Glyceollins, which are derived from daidzein in soybean in response to various stimuli or stresses, have been reported to activate antioxidant/detoxifying enzymes in a nuclear factor (erythroid-derived 2)-like 2 (Nrf2)-dependent manner, in addition to exerting anti-inflammatory effects in murine macrophages. As the Nrf2 signaling pathway is known to antagonize nuclear factor (NF)-κB signaling, glyceollins likely have the potential to prevent or treat inflammatory bowel disease. Thus, this study was conducted to examine whether glyceollins could inhibit dextran sulfate sodium (DSS)-induced colitis in a mouse model. Ulcerative colitis (UC) was induced in male BALB/c mice by administering drinking water with 4% DSS for 5 days. Glyceollins (4 or 10 mg/kg of body weight) were orally administered 48 h before and after DSS treatment. We found that glyceollins alleviated histological colon damage and inflammation induced by DSS treatment. More specifically, glyceollins reduced plasma levels of inflammatory cytokines, such as tumor necrosis factor-α and interleukin-6, which were otherwise markedly increased by DSS treatment. Markers of tissue damage, including malondialdehyde and 8-hydroxy-2-guanosine, were significantly increased by DSS treatment; however, this effect was mitigated through concomitant treatment with glyceollins. Furthermore, nuclear accumulation of NF-κB p65 and the expression of inducible nitric oxide synthase were upregulated by glyceollins, consistent with the observed modulation of inflammatory markers. In conclusion, glyceollins have therapeutic potential for UC and merit further clinical study.
Korean red ginseng (Panax ginseng C.A. Meyer) contains various pharmacologically active constituents including ginsenosides. Recently we found that red ginseng extract has a strong antioxidant activity and that pectinase‐mediated hydrolysis augments its radical‐scavenging activity. In addition, the content of compound‐K, a bioavailable and bioactive ginsenoside, was significantly increased in the hydrolyzed red ginseng extract compared to the non‐hydrolyzed extract. We further investigated neuroprotective and cognitive‐enhancing effects of the hydrolyzed red ginseng extract in vitro and in vivo. To induce oxidative stress‐induced neurotoxicity, mouse hippocampal HT22 cells and C57BL/6 mice were exposed to an excess glutamate and D‐galactose, respectively. For behavioral assessments, the passive avoidance, Y‐maze, and Morris water maze tasks were performed following treatment with the extracts or compound‐K. Our results from the in vitro and in vivo tests demonstrate that (1) red ginseng extract (containing compound‐K) protects neuronal cells from oxidative damage through the induction of Nrf2 and antioxidant enzymes, (2) the learning and memory impairments induced by oxidative stress were alleviated by treatment with the hydrolyzed red ginseng extract, (3) the hippocampi (particularly cell counts and nuclear arrangement) of the stressed mice was histologically pathologic, which was rarely observable from the hippocampi of the extract‐treated mice. Our findings suggest that red ginseng extract hydrolyzed by pectinase may effectively alleviate oxidative stress‐mediated memory deficits possibly through Nrf2‐related detoxification.Support or Funding InformationThis work was supported by the Food Functionality Evaluation program funded by the Ministry of Agriculture, Food and Rural Affairs through Korea Food Research Institute.
Salicornia herbacea L., also called as glasswort, is a halophyte growing in salt marshes and has been used as a seasoned vegetable and a traditional medicine for various disorders. It is a nutrient‐rich herb containing plenty of bioactive compounds such as selenium, flavonoids. In this study, we in vitro examined if ethanol extract from glasswort is neuroprotective under oxidative stress‐induced environment. Hippocampal HT22 cells were treated with 5 mM glutamate in the presence of ethanol extract from glasswort or its subfractions in five different solvents (hexane, methylene chloride, ethyl acetate, butanol, and water). Ethanol (EtOH) extract and methylene chloride‐soluble subfraction (MC fraction) of the herb were effective in protecting HT22 cells from glutamate‐induced toxicity. In addition, EtOH extract and MC fraction induced intracellular antioxidant enzyme NQO1's activity and inhibited ROS production. The levels of Nrf2 and its downstream antioxidant enzymes were significantly elevated by both EtOH extract and MC fraction. We further investigated whether MC fraction is protective against galactose‐induced cognitive decline in animal model. C57BL/6J mice were fed MC fraction, and intraperitoneally injected with D‐galactose on a daily‐basis to generate oxidative stress and cause learning and memory impairments. After 6 weeks, behavioral and biochemical tests were conducted. The group fed MC fraction decreased escape latency time, reduced DNA damage and lipid peroxidation, and enhanced NQO1 enzyme activity in tissues, compared to D‐galactose‐treated control group. Overall, these findings suggest that MC fraction of glasswort extract could be a promising agent for AD prevention.Support or Funding InformationThis work was supported by the Food Functionality Evaluation program funded by the Ministry of Agriculture, Food and Rural Affairs through Korea Food Research Institute, and by the Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Education (Project No. 2013R1A1A2013362).
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