Pien Tze Huang Protects the Liver against Carbon Tetrachloride‐Induced Damage
: Pien Tze Huang, a traditional Chinese medicine, has been extensively used as a therapeutic drug in the treatment of liver diseases. In this study, we have examined its ability to protect the liver from carbon tetrachloride (CCl4)‐induced damage in the mouse. Histological observations revealed that...
Gespeichert in:
Veröffentlicht in: | Pharmacology & toxicology 2002-10, Vol.91 (4), p.185-192 |
---|---|
Hauptverfasser: | , , , , |
Format: | Artikel |
Sprache: | eng |
Schlagworte: | |
Online-Zugang: | Volltext |
Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
Zusammenfassung: | : Pien Tze Huang, a traditional Chinese medicine, has been extensively used as a therapeutic drug in the treatment of liver diseases. In this study, we have examined its ability to protect the liver from carbon tetrachloride (CCl4)‐induced damage in the mouse. Histological observations revealed that CCl4 treatment induced extensive degenerative changes in the hepatocytes surrounding the central veins of the liver. However, these changes were much reduced by more than 28% in mice fed with 0.5 mg of Pien Tze Huang/g body weight/dose (3 doses over 36 hr) prior to CCl4 treatment. The effects of Pien Tze Huang were then further investigated in a hepatoma cell line. Flow analysis showed that it had no significant effects on cell proliferation. When the ability of Pien Tze Huang to influence various response elements of important signal transduction pathways was examined in the hepatoma cell line, it was found that Pien Tze Huang stimulated an increase in the response of AP1, CRE and NFκB responsive elements. The transcriptional factors of these responsive elements are known to play important roles in regulating cell death and survival. We thus postulate that the ability of Pien Tze Huang to protect the liver from damage is attained through its ability to modulate the activity of these important signal transduction pathways. |
---|---|
ISSN: | 0901-9928 1600-0773 |
DOI: | 10.1034/j.1600-0773.2002.910406.x |