ABSTRACT
Crocodile oil (CO) is generated from the fatty tissues of crocodiles as a by-product of commercial aquaculture. CO is extensively applied in the treatment of illnesses including asthma, emphysema, skin ulcers, and cancer, as well as wound healing. Whether CO has anti-inflammatory properties and encourages an immune response remains uncertain. The impact of CO on inflammatory conditions in lipopolysaccharide (LPS)-stimulated RAW 264.7 cells and the mechanisms behind it were examined in this work. Cells were treated with 0.125-2% CO dissolved in 0.5% propylene glycol with or without LPS. The production and expression of inflammatory cytokines and mediators were also examined in this research. CO reduced the synthesis and gene expression of interleukin-6 (IL-6). Consistently, CO inhibited the expression and synthesis of inflammatory markers including cyclooxygenase-2 (COX-2), prostaglandin E2 (PGE2), nitric oxide (NO), and nuclear factor kappa B (NF-κB). Furthermore, CO reduced the effects of DNA damage. CO also increased the cell-cycle regulators, cyclins D2 and E2, which improved the immunological response. CO might thus be produced as a nutraceutical supplement to help avoid inflammatory diseases.
Subject(s)
Alligators and Crocodiles , Lipopolysaccharides , Animals , Cyclooxygenase 2/metabolism , Immunity , Inflammation/drug therapy , Inflammation/metabolism , Lipopolysaccharides/pharmacology , Macrophages , Mice , NF-kappa B/metabolism , Nitric Oxide/metabolism , Nitric Oxide Synthase Type II/metabolism , Oils , RAW 264.7 CellsABSTRACT
BACKGROUND: Caulerpa lentillifera (CL) is a green seaweed, and its edible part represents added value as a functional ingredient. CL was dried and extracted for the determination of its active compounds and the evaluation of its biological activities. The major constituents of CL extract (CLE), including tannic acid, catechin, rutin, and isoquercetin, exhibited beneficial effects, such as antioxidant activity, anti-diabetic activity, immunomodulatory effects, and anti-cancer activities in in vitro and in vivo models. Whether CLE has an anti-inflammatory effect and immune response remains unclear. METHODS: This study examined the effect of CLE on the inflammatory status and immune response of lipopolysaccharide (LPS)-stimulated RAW 264.7 cells and the mechanisms involved therein. RAW264.7 cells were treated with different concentrations of CLE (0.1-1000 µg/mL) with or without LPS (1 µg/mL) for 24 h. Expression and production of the inflammatory cytokines, enzymes, and mediators were evaluated. RESULTS: CLE suppressed expression and production of the pro-inflammatory cytokines IL-6 and TNF-α. Moreover, CLE inhibited expression and secretion of the inflammatory enzyme COX-2 and the mediators PGE2 and NO. CLE also reduced DNA damage. Furthermore, CLE stimulated the immune response by modulating the cell cycle regulators p27, p53, cyclin D2, and cyclin E2. CONCLUSIONS: CLE inhibits inflammatory responses in LPS-activated macrophages by downregulating inflammatory cytokines and mediators. Furthermore, CLE has an immunomodulatory effect by modulating cell cycle regulators.
Subject(s)
Anti-Inflammatory Agents/pharmacology , Catechin/pharmacology , Caulerpa/chemistry , Quercetin/analogs & derivatives , Rutin/pharmacology , Tannins/pharmacology , Animals , Catechin/isolation & purification , Cytokines/genetics , Dose-Response Relationship, Drug , Gene Expression Regulation/drug effects , Immunity/drug effects , Lipopolysaccharides/adverse effects , Mice , Quercetin/isolation & purification , Quercetin/pharmacology , RAW 264.7 Cells , Rutin/isolation & purification , Tannins/isolation & purificationABSTRACT
The present study assessed the effect of freshwater hybrid catfish oil (FFO) on the inflammatory status of lipopolysaccharide (LPS)-stimulated RAW264.7 cells and investigated the underlying mechanisms. RAW264.7 cells were supplemented with various concentrations [0.125-2% in 0.5% propylene glycol (v/v)] of FFO with or without LPS (1 µg/ml) for 24 h. Inflammatory cytokines and mediators were quantified using ELISA and reverse transcription-quantitative PCR. The results revealed that FFO treatment inhibited the secretion and mRNA expression of the pro-inflammatory cytokines IL-6, IL-1ß, TNF-α. In line with this, FFO suppressed the expression and secretion of the inflammatory mediators cyclooxygenase-2 and prostaglandin E2. FFO also reduced apoptotic body formation and DNA damage. Correspondingly, FFO enhanced the immune response by modulating the cell cycle regulators p53, cyclin D2 and cyclin E2. Accordingly, FFO may be developed as a nutraceutical product to prevent inflammation.
