• Journal of Life Science
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• v.29 no.3
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• pp.295-302
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• 2019

Liquiritigenin (LG) is a chiral flavonoid isolated from the roots of licorice. It exhibits multiple biological activities including anti-oxidant, anti-cancer, and anti-inflammatory effects. In particular though, the anti-cancer activity of LG in oral squamous cell carcinoma has yet to be elucidated, and LG-induced apoptosis in oral squamous cell carcinoma remains poorly understood. In the present study, we tested the role of LG in inducing apoptosis in oral squamous cell carcinoma cells. LG treatment of HN22 cells resulted in a dose-dependent inhibition of cell viability as detected by a 3-(4,5-dimethylthiazol-2-yl)-2,5 diphenyltetrazolium bromide assay. The induction of apoptosis in terms of Annexin V/7-Aminoactinomycin D staining, sub-G1 population, and multi-caspase activity were assessed with a $Muse^{TM}$ Cell Analyzer. Flow cytometric analysis revealed that LG treatment resulted in G2/M arrest in cell cycle progression and downregulation of cyclin B1 and CDC2 expression in a concentration-dependent manner. It also resulted in significant upregulation of p27. In addition, LG was seen to trigger the generation of reactive oxygen species and induce CCAAT/enhancer-binding protein homologous protein and 78-kDa glucose-regulated protein in concentration-dependent upregulation. The LG treatment of HN22 cells led to a loss of mitochondrial membrane potential (${\Delta}{\Psi}m$); it also reduced the levels of anti-apoptotic protein and increased the expression of apoptotic protease activating factor-1, cleaved poly (ADP-ribose)polymerase and Bax. Overall, our results indicate that the pro-apoptotic effects of LG in HN22 cells depend on the activation of both intrinsic and extrinsic signaling pathways. Thus, our results suggest that LG constitutes a natural compound with a potential role as an anti-tumor agent in oral squamous cell carcinoma.

• Journal of Food Hygiene and Safety
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• v.34 no.4
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• pp.388-395
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• 2019

The object of the present study was to examine the effect of selenium-treated Spinacia oleracea L. on antioxidative defense system and oxidative damage in rats fed high-fat and high-cholesterol diets. Experimental rats were divided into six groups which were composed of normal diet group (N), high-fat and high-cholesterol diet group (HF), high-fat and high-cholesterol diet with 5% or 10% non-treated spinach supplemented group (SPA or SPB) and high-fat and high-cholesterol diet with 5% or 10% selenium-treated spinach-supplemented group (SSA or SSB). In the antioxidant enzyme activities of hepatic glutathione peroxidase and superoxide dismutase, activities increased in supplementation of non-treated or selenium-treated spinach groups compared to HF group. However, there was no significant difference in the activity of hepatic catalase among all experimental groups. The microsomal superoxide radical content of the SSB group was significantly reduced compared to the HF group. The mitochondrial carbonyl values of the SSB group were significantly reduced compared to the HF group. Thiobarbituric acid reaction substance (TBARS) values in RBC and liver were also reduced in non-treated or selenium-treated spinach-supplemented groups compared to the HF group. The hepatic TBARS values of the supplementation of selenium-treated spinach groups significantly decreased compared to the supplementation of non-treated spinach groups. These results suggest that selenium-treated spinach may reduce oxidative damage by the activation of antioxidative defense system in rats fed high-fat and high-cholesterol diets.

• Journal of Life Science
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• v.29 no.11
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• pp.1273-1280
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• 2019

Age-related macular degeneration (AMD) is one of the leading causes of blindness in the elderly population, and damage to retinal pigment epithelial (RPE) cells due to oxidative stress contributes to the development of AMD. Glycyrrhiza uralensis Fischer is one of the most widely used herbal medicines for the treatment of various diseases in Asian countries. Although recent studies indicated that treatment with G. uralensis can protect cells from oxidative stress, its mechanisms in RPE cells remain unknown. We evaluated the effect of a G. uralensis ethanol extract (GU) on $H_2O_2$-induced oxidative injury in ARPE-19 RPE cells. The GU pretreatment attenuated reactive oxygen species (ROS) generation induced by $H_2O_2$, which was associated with induced expression of nuclear factor erythroid-derived-2-like 2 (Nrf2) and heme oxygenase-1 (HO-1). GU also suppressed $H_2O_2$-induced DNA damage and mitochondrial dysfunction. The inhibitory effect of GU on $H_2O_2$-induced apoptosis was associated with the protection of caspase-3 activation. Overall, GU appeared to protect RPE cells from oxidative injury by inhibiting DNA damage and reducing apoptosis. Further studies are needed to determine the regulation of Nrf2-mediated HO-1 expression, but our results suggest the possibility of using GU to reduce the risk of AMD.