• Biomolecules & Therapeutics
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• v.3 no.3
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• pp.223-228
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• 1995

In an attempt to define the effects of biphenyldimethyl dicarboxylate (DDB) on the lipid peroxidation and oxygen free radical scavenging enzymes activities in mercuric chloride-induced hepatotoxic rats, we studied malondialdehyde (MDA) level and the activities of catalase and superoxide dismutase (SOD) in liver of the rats at 24 hr after the injection of mercuric chloride. Sprague-Dalwey albino rats were injected subcutaneously with mercuric chloride (5 mg/kg) only and mercuric chloride (5 mg/kg) plus. DDB (200 mg/kg/day, p.o) is administered for 4 days prior to 3 days from the injection of mercuric chloride. The group treated with mercuric chloride showed significantly higher MDA level and lower catalase and SOD activities as compared with that of control group. The group treated with mercuric chloride plus DDB showed significantly lower MDA level and catalase activity and higher SOD activity as compared with that of mercuric chloride-treated group. These results suggest that the excessive oxygen free radicals resulting from the depression of superoxide dismutase activity is an important determinant in the pathogenesis of mercuric chloride-induced hepatotoxicity and DDB has antioxidant effects.

• The Korean Journal of Pharmacology
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• v.30 no.2
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• pp.217-225
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• 1994

In an attempt to define the effects of Biphenyldimethyl dicarboxylate(DDB) on the lipid peroxidation, oxygen free radical scavenging enzymes activities and hepatic functions in ethanol-induced hepatotoxic rats, we studies malondialdehyde(MDA) level and the activities of catalse, superoxide dismutase(SOD), glutamic-oxaloacetic transaminase(GOT) and glutamic-pyruvic transaminase(GPT) in liver of the rats at 24, 48 and 72 hr after the injection of ethanol and DDB. Sprague-Dalwey albino rats weighing 250 to 280gm were injected intraperitoneally with ethanol(2.5 gm/kg ) only and ethanol plus DDB(300mg/kg ). The result obtained can be summarized as follows : 1) The group treated with ethanol showed significantly higher MDA level and lower catalase and SOD activities at 24, 48 and 72hr after the injection as compared with that of control group. 2) The group treated with ethanol showed significantly higher GOT and GPT activities at 24, 48 and 72hr after the injection as compared with that of control group. 3) The group treated with ethanol plus DDB showed significantly lower MDA level and higher catalase and SOD activities at 24, 48 and 72 hr after the injection as compared with that of ethanol group. 4) The group treated with ethanol plus DDB showed significantly lower GOT and GPT activities at 24, 48 and 72 hr after the injection as compared with that of ethanol group. These results suggest that the excessive oxygen free radicals resulting from the depression of the activities of catalase and superoxide dismutase is an important determinant in pathogenesis of ethanol-induced hepatotoxicity and DDB has antioxidant effects.

• YAKHAK HOEJI
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• v.42 no.1
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• pp.82-88
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• 1998

The effect of hepatoprotective agents and bile acids on tumor necrosis factor-alpha, (TNF-${\alpha}$) production in murine and human macrophage cell line (RAW264.7 and U937) was inve stigated. The hepatoprotective agents including silymarin and its major component, silybin, significantly inhibited TNF-alpha production in a concentration dependent manner ($IC_50$ of silybin=67.7${\mu}g$/ml (140.3${\mu}g$M)). In differentiated U937 cells, especially, silybin showed more effective inbitory activity ($IC_50$=35.1${\mu}g$g/ml (72.7${\mu}g$M)). These results suggest that silymarin and silybin may inhibit TNF-alpha production in the process of hepatic diseases in human. However, biphenyldimethyl dicarboxylate (DDB) was not effective. In the case of bile acids, chenodeoxycholic acid (CDCA) showed a concentration dependent inhibitory effect on TNF-alpha production ($IC_50$ of CDCA= 71.5${\mu}g$g/ml (182.1${\mu}g$M)). In contrast, glycine or taurine conjugated form (G-CDCA or T-CDCA) restored to the control level or significantly increased TNF-${\alpha}$ production. And also ursodeoxycholic acid (UDCA) and its conjugated forms (G-UDCA and T-UDCA) showed a variety of patterns on TNF-${\alpha}$ production by changes of functional groups and concentration. These results also indicate that bile acids may regulate TNF-${\alpha}$ production in normal hepatic function or disease conditions.

• Journal of Life Science
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• v.15 no.3 s.70
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• pp.461-467
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• 2005

This study was conducted to investigate the biological activity and hepatoprotective effect of DWP-04 [DDB : selenium yeast: glutathione (31.1 : 6.8 : 62.1(w/w/w)] in D-galactosamine (GaIN) intoxicated rats. The DWP-04 (50, 100 or 200 mg/kg) or its vehicle was orally administered everyday before the start of GaIN injection (400 mg/kg, ip) for two weeks and animal decapitated for 24 hrs after GaIN­injected. The activities of serum enzymes, markers of liver function, were increased in the GaIN group compared to normal group and significantly lowered in the DWP-04 pretreated group than in the GaIN group. Hepatic lipid peroxide level and activities of phase 1 enzymes were significantly higher than those of GaIN group compared to normal group and lower in the DWP-04 pretreated group than in the GaIN group, and phase II enzyme activities in liver were lower in the GaIN group than in the normal group and were increased in the DWP-04 pretreated group than in the GaIN group. Total hepatic glutathione content and glutathione biosynthesis enzymes were lower in the GaIN group than in the normal group and were increased in the DWP-04 pretreated group than in the GaIN group. Therefore, the current results indicated that DWP-04 administration alleviated the GaIN-induced adverse effect through enhancing the antioxidant enzyme activities.