• Journal of the Korean Society of Food Science and Nutrition
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• v.36 no.10
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• pp.1271-1278
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• 2007

In this study, the ability of Styela clava or Styela plicata to reduce ethanol-induced hepatotoxicity and hepatic and leucocytic DNA damages was evaluated. Twenty four male SD rats were given 25% ethanol containing water (ad lib, p.o.) and divided into 3 groups; ethanol treated control group (EtOH), ethano1+3% S. clava (EtOH+SC), and ethano1+3% S. plicata (EtOH+SP). After 6 weeks, the supplementation of S. clava reduced the plasma ALT, ALP and LDH activities significantly (p<0.05), while S. plicata induced significant decrease in the plasma LDH activity only. The comet assay was employed to quantify the alcohol-induced DNA damage in rat hepatocytes and leucocytes. A significant protective effect on hepatic and leucocytic DNA damages was observed in S. clava or S. plicata supplemented groups compared to the EtOH control group. The hepatic DNA damage was correlated positively with plasma ALP and LDH activities. These results demonstrated that S. clava or S. plicata supplementation protected alcohol-induced hepatic and leucocytic DNA damage.

• Journal of the Korean Society of Food Science and Nutrition
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• v.35 no.10
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• pp.1336-1342
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• 2006

This study was performed to investigate the effect of ethanol extract of Chaenomeles sinensis Koehne (CS) on alcohol-induced liver damage in rats. Male Sprague-Dawley rats weighing $135{\pm}10g$ were divided into 6 groups for 4 weeks; normal group (ND), alcohol (35%, 10 mL/kg/day) treated group (ET), CS ethanol extract 200 mg/kg/day treated group (ND-CSL), CS ethanol extract 400 mg/kg/day treated group (ND-CSH), CS ethanol extract 200 mg/kg/day and alcohol treated group (ET-CSL), and CS ethanol extract 400 mg/kg/day and alcohol treated group (ET-CSH). The body weight gain and food efficiency ratio were no differences between ND and ET. There were increases in the activities of serum alanine aminotransferase (ALT), asparate aminotransferase (AST), and alkaline phosphatase (ALP) in ET. On the other hand, the administration of CS decreased ALT, AST and ALP activities in serum. It was also observed that the hepatic activities of superoxide dismutase (SOD), catalase, glutathione peroxidase (GSH-Px) and xanthine oxidase (XO) increased by alcohol treatment were also markedly decreased in the CS administered groups as compared with ET. The activities of hepatic SOD, catalase, GSH-Px and XO were riot significantly different among the normal diet groups. Contents of thiobarbituric acid reactive substances (TBARS) were increased by the administration of alcohol, on the other hand, the administration of CS reduced TBARS value in the liver. In addition, the content of glutathione (GSH) in the liver was decreased by alcohol administration, however, GSH increased after administering CS. In conclusion, the administration of alcohol develops the hyperoxidation of liver lipids through tile increase in enzymes activity related to the lipid peroxiation, however, it was decreased after administring CS. Thus, CS may have a possible protective effect on ethanol-induced hepatotoxicity in rat liver.

• Journal of the Korean Society of Food Science and Nutrition
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• v.35 no.5
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• pp.549-556
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• 2006

The purpose of this study was to assess the effects of mulberry leaf extract supplement on blood glucose, glycated hemoglobin ($HbA_{1C}$) and serum lipids in type II diabetic patients, and also to assess safety in liver function after mulberry leaf extract supplement. The study was a randomized placebo-controlled trial and total 23 type II diabetic patients were divided into a MLE group taking 1,000 mg mulberry leaf extract supplement per day as experimental group and a placebo group taking 1,000 mg cellulose Powder supplement per day for 12 weeks. After 2 weeks of wash-out period, fasting blood glucose, $HbA_{1C}$, serum lipid levels and liver function test were analyzed before and after treatment of 12 weeks. The general baseline characteristics, nutrient intake and life style factors of study subjects were similar between two groups during intervention. The concentrations of fasting blood glucose and $HbA_{1C}$ (p<0.05) decreased significantly after mulberry leaf extract supplement in MLE group, while there were no changes found in placebo group. We also found it showed that mulberry leaf extract supplement for 12 weeks decreased significantly (p<0.05) the fasting blood glucose in poor fasting blood glucose group and $HbA_{1C}$ concentration in poor $HbA_{1C}$ group. The concentrations of LDL-cholesterol (p<0.05) and triglyceride (p<0.01) decreased significantly in MLE group after 12 weeks of taking the supplement, while there were no changes found in placebo group. The mulberry leaf extract supplement for 12 weeks didn't show hepatotoxicity. These results suggested that mulberry leaf extract supplement could be effective in improving fasting blood glucose and $HbA_{1C}$ levels in the diabetic patients, specially having high concentrations of fasting blood glucose and $HbA_{1C}$ among type II diabetic patients.

• Tuberculosis and Respiratory Diseases
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• v.45 no.3
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• pp.509-518
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• 1998

Background: Short-course chemotherapy for 6 months is well established for pulmonary tuberculosis. However, little is known about the efficacy of the short-course chemotherapy for tuberculous pleural effusion. Tuberculous pleural effusion itself may be self-limiting without any treatment, but about two thirds of the patients with tuberculous pleural effusion may subsequently develop pulmonary tuberculosis within 5 years. After completing treatment for tuberculous pleural effusion. prolonged follow-up is necessary for evaluating the efficacy of the treatment There is still no report on the efficacy of 6-month regimens for tuberculous pleural effusion in Korea, where the incidence of tuberculous disease and drug resistance is high. We studied the efficacy of 6 month short-course chemotherapy comparing with 9 month chemotherapy. Method : Retrospective study was done through medical record review in 238 patients with tuberculous pleural effusion who admitted to Asan Medical Center during May 1989-May 1993. The diagnosis of tuberculous pleural effusion was made by bacteriologic or histopathologic study. Results: Among 238 patients, 38 patients were dropped out during follow-up period. In 2 patients, second line drugs were prescribed according to known drug resistance results. And, in 23 patients, treatment longer than 9 months was done due to accompanying extrapulmonary tuberculosis or durg resistance. In 8 patients, treatment regimen was changed due to hepatotoxicity. Remaining 167 cases (70.2%) completed the treatment as scheduled ; 6 month chemotherapy in 88 cases and 9 month chemotherapy in 79 cases. In 60 patients (35.9%) with pleural effusion only in chest X-ray finding, sputum smear or culture for M.tuberculosis was positive in 6 cases (10.0%), and in 63 patients (37.7%) with radiologically inactive pulmonary tuberculosis, sputum smear or culture was positive in 18 cases (28.6%). In 44 patients (26.3%) with radiologically active pulmonary tuberculosis, the sputum smear or culture was positive in 24 cases (54.5%). In 6-month chemotherapy group (n=88), during mean 23 months (range; 1~61months) follow-up period, pulmonary tuberculosis developed in 1 case (1.4%). In 9-month chemotherapy group(n=79), during mean 23 months (range; 3~70months) follow-up period, pulmonary tuberculosis developed in 2 cases (2.5%). All the cases who developed pulmonary tuberculosis also showed active pulmonary tuberculosis on initial chest X-ray before treatment Conclusion: In patients with tuberculous pleural effusion, the incidence of pulmonary tuberculosis after 6 month chemotherapy showed no difference from that after 9 month chemotherapy. Thus, 6 month short-course chemotherapy seems to be an effective treatment for tuberculous pleural effusion.

• Journal of Ginseng Research
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• v.32 no.4
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• pp.382-389
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• 2008

To achieve a better understanding of protective effects of water extracts of Panax ginseng against TCDD-induced toxicities, we monitored physiological and clinical changes in rat for 4 weeks after administrations of each Panax Ginseng extract or TCDD, and co-administration of the two materials. For this study, 120 male Sprague-Dawley (SD) rats weighing 190-210 g each (8 weeks old) were divided into four groups: TCDD-administered, co-administered group with TCDD and ginseng extract, ginseng extract-administered, and control group. The TCDD-administered group received single dose of TCDD in a corn oil vehicle ($25\;{\mu}g/kg$ body weight) by intraperitoneal administration on Day 1. The Panax ginseng extracts-administered group received intraperitoneally 100 mg/kg body weight every other day for one month. For the co-administered group with TCDD and ginseng extracts, Panax ginseng extracts were intraperitoneally administered to rats at 100 mg/kg body weight every other day for one month after a single intraperitoneal dose of $25\;{\mu}g$ of TCDD/kg body weight on Day 1. Panax ginseng extracts attenuated the mortality induced by TCDD administration. The extracts also slightly attenuated the TCDD-induced body weight loss. Administration of TCDD alone increased liver weight at 2, 5, and 16 days after administration of TCDD. Administration of Panax ginseng extracts rather decreased liver weight through whole the experimental period, but which was statistically insignificant. Administration of TCDD alone at $25\;{\mu}g/kg$ body weight increased both serum enzyme activities of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) at 32 days, indicating that liver damage occurred maximally at that time. Ginseng extract administration caused insignificant changes in serum ALT, but gradually decreased in AST as the exposure time increased. Coadministration of TCDD and ginseng extracts caused serum AST activity to significant recovery to normal value at 16 days and 32 days after exposure to TCDD. The extracts also significantly decreased the TCDD-induced ALT activity after 16 days of TCDD administration. These results suggest that Panax ginseng extracts may possess a protective effect against TCDD-induced toxicities including hepatotoxicity in rats.