• Nutrition Research and Practice
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• v.16 no.6
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• pp.729-744
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• 2022

BACKGROUND/OBJECTIVES: 4-Hydroxy-2-nonenal (HNE) is a biomarker for oxidative stress to induce inflammation. Methionine is an essential sulfur-containing amino acid with antioxidative activity. On the other hand, the evidence on whether and how methionine can depress HNE-derived inflammation is lacking. In particular, the link between the regulation of the nuclear factor-κB (NF-κB) signaling pathway and methionine intake is unclear. This study examined the link between depression from HNE accumulation and the anti-inflammatory function of ⳑ-methionine in rats. MATERIALS/METHODS: Male Wistar rats (3-week-old, weighing 70-80 g) were administered different levels of ⳑ-methionine orally at 215.0, 268.8, 322.5, and 430.0 mg/kg body weight for two weeks. The control group was fed commercial pellets. The hepatic HNE contents and the protein expression and mRNA levels of the inflammatory mediators were measured. The interleukin-10 (IL-10) and glutathione S-transferase (GST) levels were also estimated. RESULTS: Compared to the control group, hepatic HNE levels were reduced significantly in all groups fed ⳑ-methionine, which were attributed to the stimulation of GST by ⳑ-methionine. With decreasing HNE levels, ⳑ-methionine inhibited the activation of NF-κB by up-regulating inhibitory κBα and depressing phosphoinositide 3 kinase/protein kinase B. The mRNA levels of the inflammatory mediators (cyclooxygenase-2, interleukin-1β, interleukin-6, inducible nitric oxide synthase, tumor necrotic factor alpha) were decreased significantly by ⳑ-methionine. In contrast, the protein expression of these inflammatory mediators was effectively down regulated by ⳑ-methionine. The anti-inflammatory action of ⳑ-methionine was also reflected by the up-regulation of IL-10. CONCLUSIONS: This study revealed a link between the inhibition of HNE accumulation and the depression of inflammation in growing rats, which was attributed to ⳑ-methionine availability. The anti-inflammatory mechanism exerted by ⳑ-methionine was to inhibit NF-κB activation and to up-regulate GST.

• Journal of the Korean Society of Food Science and Nutrition
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• v.37 no.9
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• pp.1126-1135
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• 2008

This study was carried out to investigate the anti-oxidative and anti-inflammatory actions of genistein in BALB/c mice injected with lopopolysaccharide (LPS), called endotoxin. Mice (10 weeks of age) weighing approximately 20 g were divided into 4 groups. Endotoxin shock was induced by intraperitoneal injection of LPS (100 mg/kg BW). LPS and genistein+LPS groups were injected with LPS 30 min after phosphate buffered saline (PBS) solution and genistein (200 mg/kg BW) injections, respectively. Genistein group was injected with genistein, followed by PBS, while PBS group received two injections of PBS. Superoxide anion generation of peritoneal macrophage cells was significantly (p<0.05) lower in the genistein+LPS group than in the LPS injection group at 8 h after intraperitoneal injection, while SOD activity was significantly higher in genistien+LPS group than LPS group. Tumor necrosis factor-$\alpha$ levels of plasma were significant lower (p<0.05) in the genistein+LPS injection group than LPS group at 8 h after intraperitoneal injection. Plasma TBARS was lower in genistein+LPS group than LPS group, while hepatic TBARS were not different among groups. Hepatic glutathione concentrations and antioxidant enzyme activities were ignificantly higher in the genistein+LPS group than in the LPS group at 1 h and 8 h after intraperitoneal injection. Nuclear factor-kappa B (NF-${\kappa}B$) transactivation was significantly (p<0.05) inhibited in LPS group. These results demonstrate genistein may ameliorate inflammatory diseases through inhibition of NF-${\kappa}B$ transactivation and oxidative stress, which may be mediated partially by anti-oxidative effect of genistein.