No abstract

GCBE has a potential anti-obesity effect with lowering body fat accumulation by regulating adipogenesis and lipid metabolism-related genes and proteins in WAT and liver.

No abstract

Nobiletin and tangeretin are polymethoxy flavonoids (PMFs), found in rich quantities in the peel of citrus fruits. In the present study, we assessed the biological effect of the PMFs on liver damage using a mouse model of binge drinking. First, we extracted PMFs from the peels of Citrus aurantium to make Citrus aurantium extract (CAE). Male C57BL/6 mice were orally treated with silymarin and CAE (50, 100, and 200 mg/kg) for 3 days prior to ethanol (5 g/kg, total of 3 doses) oral gavage. Liver injury was observed in the ethanol alone group, as evidenced by increases in serum hepatic enzymes and histopathologic alteration, as well as by hepatic oxidative status disruption. CAE improved serum marker and hepatic structure and restored oxidative status by enhancing antioxidant enzyme levels and by reducing lipid peroxidation levels. In addition, CAE evidently suppressed inflammation and apoptosis in the livers of mice administered with ethanol, by 85% (tumor necrosis factor-α) and 44% compared to the control group, respectively. Furthermore, CAE activated lipid metabolism related signals and enhanced phosphorylation of AMP-activated protein kinase (AMPK) and nuclear factor E2-related factor 2 (Nrf2) with several cytoprotective proteins including heme oxygenase-1, NAD(P)H quinone oxidoreductase 1, and γ-glutamylcysteine synthetase. Taken together, the present study demonstrated that, CAE possesses antioxidant, anti-inflammatory, and antiapoptotic activity against ethanol-induced liver injury.

In this study, we optimized fermentation conditions for the solid state fermentation of rice bran with Monascus pilosus KCCM60084, and the antioxidant activities were investigated. Optimal fermentation conditions were determined by the production of Monacolin K, a functional secondary metabolites with cholesterol lowering activity. The highest Monacolin K production were 2.88 mg/g observed on day 10 with 45% moisture content in the substrate when inoculated with 5% inoculum (w/w). Reducing power, iron chelating activity and ABTS + radical scavenging activity were significantly enhanced after fermentation by 60, 80, and 38% respectively. Furthermore, the content of total flavonoid were found to be increased by 4.58 fold. Based on these results, Monascus-fermented rice bran showed strong possibility to be used as a natural antioxidant agent due to its enhanced antioxidant activity.

Platelet-derived growth factor (PDGF)-BB can induce abnormal proliferation and migration of vascular smooth muscle cells (VSMC) that are involved in the development of CVD. In our preliminary study, phytoalexin glyceollins (glyceollins I, II and III) isolated from soyabean seeds cultured with Aspergillus sojae showed strong antioxidant and anti-inflammatory activity. Since antioxidants showed beneficial effects on chronic inflammatory diseases, the purpose of the present study was to examine the effects of glyceollins on PDGF-induced proliferation and migration in human aortic smooth muscle cells (HASMC). Incubation of resting HASMC with glyceollins for 24 h significantly diminished PDGF-increased cell number and DNA synthesis in a dose-dependent manner without any cytotoxicity. In addition to blocking of the PDGF-inducible progression through the G 0 /G 1 to the S phase of the cell cycle, glyceollins down-regulated the expression of cyclindependent kinase (CDK)2 and cyclin D1, and up-regulated the expression of CDK inhibitors such as p27 kip1 and p53.Glyceollins also effectively inhibited reactive oxygen species generation and phosphorylation of PDGF receptor-b, phospholipase Cg1, Akt and extracellular signal-regulated kinase 1/2 by PDGF stimulation. Furthermore, glyceollins were found to inhibit PDGF-induced dissociation of actin filaments and cell migration. Thus, the results suggest that glyceollins could become a potent therapeutic agent for regulating VSMC-associated vascular disease such as atherosclerosis and restenosis after angioplasty.

No abstract

In this study, tomentosin, a sesquiterpene lactone was isolated from Inulae flos and its biological activities were investigated. The effects of tomentosin on the production of inflammatory mediators as well as on nuclear factor (NF)-κB and mitogen-activated protein (MAP) kinase activation were evaluated in RAW264.7 cells. Tomentosin decreased the production of nitric oxide (NO) and prostaglandin E 2 (PGE 2 ) by suppressing the protein expression of inducible NO synthase (iNOS) and cyclooxygenase (COX)-2, respectively. Additionally, tomentosin reduced the release of pro-inflammatory cytokines, such as tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6). Tomentosin not only attenuated lipopolysaccharide (LPS)-induced NF-κB activation via the abrogation of inhibitory (I)κBα degradation and caused a subsequent decrease in nuclear p65 level, but it also suppressed the phosphorylation of MAP kinases (p38 and c-Jun N terminal kinase (JNK)). These results indicate that tomentosin exerts anti-inflammatory activities through the inhibition of inflammatory mediators (NO, iNOS, PGE 2 , COX-2, TNF-α, and IL-6) by regulating NF-κB activation and phosphorylation of p38/JNK kinases in macrophages, thus suggesting that tomentosin could be a potential agent for the treatment of inflammatory diseases. Key words tomentosin; inflammatory mediator; nuclear factor (NF)-κB; mitogen-activated protein (MAP) kinaseInflammation is the host response to infection and injury, but if it is left uncontrolled, the inflammatory mediators become involved in the pathogenesis of many inflammatory disorders.1) Macrophages play a crucial role in both the specific and non-specific immune responses to microbial and viral infections. When activated by stimuli such as lipopolysaccharide (LPS), macrophages produce a variety of inflammatory mediators such as prostaglandin E 2 (PGE 2 ) and nitric oxide (NO) and pro-inflammatory cytokines including tumor necrosis factor-α (TNF-α), interleukin-1beta (IL-1β) and IL-6.Expression of these inflammatory mediators is regulated by the activation of nuclear factor-kappaB (NF-κB).2) Also, inflammatory mediators including cytokines or mitogenactivated protein (MAP) kinases such as p38 and c-Jun N terminal kinase (JNK) stimulate the pathways by activating the inhibitor κB kinase (IKK).3,4) In unstimulated cells, NF-κB is located in the cytoplasm as an inactive complex bound to its inhibitory protein (IκB). During the process of inflammation, the IKK phosphorylates IκB, inducing its ubiquitination and degradation of IκBα. The free NF-κB then translocates to the nucleus, where it binds to κB-binding sites in the promoter regions of target genes and regulates the expression of various genes, including inducible NO synthase (iNOS) and cyclooxygenase 2 (COX-2), and inflammatory cytokines. 5-7)Our previous studies have shown that the ethanol extract of Inulae flos is a potent inhibitor of inflammatory mediators. 8)Recently, it was shown that britanin isolated from Inulae flos inhibited the production of inflammatory medi...