A novel experimental model of acute hypertriglyceridemia induced by schisandrin B

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Abstract

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—Emax (maximal effect) = 6mmol/L (384% increase, P < 0.001); KD (affinity) = 0.59mmol/kg; pD2 (an index of affinity) = 6.62; liver—Emax = 21μmol/g (68% increase, P < 0.001); KD = 0.37mmol/kg; pD2 = 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.

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