Preventive effect of Oren-gedoku-to (Huanglian-Jie-Du-Tang) extract on the progression of D-galactosamine-induced liver injury.
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Accession number;03A0126865
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| Title;Preventive effect of Oren-gedoku-to (Huanglian-Jie-Du-Tang) extract on the progression of D-galactosamine-induced liver injury. |
| Author;
OTA YOSHIJI
(Fujitahoken'eiseidai I Kagaku)
KONGO MUTSUMI
(Fujita Health Univ.)
HAYASHI TAKAHIRO
(Fujitahoken'eiseidai Byoin Yakuzaibu)
INAGAKI SHOJI
(Fujitahoken'eiseidai Byoin Yakuzaibu)
KISHIKAWA TERUAKI
(Fujita Health Univ.)
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Journal Title;Journal of Traditional Medicines
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Journal Code:Y0941A
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ISSN:1340-6302
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VOL.19;NO.6;PAGE.223-229(2002)
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| Figure&Table&Reference;FIG.5, REF.31 |
| Pub. Country;Japan |
| Language;Japanese |
| Abstract;We examined the preventive effect of Oren-gedoku-to (Huanglian-Jie-Du-Tang) extract (Tsumura TJ-15) on the progression of D-galactosamine (GAL)-induced liver injury in rats. In rats receiving a single intraperitoneal injection of GAL (500 mg/kg body weight), an apparent liver injury occurred 6 h after treatment and the liver injury progressed at 24 h, judging from the levels of serum liver cell damage markers such as aminotransferases, albumin, and triglyceride. Oral administration of TJ-15 (500 mg/kg body weight) to GAL-treated rats, which was conducted 6 h after hepatotoxin treatment, prevented liver injury progression observed at 24 h after hepatotoxin treatment. The hepatic concentrations of triglyceride and thiobarbituric acid reactive substances, an index of lipid peroxidation, and the hepatic activity of 5'-nucleotidase, a marker enzyme of plasma membranes, in GAL-treated rats increased 24 h, but not 6 h, after treatment. The hepatic activity of myelpoperoxidase, an index of tissue neutrophil infiltration, in GAL-treated rats increased 6 h after treatment and this increase in activity was enhanced at 24 h. The post-oral administration of TJ-15 attenuated all these changes observed at 24 h after GAL treatment. These results indicate that TJ-15 exerts a preventive effect on the progression of GAL-induced liver injury in rats possibly through its inhibitory actions against lipid peroxidation, triglyceride accumulation, plasma membrane destruction, and neutrophil infiltration in the liver tissue. (author abst.) |
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