The Experts below are selected from a list of 291 Experts worldwide ranked by ideXlab platform
Hye Gwang Jeong - One of the best experts on this subject based on the ideXlab platform.
-
protective effect of acteoside on carbon Tetrachloride induced hepatotoxicity
Life Sciences, 2004Co-Authors: Kyung Jin Lee, Eunrhan Woo, Chul Yung Choi, Dong Weon Shin, Dong Gun Lee, Ho Jin You, Hye Gwang JeongAbstract:This study investigated the protective effects of acteoside, a phenylethanoid glycoside, on the carbon Tetrachloride-induced hepatotoxicity as well as the possible mechanisms involved in this protection in mice. Pretreatment with acteoside prior to the administration of carbon Tetrachloride significantly prevented the increased serum enzymatic activities of alanine and aspartate aminotransferase in a dose-dependent manner. In addition, pretreatment with acteoside significantly prevented the increase in hepatic malondialdehyde formation and the depletion of the reduced glutathione content in the liver of carbon Tetrachloride-intoxicated mice. Carbon Tetrachloride-induced hepatotoxicity was also essentially prevented, as indicated by a liver histopathologic study. The effects of acteoside on cytochrome P450 (P450) 2E1, the major isozyme involved in carbon Tetrachloride bioactivation were also investigated. Treatment of the mice with acteoside resulted in a significant decrease in the P450 2E1-dependent pnitrophenol and aniline hydroxylation in a dose-dependent manner. Consistent with these observations, the P450 2El protein levels were also lower. Acteoside exhibited anti-oxidant effects on FeCl2-ascorbate induced lipid peroxidation in a mouse liver homogenate, and on superoxide radical scavenging activity. These results suggest that the protective effects of acteoside against the carbon Tetrachloride-induced hepatotoxicity possibly involve mechanisms related to its ability to block the P450-mediated carbon Tetrachloride bioactivation and free radical scavenging effects.
-
hepatoprotective effects of 18β glycyrrhetinic acid on carbon Tetrachloride induced liver injury inhibition of cytochrome p450 2e1 expression
Pharmacological Research, 2002Co-Authors: Hye Gwang Jeong, Ho Jin You, Sung Jun Park, Ae Ran Moon, Young Chul Chung, Shin Keon Kang, Hyo Kon ChunAbstract:The protective effects of 18beta-glycyrrhetinic acid (GA), the aglycone of glycyrrhizin (GL) derived from licorice, on carbon Tetrachloride-induced hepatotoxicity and the possible mechanisms involved in this protection were investigated in mice. Pretreatment with GA prior to the administration of carbon Tetrachloride significantly prevented an increase in serum alanine, aspartate aminotransferase activity and hepatic lipid peroxidation in a dose-dependent manner. In addition, pretreatment with GA also significantly prevented the depletion of glutathione (GSH) content in the livers of carbon Tetrachloride-intoxicated mice. However, reduced hepatic GSH levels and glutathione-S-transferase activities were unaffected by treatment with GA alone. Carbon Tetrachloride-induced hepatotoxicity was also prevented, as indicated by a liver histopathologic study. The effects of GA on the cytochrome P450 (P450) 2E1, the major isozyme involved in carbon Tetrachloride bioactivation, were also investigated. Treatment of mice with GA resulted in a significant decrease of the P450 2E1-dependent hydroxylation of p-nitrophenol and aniline in a dose-dependent manner. Consistent with these observations, the P450 2E1 expressions were also decreased, as determined by immunoblot analysis. GA also showed antioxidant effects upon FeCl(2)-ascorbate-induced lipid peroxidation in mice liver homogenate and upon superoxide radical scavenging activity. These results show that protective effects of GA against the carbon Tetrachloride-induced hepatotoxicity may be due to its ability to block the bioactivation of carbon Tetrachloride, primarily by inhibiting the expression and activity of P450 2E1, and its free radical scavenging effects.
-
inhibition of cytochrome p450 2e1 expression by oleanolic acid hepatoprotective effects against carbon Tetrachloride induced hepatic injury
Toxicology Letters, 1999Co-Authors: Hye Gwang JeongAbstract:The protective effects of oleanolic acid on carbon Tetrachloride-induced hepatotoxicities and the possible mechanisms involved in this protection were investigated in mice. Pretreatment with oleanolic acid prior to the administration of carbon Tetrachloride significantly prevented the increase in serum alanine aminotransferase and lactate dehydrogenase activity and liver lipid peroxidation in a dose-dependent manner. Hepatic glutathione levels and glutathione-S-transferase activities were not affected by treatment with oleanolic acid alone but pretreatment with oleanolic acid protects carbon Tetrachloride-induced depletion of hepatic glutathione levels. The effects of oleanolic acid on the cytochrome P450 (P450) 2E1, the major isozyme involved in carbon Tetrachloride bioactivation were investigated. Treatment of mice with oleanolic acid resulted in a significant decrease of P450 2E1-dependent p-nitrophenol and aniline hydroxylation in a dose-dependent manner. Consistent with these observations, the P450 2E1 expressions were also decreased, as determined by immunoblot analysis. These results show that the protective effects of oleanolic acid against the carbon Tetrachloride-induced hepatotoxicity may, at least in part, be due to its ability to block bioactivation of carbon Tetrachloride mainly by the inhibition of expression and activities of P450 2E1.
Hyo Kon Chun - One of the best experts on this subject based on the ideXlab platform.
-
hepatoprotective effects of 18β glycyrrhetinic acid on carbon Tetrachloride induced liver injury inhibition of cytochrome p450 2e1 expression
Pharmacological Research, 2002Co-Authors: Hye Gwang Jeong, Ho Jin You, Sung Jun Park, Ae Ran Moon, Young Chul Chung, Shin Keon Kang, Hyo Kon ChunAbstract:The protective effects of 18beta-glycyrrhetinic acid (GA), the aglycone of glycyrrhizin (GL) derived from licorice, on carbon Tetrachloride-induced hepatotoxicity and the possible mechanisms involved in this protection were investigated in mice. Pretreatment with GA prior to the administration of carbon Tetrachloride significantly prevented an increase in serum alanine, aspartate aminotransferase activity and hepatic lipid peroxidation in a dose-dependent manner. In addition, pretreatment with GA also significantly prevented the depletion of glutathione (GSH) content in the livers of carbon Tetrachloride-intoxicated mice. However, reduced hepatic GSH levels and glutathione-S-transferase activities were unaffected by treatment with GA alone. Carbon Tetrachloride-induced hepatotoxicity was also prevented, as indicated by a liver histopathologic study. The effects of GA on the cytochrome P450 (P450) 2E1, the major isozyme involved in carbon Tetrachloride bioactivation, were also investigated. Treatment of mice with GA resulted in a significant decrease of the P450 2E1-dependent hydroxylation of p-nitrophenol and aniline in a dose-dependent manner. Consistent with these observations, the P450 2E1 expressions were also decreased, as determined by immunoblot analysis. GA also showed antioxidant effects upon FeCl(2)-ascorbate-induced lipid peroxidation in mice liver homogenate and upon superoxide radical scavenging activity. These results show that protective effects of GA against the carbon Tetrachloride-induced hepatotoxicity may be due to its ability to block the bioactivation of carbon Tetrachloride, primarily by inhibiting the expression and activity of P450 2E1, and its free radical scavenging effects.
Ho Jin You - One of the best experts on this subject based on the ideXlab platform.
-
protective effect of acteoside on carbon Tetrachloride induced hepatotoxicity
Life Sciences, 2004Co-Authors: Kyung Jin Lee, Eunrhan Woo, Chul Yung Choi, Dong Weon Shin, Dong Gun Lee, Ho Jin You, Hye Gwang JeongAbstract:This study investigated the protective effects of acteoside, a phenylethanoid glycoside, on the carbon Tetrachloride-induced hepatotoxicity as well as the possible mechanisms involved in this protection in mice. Pretreatment with acteoside prior to the administration of carbon Tetrachloride significantly prevented the increased serum enzymatic activities of alanine and aspartate aminotransferase in a dose-dependent manner. In addition, pretreatment with acteoside significantly prevented the increase in hepatic malondialdehyde formation and the depletion of the reduced glutathione content in the liver of carbon Tetrachloride-intoxicated mice. Carbon Tetrachloride-induced hepatotoxicity was also essentially prevented, as indicated by a liver histopathologic study. The effects of acteoside on cytochrome P450 (P450) 2E1, the major isozyme involved in carbon Tetrachloride bioactivation were also investigated. Treatment of the mice with acteoside resulted in a significant decrease in the P450 2E1-dependent pnitrophenol and aniline hydroxylation in a dose-dependent manner. Consistent with these observations, the P450 2El protein levels were also lower. Acteoside exhibited anti-oxidant effects on FeCl2-ascorbate induced lipid peroxidation in a mouse liver homogenate, and on superoxide radical scavenging activity. These results suggest that the protective effects of acteoside against the carbon Tetrachloride-induced hepatotoxicity possibly involve mechanisms related to its ability to block the P450-mediated carbon Tetrachloride bioactivation and free radical scavenging effects.
-
hepatoprotective effects of 18β glycyrrhetinic acid on carbon Tetrachloride induced liver injury inhibition of cytochrome p450 2e1 expression
Pharmacological Research, 2002Co-Authors: Hye Gwang Jeong, Ho Jin You, Sung Jun Park, Ae Ran Moon, Young Chul Chung, Shin Keon Kang, Hyo Kon ChunAbstract:The protective effects of 18beta-glycyrrhetinic acid (GA), the aglycone of glycyrrhizin (GL) derived from licorice, on carbon Tetrachloride-induced hepatotoxicity and the possible mechanisms involved in this protection were investigated in mice. Pretreatment with GA prior to the administration of carbon Tetrachloride significantly prevented an increase in serum alanine, aspartate aminotransferase activity and hepatic lipid peroxidation in a dose-dependent manner. In addition, pretreatment with GA also significantly prevented the depletion of glutathione (GSH) content in the livers of carbon Tetrachloride-intoxicated mice. However, reduced hepatic GSH levels and glutathione-S-transferase activities were unaffected by treatment with GA alone. Carbon Tetrachloride-induced hepatotoxicity was also prevented, as indicated by a liver histopathologic study. The effects of GA on the cytochrome P450 (P450) 2E1, the major isozyme involved in carbon Tetrachloride bioactivation, were also investigated. Treatment of mice with GA resulted in a significant decrease of the P450 2E1-dependent hydroxylation of p-nitrophenol and aniline in a dose-dependent manner. Consistent with these observations, the P450 2E1 expressions were also decreased, as determined by immunoblot analysis. GA also showed antioxidant effects upon FeCl(2)-ascorbate-induced lipid peroxidation in mice liver homogenate and upon superoxide radical scavenging activity. These results show that protective effects of GA against the carbon Tetrachloride-induced hepatotoxicity may be due to its ability to block the bioactivation of carbon Tetrachloride, primarily by inhibiting the expression and activity of P450 2E1, and its free radical scavenging effects.
Eun-jeon Park - One of the best experts on this subject based on the ideXlab platform.
-
protective effect of curcumin in rat liver injury induced by carbon Tetrachloride
Journal of Pharmacy and Pharmacology, 2010Co-Authors: Eun-jeon Park, Chul Hyun Jeon, Jaebaek Kim, Dong Hwan SohnAbstract:This study was carried out to investigate the protective effects of curcumin on acute or subacute carbon Tetrachloride-induced liver damage in rats. Acute hepatotoxicity was induced by intraperitoneal injection of carbon Tetrachloride after 4 consecutive days of curcumin treatment. Subacute hepatotoxicity was induced by oral administration of carbon Tetrachloride twice a week during 4 weeks of curcumin treatment. In rats with acute liver injury, curcumin (100 and 200 mg kg(-1)) lowered the activity of serum alanine aminotransferase to 52-53% (P < 0.05) and aspartate aminotransferase to about 62% (P < 0.05) those of control rats. In rats with subacute liver injury, curcumin (100 mg kg(-1)) lowered the activity of serum alanine aminotransferase to 34% (P < 0.01) and alkaline phosphatase to 53% (P < 0.05) of control rats. The liver hydroxyproline content in the curcumin (100 mg kg(-1))-treated group was reduced to 48% of the carbon Tetrachloride control group (P < 0.01). Malondialdehyde levels in curcumin (100 mg kg(-1)) treated rat liver was decreased to 67% of the control rat liver (P < 0.01) in subacute injury. It was concluded that curcumin improved both acute and subacute liver injury induced by carbon Tetrachloride in rats.
-
the ethanol soluble part of a hot water extract from artemisia iwayomogi inhibits liver fibrosis induced by carbon Tetrachloride in rats
Journal of Pharmacy and Pharmacology, 2000Co-Authors: Eun-jeon Park, Ji-xing Nan, Ji-young Kim, Hee-chul Kang, Jung Hwan Choi, So Jung Lee, Bo Hye Lee, Sun Jin Kim, Jaehyun Lee, Y. C. KimAbstract:This study was carried out to investigate the protective effects of the hot-water extract from Artemisia iwayomogi (Compositae) on carbon Tetrachloride-induced liver fibrosis in rats. Liver injury was induced by oral administration of carbon Tetrachloride (1 mL kg−1) twice a week during 4 weeks of A. iwayomogi treatment. Extracts from A. iwayomogi were prepared and administered to rats orally (2 g kg−1 as A. iwayomogi for 4 weeks) as follows: group 1, hot-water extract; group 2, ethanol-soluble part of hot-water extract; group 3, ethanol-insoluble part of hot-water extract; and group 4, methanol extract. In rats treated with the ethanol-soluble part of the hot-water extract, liver hydroxyproline content was reduced to 74% that of carbon Tetrachloride control rats (P < 0.05). Protein expression of alpha smooth muscle cell like actin was also decreased in rats treated with the ethanol-soluble part of the hot-water extract, which indicates inhibition of hepatic stellate cell activation. Liver malondialdehyde levels were significantly lowered in rats treated with the ethanol-soluble part of hot-water extract (P < 0.05). Serum cholesterol levels in rats treated with hot-water extract, ethanol-soluble or -insoluble parts of hot-water extract or methanol extract were significantly reduced when compared with those of carbon Tetrachloride control rats (P < 0.05). The ethanol-soluble part of the hot-water extract from A. iwayomogi inhibited fibrosis and lipid peroxidation in rats with liver fibrosis induced by carbon Tetrachloride. Both hot-water extract (either ethanol-soluble or -insoluble) and methanol extract of A. iwayomogi also lowered serum cholesterol levels in fibrotic rats.
R P Mason - One of the best experts on this subject based on the ideXlab platform.
-
the detection of halocarbon derived radical adducts in bile and liver of rats
Drug Metabolism and Disposition, 1991Co-Authors: K T Knecht, R P MasonAbstract:The free radical metabolism of halocarbons has been studied in living animals by the techniques of spin trapping and electron paramagnetic resonance. Earlier work demonstrated that radical adducts of carbon Tetrachloride can be detected in the bile of living rats treated with carbon Tetrachloride and the spin trap phenyl-N-t-butyl nitrone. In this study, the biles and livers of treated animals have been examined in order to determine the factors that could affect the content of radical adduct detected in bile (e.g. bile flow rate). The approaches used include the quantitation of radiolabeled spin trap and of the trichloromethyl radical adduct in bile and liver, and the pharmacological manipulation of bile flow. Other halogenated hydrocarbons are thought to form free radicals in vivo, and have also been studied by these techniques. Bromotrichloromethane, a brominated analog of carbon Tetrachloride, readily forms the same radical adducts as carbon Tetrachloride. No radical adduct from chloroform, the corresponding hydrogenated analog, is detectable in bile. Radical adduct is only detectable in bile from bromoform-treated rats after the production of hypoxia.
-
the detection of halocarbon derived radical adducts in bile and liver of rats
Drug Metabolism and Disposition, 1991Co-Authors: K T Knecht, R P MasonAbstract:The free radical metabolism of halocarbons has been studied in living animals by the techniques of spin trapping and electron paramagnetic resonance. Earlier work demonstrated that radical adducts of carbon Tetrachloride can be detected in the bile of living rats treated with carbon Tetrachloride and the spin trap phenyl-N-t-butyl nitrone. In this study, the biles and livers of treated animals have been examined in order to determine the factors that could affect the content of radical adduct detected in bile (e.g. bile flow rate). The approaches used include the quantitation of radiolabeled spin trap and of the trichloromethyl radical adduct in bile and liver, and the pharmacological manipulation of bile flow. Other halogenated hydrocarbons are thought to form free radicals in vivo, and have also been studied by these techniques. Bromotrichloromethane, a brominated analog of carbon Tetrachloride, readily forms the same radical adducts as carbon Tetrachloride. No radical adduct from chloroform, the corresponding hydrogenated analog, is detectable in bile. Radical adduct is only detectable in bile from bromoform-treated rats after the production of hypoxia.
