A novel experimental model of acute hypertriglyceridemia induced by schisandrin B.
Mice were intragastrically treated with single doses (0.05-0.8g/kg) of schisandrin B (a dibenzocyclooctadiene derivative isolated from the fruit of Schisandra chinensis). Twenty-four hours after schisandrin B administration, the serum triglyceride level was increased by 10-235% in a dose-dependent manner. However, the serum low density lipoprotein cholesterol level was significantly decreased by 28% at a dose of 0.8g/kg. When given once daily (0.01-0.2g/kg) for 4days, schisandrin B also dose-dependently elevated the serum triglyceride level (17-134%). Kinetics parameters estimated by Scott's plot analysis of schisandrin B-induced changes in serum and hepatic triglyceride levels were determined: serum-E(max) (maximal effect)=6mmol/L (384% increase, P<0.001); K(D) (affinity)=0.59mmol/kg; pD(2) (an index of affinity)=6.62; liver-E(max)=21mumol/g (68% increase, P<0.001); K(D)=0.37mmol/kg; pD(2)=6.83. The efficacy of schisandrin B in increasing the triglyceride level was 5.6-fold higher in serum than in liver tissue. Fenofibrate (0.2g/kg) treatment, when in combination with schisandrin B (0.2g/kg), for 4days significantly reduced the schisandrin B-induced increase in serum triglyceride level (by 81%, P<0.001). Hepatic triglyceride level was also decreased (by 100%, P<0.001) by co-treatment with fenofibrate. Our results suggest that schisandrin B treatment can be used to establish a mouse model of acute hypertrigylceridemia.[1]References
- A novel experimental model of acute hypertriglyceridemia induced by schisandrin B. Pan, S.Y., Dong, H., Han, Y.F., Li, W.Y., Zhao, X.Y., Ko, K.M. Eur. J. Pharmacol. (2006) [Pubmed]
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