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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, 2004
    Co-Authors: Kyung Jin Lee, Eunrhan Woo, Chul Yung Choi, Dong Weon Shin, Dong Gun Lee, Ho Jin You, Hye Gwang Jeong
    Abstract:

    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, 2002
    Co-Authors: Hye Gwang Jeong, Ho Jin You, Sung Jun Park, Ae Ran Moon, Young Chul Chung, Shin Keon Kang, Hyo Kon Chun
    Abstract:

    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, 1999
    Co-Authors: Hye Gwang Jeong
    Abstract:

    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.

Leeyan Sheen - One of the best experts on this subject based on the ideXlab platform.

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, 2002
    Co-Authors: Hye Gwang Jeong, Ho Jin You, Sung Jun Park, Ae Ran Moon, Young Chul Chung, Shin Keon Kang, Hyo Kon Chun
    Abstract:

    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, 2004
    Co-Authors: Kyung Jin Lee, Eunrhan Woo, Chul Yung Choi, Dong Weon Shin, Dong Gun Lee, Ho Jin You, Hye Gwang Jeong
    Abstract:

    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, 2002
    Co-Authors: Hye Gwang Jeong, Ho Jin You, Sung Jun Park, Ae Ran Moon, Young Chul Chung, Shin Keon Kang, Hyo Kon Chun
    Abstract:

    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.

Stryjecka M Zimmer - One of the best experts on this subject based on the ideXlab platform.