Abstract
Pretreating female Balb/c mice with schisandrin B (Sch B) at increasing daily doses
(1-4 mmol/kg) for 3 days caused dose-dependent increases in hepatic glutathione S-transferase (GST) and glutathione reductase (GRD) activities. However, the activities
of glucose-6-phosphate dehydrogenase (G6PDH), Se-glutathione peroxidase (GPX), and γ-glutamylcysteine synthetase (GCS) were down-regulated
to varying degrees in a dose-dependent manner. While there were biphasic changes in
hepatic reduced glutathione (GSH) level as well as susceptibility of hepatic tissue
homogenates to in vitro peroxide-induced GSH depletion, a gradual decrease in hepatic malondialdehyde content
was observed. The beneficial effect of Sch B on the hepatic GSH antioxidant system
became more evident after CC14 challenge. The same Sch B pretreatment regimen caused a dose-dependent protection
against carbon tetrachloride (CCl4)-induced hepatotoxicity. The hepatoprotection was associated with significant enhancement
in hepatic GSH status, as indicated by the substantial increase in tissue GSH levels
and the corresponding decrease in susceptibility of tissue homogenates to GSH depletion.
Where the activities of GST and GRD were increased linearly over non-CCl4 control values, there was also a gradual elevation in G6PDH activity upon administration
of increasing doses of Sch B. In contrast, GPX activity was moderately down-regulated.
The ensemble of results suggests that the hepatoprotection afforded by Sch B pretreatment
may mainly be attributed to the enhancement in the functioning of the hepatic GSH
antioxidant system, possibly through stimulating the activities of GSH related enzymes.
Key words
Schisandra chinensis
- Schisandraceae/Magnoliaceae - schisandrin B - glutathione S-transferases - glutathione reductase - glucose-6-phosphate dehydrogenase - carbon
tetrachloride
