Comparison of the inhibition effects of naringenin and its glycosides on LPS-induced inflammation in RAW 264.7 macrophages.

BACKGROUND: Inflammation is intricately linked to the development of various diseases, such as diabetes, cardiovascular diseases, and cancer. Flavonoids, commonly found in plants, are known for their diverse health benefits, including antioxidant and anti-inflammatory properties. These compounds are categorized into different classes based on their chemical structure. structures. However, limited research has compared the effects of flavonoid aglycones and flavonoid glycosides. This study aims to assess the anti-inflammatory effects of naringenin and its glycosides (naringin and narirutin) in RAW264.7 macrophages. METHODS AND RESULTS: RAW264.7 cells were treated with naringenin, naringin, and narirutin, followed by stimulation with lipopolysaccharide. The levels of inflammatory mediators, including tumor necrosis factor α (TNF-α), interleukin-1ß (IL-1ß), nitric oxide (NO), inducible NO synthase (iNOS), and cyclooxygenase-2 (COX-2), were assessed. Additionally, the study examined nuclear factor-κB (NF-κB) and mitogen-activated protein kinase (MAPK) activation using western blot analysis. Among the compounds tested, narirutin exhibited the most potent anti-inflammatory effect against TNF-α, NO, and iNOS. Naringin and narirutin showed comparable inhibitory effects on IL-1ß and COX-2. Both naringin and narirutin suppressed the expression of pro-inflammatory mediators by targeting different levels of the NF-κB and MAPK pathways. Naringenin demonstrated the weakest anti-inflammatory effect, primarily inhibiting NF-κB and reducing the phosphorylation levels of p38. CONCLUSIONS: This study suggests that the presence of glycosides on naringenin and the varied binding forms of sugars in naringenin glycosides significantly influence the anti-inflammatory effects compared with naringenin in RAW 264.7 macrophages.

Tea seed saponin­reduced extract ameliorates palmitic acid­induced insulin resistance in HepG2 cells.

Tea (Camellia sinensis) seed cake is a potential resource that contains a wealth of bioactive compounds. However, the high toxicity of tea saponins in tea seed cake restricts its applications. The present study aimed to i) develop a method of extracting bioactive compounds and reducing tea saponins during the process of tea seed cake extraction and ii) investigate the anti­insulin resistance effect of tea seed saponin­reduced extract (TSSRE) in a palmitic acid (PA)­induced insulin resistance HepG2­cell model. The concentration of tea saponins in TSSRE was ~10­fold lower than that in tea seed crude extract (TSCE) after the saponin­reduction process. In addition, TSSRE cytotoxicity was significantly lower than that of TSCE in HepG2 cells. TSSRE treatment improved glucose consumption as well as glucose transporter (GLUT) 2 and GLUT4 expression levels in PA­stimulated HepG2 cells. Moreover, TSSRE enhanced the phosphorylation of the insulin receptor substrate 1/protein kinase B/forkhead box protein O1/glycogen synthase kinase 3ß and inhibited the elevated expression of phosphoenolpyruvate carboxykinase in PA­exposed HepG2 cells. The effect of TSSRE on the mediation of the insulin signaling pathway was attributed to the inhibition of PA­induced mitogen­activated protein kinase activation. The findings of the present study indicated that TSSRE ameliorates hepatic insulin resistance by ameliorating insulin signaling and inhibiting inflammation-related pathways.