Attenuation by Oren-gedoku-to Extract (TJ-15) of Disruption of Hepatic Reactive Oxygen Species Metabolism with Progression of Carbon Tetrachloride-Induced Acute Liver Injury in Rats

DOI 参考文献27件
  • Ohta Yoshiji
    Department of Chemistry, School of Medicine, Fujita Health University
  • Kongo-Nishimura Mutsumi
    Department of Pediatric Surgery, School of Medicine, Fujita Health University
  • Hayashi Takahiro
    Department of Pharmacy, Fujita Health University Hospital
  • Matsura Tatsuya
    Division of Medical Biochemistry, Department of Pathophysiology and Therapeutic Science, Faculty of Medicine, Tottori University
  • Yamada Kazuo
    Division of Medical Biochemistry, Department of Pathophysiology and Therapeutic Science, Faculty of Medicine, Tottori University

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We attempted to elucidate how Oren-gedoku-to (Huanglian-Jie-Du-Tang) extract (TJ-15), a Chinese herbal medicine, attenuates the disruption of hepatic reactive oxygen species metabolism with the progression of carbon tetrachloride (CCl4)-induced acute liver injury in rats. TJ-15 (100, 250 or 500 mg/kg body weight) was orally administered to rats injected with CCl4 (1 ml/kg, i.p.) at 6 h after the toxicant treatment. Post-administered TJ-15 reduced progressive liver injury in CCl4-treated rats at 24 h after the toxicant treatment dose-dependently. The liver of rats treated with CCl4 alone showed increases in the concentration of thiobarbituric acid-reactive substances, an index of lipid peroxidation, and xanthine oxidase activity and decreases in reduced glutathione and ascorbic acid concentrations and superoxide dismutase, catalase, and glutathione reductase activities at 24 h after the toxicant treatment. The liver of CCl4-treated rats showed no change in Se-glutathione peroxidase activity and an increase in hepatic glucose-6-phosphate dehydrogenase activity at 24 h after the toxicant treatment. Post-administered TJ-15 attenuated the increases in hepatic thiobarbituric acid-reactive substances and xanthine oxidase activity and the decreases in hepatic reduced glutathione and ascorbic acid concentrations and superoxide dismutase, catalase, and glutathione reductase activities dose-dependently but did not affect the hepatic Se-glutathione peroxidase activity and the increased hepatic glucose-6-phosphate dehydrogenase activity. These results indicate that orally administered TJ-15 attenuates the disruption of hepatic reactive oxygen species metabolism with the progression of CCl4-induced acute liver injury in rats through its direct and indirect antioxidant actions. The results also suggest that this attenuating effect of TJ-15 could contribute to its preventive effect on the progression of CCl4-induced acute liver injury.

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