• Nutrition Research and Practice
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• v.5 no.2
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• pp.150-156
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• 2011

Few studies have shown the correlation between metabolic syndrome and bone mineral density (BMD). The main pathogenic mechanisms of metabolic syndrome rely on chronic low-level inflammatory status and oxidative stress. There are few studies that examine the gender-specific effects of inflammation and antioxidants on BMD. In this study, we evaluated the relative contribution of these factors in patients with metabolic syndrome. We conducted a cross-sectional study of 67 men and 46 postmenopausal women with metabolic syndrome; metabolic syndrome was defined as having three or more metabolic syndrome risk factors. BMD, body fat mass, and lean body mass were evaluated. We also examined the levels of high sensitive C-reactive protein (hs-CRP), interleukin-6 (IL-6), adiponectin, vitamin E, and C in serum. Log-transformed hs-CRP levels were significantly higher in lumbar spine osteoporotic subjects than in normal subjects for women but not for men. There was no significant difference between the normal group and the osteoporotic group in other inflammatory markers. Stepwise regression analyses for BMD of the lumbar spine showed that lean body mass and vitamin E were significant determinants in men. Lean body mass and log-transformed hs-CRP were significant determinants in women Analysis for BMD of the femoral neck showed that lean body mass was a significant determinant for both men and women. There was no significant factor among the inflammatory markers or antioxidant vitamins affecting the femoral neck BMD for either gender. In conclusion, while hs-CRP is an independent predictor of the BMD of the lumbar spine in women, vitamin E showed profound effects on BMD in men but not women with metabolic syndrome.

• Journal of Food Hygiene and Safety
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• v.26 no.2
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• pp.107-113
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• 2011

Plantago asiatica L. (PA), which is widely distributed in Korea, Japan and China, has traditionally been used as a popular folk medicine for the treatment of liver diseases. A variety of activities of PA was reported, that is hepatoprotective, anti-inflammatory, anti-glycation and anti-oxidant effect. Ferric nitrilotriacetate (Fe-NTA) is a potent nephrotoxic agent and has been reported to induce renal proximal tubular necrosis. In the present study, pre-treatment with PA extract (PAE) in Wistar rat followed by Fe-NTA i.p. treatment (13.5 mg Fe/kg body weight) was performed to detect the renal protective effect of PAE. Only Fe-NTA treated group showed increases in the level of serum blood urea nitrogen (BUN) and serum creatinine (Cr), and renal tissue malondialdehyde (MDA), product of lipid peroxidation. Moreover, the level of biomarkers indicate the antioxidants status, reduced glutathione (GSH), glutathione-S-transferase (GST) and glutathione reductase (GR) were decreased. However, PAE pre-treated group showed decreases in the levels of serum BUN, serum Cr and renal tissue MDA in concentration dependent manner and increases in the level of GSH, GST and GR. These results are significantly different (p < 0.05) to the other groups. Our data suggest that PAE may be used as an chemopreventive material against Fe-NTA-mediated renal oxidative stress.

• Journal of the Korean Society of Food Science and Nutrition
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• v.36 no.6
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• pp.708-719
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• 2007

Glutathione S-transferase genotypes GSTT1, GSTM1 and GSTP1 were characterized in 104 healthy male and female subjects and compared with parameters of oxidative stress at the level of DNA and lipids, with antioxidant enzymes, and with plasma antioxidants in smokers and non.smokers. Of the 104 subjects studied, 57.4% were GSTT1 present and 47.6% were GSTM1 present. The GSTP1 polymorphisms a and b were represented as follows: a/a, 75.5%; a/b, 21.6%; b/b type, 2.9%. The GSTT1 null genotype was associated with decreased glutathione in erythrocytes and elevated lymphocytes DNA damage. GST-Px was higher in GSTT1 null compared with GSTT1 present type. The homozygous GSTP1 genotype was not associated with any antioxidant status or DNA damage. The difference in plasma ${\alpha}$-carotene and erythrocytes GSH-Px and GST activities between smokers and non-smokers was detected in the GSTT1 null genotype. Plasma ${\gamma}$-tocopherol and ${\beta}$-carotene decreased significantly in smokers having GSTM1 null genotype. When GSTT1 and GSTM1 were combined, plasma lycopene and erythrocyte GST were reduced in smokers in both null types of these genes. As for GSTP1 genotype, plasma ${\alpha}$-carotene and erythrocytes GSH-Px decreased significantly in smokers with GSTP1 b/b, while erythrocytes GSH-Px activities decreased in smokers with GSTP1 a/b. The different ${\beta}$-carotene level between smokers and non-smokers was seen with both GSTP1 a/a and a/b genotype. It seems that polymorphisms in the phase II metabolizing enzyme glutathione S-transferase may be important determinants of commonly measured biomarkers.

• Korean Journal of Food Science and Technology
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• v.54 no.3
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• pp.288-296
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• 2022

This study aimed to verify the effect of Citrus unshiu peel water extract (CUP) on a mouse model of acute gastritis (AG) induced by HCl/ethanol. Several studies have found that CUP has anti-inflammatory effects. The AG model was induced by oral administration of 150 mM HCl/60% ethanol (550 µL) to all groups except the control group. Also, for drug treatment, sucralfate (10 mg/kg) and CUP (100 or 200 mg/kg) were orally administered for 90 minutes before induction. The effect of CUP treatment was confirmed by gross gastric mucosal damage measurement, and the levels of Glutamic Oxaloacetic Transaminase (GOT), Glutamic Pyruvic Transaminase (GPT), and myeloperoxidase were reduced as well as the levels of oxidative stress biomarkers and their related proteins. In addition, the levels of inflammatory proteins, mediators, and cytokines were significantly downregulated byPI3K/Akt signaling. Taken together, these results show that CUP treatment alleviates AG by regulating PI3K/Akt signaling.

• Journal of Life Science
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• v.31 no.10
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• pp.885-897
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• 2021

Schisandrae Fructus (SF) and Corni Fructus (CF) have been used for a long time for the prevention and treatment of various diseases. Although reports have highlighted the possibility of inhibiting the onset and progression of benign prostatic hyperplasia (BPH), studies on related mechanisms are still lacking. In this study, we investigated the potential of SF and CF in improving BPH by using a dihydrotestosterone (DHT)-induced in vitro BPH model using LNCaP prostate carcinoma cells. According to our results, water and ethanol extracts of SF and CF significantly inhibited the proliferation of LNCaP cells by DHT treatment and markedly downregulated the expression of DHT-induced BPH biomarkers and growth factors. They also regulated the expression of apoptosis regulatory factors and significantly reduced DHT-mediated oxidative stress. In addition, the protective effect on major factors involved in the pathogenesis of BPH was more effective in the ethanol extract treatment group than in the water extract group. Furthermore, the improvement effect on BPH was higher in the 1:1 combined treatment group than in the ethanol extract alone treatment group of SF and CF, and 60% ethanol extracts showed a better effect than 40% ethanol extracts. Therefore, our findings demonstrate that SF and CF can protect against BPH by preventing the hyperproliferation of prostate cells through the inhibition of the androgen signaling pathway, which was correlated with their antioxidant activities. Therefore, SF and CF extracts may be useful in the clinical treatment of BPH, and the combination of these two extracts can be synergistic.

• Journal of the Korean Society of Food Science and Nutrition
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• v.39 no.3
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• pp.343-349
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• 2010

The liver is the major target of ethanol toxicity and oxidative stress plays a role in development of alcoholic liver disease. This study was performed to investigate the effects of green tea extracts (GTE) on acute ethanol-induced hepatotoxicity in rats. Experimental animals were divided into 4 groups, control, GTE, ethanol, and GTE+ethanol treatment, with 5 rats in each group. Ethanol (6 g/kg body weight (BW)) and GTE (200 mg/kg BW) were treated by gavage. At 1 hour, 3 hours and 20 days (6 g/kg BW every 2 days for total 10 doses) after ethanol and/or GTE treatments, animals were killed; hepatic tumor necrosis factor-alpha (TNF-$\alpha$) and glutathione level, serum aspartate aminotransferase (AST), serum alanine aminotransferase (ALT), hepatic antioxidant enzymes (SOD, CAT, GPx) activities and hepatic thiobarbituric acid reactive substances (TBARS) were measured. At 1 hour and 3 hours, hepatic TNF-$\alpha$ levels were increased significantly in ethanol group and ethanol+GTE group but that levels was significantly lower in ethanol+GTE group compared with ethanol group. Hepatic glutathione level was decreased by ethanol treatment but GTE prevented the ethanol-induced glutathione decrement. The levels of liver marker enzymes (AST, ALT), liver antioxidant enzymes (SOD, CAT, GPx) and lipid peroxidation marker (TBARS) were not changed in rats of 1 and 3 hours after ethanol treatment. After 20 days, GTE decreased the changes of liver marker enzymes (AST, ALT) activities and TBARS level by ethanol. This study shows that GTE beneficially modulates TNF-$\alpha$ and glutathione levels in liver of ethanol administered rats. The GTE supplementation could be beneficial to liver by decreasing early changes of biomarkers of liver damage caused by ethanol.