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Changes in butyrylcholinesterase activity and serum lipids after oxprenolol and glibenclamide treatments in non-diabetic rats.

Arzneimittelforschung. 2006;56(2):64-9. doi:10.1055/s-0031-1296703
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摘要


The effects of chronic treatment with oxprenolol (CAS 6452-72-7, OXP, 15 mg/ kg/ day) or glibenclamide (CAS 10238-21-8, GL, 2.5 mg/kg/day), or their combination administered for 6 and 12 weeks, on the butyrylcholinesterase (BuChE) activity in plasma and liver and on the plasma levels of triglycerides, total cholesterol and high density lipoprotein (HDL)-cholesterol were studied in normal, non-diabetic female rats. In all treated groups a significant increase of plasma BuChE activity was obtained after 6 weeks of either OXP (46 %), or GL (36 %) treatment, or of their concurrent application (24 %). After 12 weeks of treatment, the increase in enzyme activity was significant only in the OXP group. The BuChE activity in the liver was increased (between 3-25 %) in all treated groups except in one during 6 and 12 weeks of treatment. These effects of either OXP or GL, or their combination on BuChE activity in liver suggest their stimulating effects on enzyme synthesis. The changes of total plasma cholesterol in all groups were insignificant. On the other hand, HDL-cholesterol was significantly decreased in all treated groups. After 6 weeks of treatment, GL, OXP, or their combination caused a decrease in plasma HDL cholesterol by 19, 50 or 22 % respectively, when compared with the control group. After 12 weeks of GL, OXP, or GL+OXP administration, HDL-cholesterol plasma levels in treated groups were 32, 25 and 22 % lower than in the control group. Treatment with GL, OXP, or GL+OXP during 6 weeks had no significant effect on triglycerides level. However, after 12 weeks of GL, OXP, or GL+OXP administration, the triglycerides levels were significantly increased (9, 47 and 36 %) when compared with the control group. These results showed that the increase in BuChE activity might be the first sign of altered triglyceride and lipoprotein metabolism.

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