UVB-induced cytotoxicity (60 mJ/cm2) and the expression of proinflammatory proteins such as cyclooxygenase-2 (COX-2), tumor necrosis factor-α (TNF-α), and inducible nitric oxide synthase (iNOS). Furthermore, SFE-EtOAc significantly reduced UVB-induced production of proinflammatory mediators including prostaglandin E2 (PGE2) and nitric oxide (NO). In BALB/c mice, topical application of SFE-EtOAc prior to UVB irradiation (200 mJ/cm2) effectively suppressed the UVB-induced protein expression of COX-2, iNOS, and TNF-α and subsequently attenuated generation of PGE2 and NO as well. In another experiment, SFE-EtOAc pretreatment suppressed UVB-induced reactive oxygen species production and exhibited an antioxidant potential by upregulation of antioxidant enzymes such as catalase and Cu/Zn-superoxide dismutase in HaCaT cells. These results suggest that SFE-EtOAc could be an effective anti-inflammatory agent protecting against UVB irradiation-induced skin damages.

Sargassum Seaweed as a Source of Anti-Inflammatory Substances and the Potential Insight of the Tropical Species: A Review

“…These facts indicated that the relatively lipophilic compounds tended to be responsible for the anti-inflammatory activity. This was supported by several other studies showing a similar tendency that a relatively lipophylic extract or fraction has a promising anti-inflammatory effect [19,20,21,22,23,24,25,26,27,28,29,30,31,32,33].…”

“…Several other manifestations of the Sargassum ’s bioactive compounds against inflammatory conditions are include elevated intrinsic antioxidant activity (catalase, superoxide dismutase, glutathione peroxidase, and glutathione reductase) [24,123,138], decreased production of ROS [24,33,142], decreased pro-inflammatory cell population (T-helper, T-cytotoxic, granulocytes, eosinophils, and monocytes) [76], stabilization of the lysosomal membrane (which inhibits lysosomal enzymes, such as cathepsin D, glucosaminidase, glucuronidase, etc.) [99,105,139], decreased edema volume and neutrophil infiltration in rat edema model [104], decreased production of osteoclastogenic factors (such as RANKL and osteoprotegerin in the IL-1β-induced MG-63 osteoblast cells) [147], improvement of dyslipidemia conditions [50,99], and amelioration of insulin resistance [33,44].…”

Valuing Bioactive Lipids from Green, Red and Brown Macroalgae from Aquaculture, to Foster Functionality and Biotechnological Applications

“…To our knowledge there are few publications that evaluated COX-2 inhibition by macroalgae lipid extracts, and the ones published used cell lines assays, but not in vitro COX-2 assays. Previous studies evaluated the COX-2 expression, evidencing a reduction of the enzyme expression in cell lines [ 72 , 73 , 74 , 75 ], but polar lipid extracts from terrestrial plants and microalgae showed modulation capacity of COX-2 using in vitro assays [ 75 , 76 ]. The ethanolic extract of the small herbaceous plant Polygonum minus (Huds) achieved 25% of COX-2 inhibition at concentration of 100 μg/mL [ 76 ] which is in the same order of magnitude we obtained in the present study (about 80% inhibition at a concentration of 500 μg/mL).…”

Protective effect of fermented Cyclopia intermedia against UVB-induced damage in HaCaT human keratinocytes

“…Keratinocytes respond to the major changes in inflammation and immunomodulation observed after UVB exposure, at least in part via UVB-induced expression of inflammatory enzymes and release of pro-inflammatory mediators [ 35 ]. Chronic UVB irradiation was shown to increase the production of some pro-inflammatory cytokines, such as TNF-α, IL-1β, IL-6, and IL-8, leading to cell death in HaCaT cells [ 36 ].…”