The effect of the free cholesterol alone and the mixture of cholesterol and β muricholic acid on the synthesis of cholesterol and bile acids were otherved in cultured HepG2 cells.It was found that the free cholestero...The effect of the free cholesterol alone and the mixture of cholesterol and β muricholic acid on the synthesis of cholesterol and bile acids were otherved in cultured HepG2 cells.It was found that the free cholesterol ( 10 μM ,60 μm) inhibited the incorporation of [14C] acetate into cholesterol. (P<0. 01). The mixture of cholesterol and βmuricholic acid (cholesterol 10 μM, 60 μM and βmuricholic acid 200 μM) produced the same effect on the incorporation of [14C] acetate into cholesterol (P< 0. 01 ) .We falled to find the change of the activity of the enzyme HMGCoA reductase despite the novo synthesis of cholesterol markely decreased .The incorporation of [14C] acetate into bile acids decreased especially in chenodeoxycholic acid in presence of cholesterol 10 μM or 60 μM, or in presence of cholesterol 10 μM, 60 μM and βmuricholic acid 200 μM. (P<0. 05). In order to recognize the iuhibitory mechanism , we further more investigated the change of the activity of the enzyme 7acholesterol. We found that in the groupe treated by either chulesterol alone or by the mixture of chulesterol andβmuricholic acid, the activity of 7acholesterol hydroxylase decreased compared with the control group (P<0. 05).I. Bjokhem and H. Danieisson have concluded that 7ahydroxycholesterol was synthesised preferentially from newly synthesized cholesterol. In our experimence, the novo synthesis of cholesterol decreased in consequence the synthesis of bile acids decreased, it was uniform with this theory.In addition, we first time demonstrated that the “feed beck” inhibitory mechanism by the bile acid itself is via the cholesterol.展开更多
文摘The effect of the free cholesterol alone and the mixture of cholesterol and β muricholic acid on the synthesis of cholesterol and bile acids were otherved in cultured HepG2 cells.It was found that the free cholesterol ( 10 μM ,60 μm) inhibited the incorporation of [14C] acetate into cholesterol. (P<0. 01). The mixture of cholesterol and βmuricholic acid (cholesterol 10 μM, 60 μM and βmuricholic acid 200 μM) produced the same effect on the incorporation of [14C] acetate into cholesterol (P< 0. 01 ) .We falled to find the change of the activity of the enzyme HMGCoA reductase despite the novo synthesis of cholesterol markely decreased .The incorporation of [14C] acetate into bile acids decreased especially in chenodeoxycholic acid in presence of cholesterol 10 μM or 60 μM, or in presence of cholesterol 10 μM, 60 μM and βmuricholic acid 200 μM. (P<0. 05). In order to recognize the iuhibitory mechanism , we further more investigated the change of the activity of the enzyme 7acholesterol. We found that in the groupe treated by either chulesterol alone or by the mixture of chulesterol andβmuricholic acid, the activity of 7acholesterol hydroxylase decreased compared with the control group (P<0. 05).I. Bjokhem and H. Danieisson have concluded that 7ahydroxycholesterol was synthesised preferentially from newly synthesized cholesterol. In our experimence, the novo synthesis of cholesterol decreased in consequence the synthesis of bile acids decreased, it was uniform with this theory.In addition, we first time demonstrated that the “feed beck” inhibitory mechanism by the bile acid itself is via the cholesterol.
