Abstract:

Destroying the balance of plasma cholesterol into hypercholesterolemia is a major risk factor for atherosclerosis.
The aim of this report was to investigate the effects of phlorizin on blood cholesterol level and gene expression of cholesterolregulating
enzymes in Golden Syrian hamsters maintained on a 0.1% cholesterol high fat diet. Totally 36 hamsters were
randomly divided into control group and three experimental groups with 3, 6, and 9 g/kg phlorizin, and serum total
cholesterol (TC), triacylglycerols (TG) and high-density-lipoprotein-cholesterol (HDL-C) were detected. Then, the contents
of cholesterol in liver and fecal neutral and acidic sterols were determined by GC. The gene expression of cholesterolregulating
proteins in the small intestine was assayed with Real-Time PCR. Serum TC and TG were significantly decreased
in 9 g/kg phlorizin group compared with those in the control group, while HDL-C in 6 and 9 g/kg phlorizin groups were
significantly increased (P ＜ 0.01). The hepatic cholesterol level in the experimental groups supplemented with 6 and 9 g/kg
phlorizin was significantly lower than that in the control group (P ＜ 0.01). Higher excretion of fecal cholesterol was observed
in the phlorizin groups. The amount of total fecal neutral sterols was increased compared with that in the control group
(P ＜ 0.05 or P ＜ 0.01). The excretion of total fecal acidic sterols was increased as the amount of phlorizin increased (6 g/kg,
P ＜ 0.05; 9 g/kg, P ＜ 0.01). It was also found that the cholesterol-lowering activity of phlorizin was associated with downregulation
of intestinal 3-hydroxy-3-methyl glutaryl-CoA (HMG-CoA) reductase, niemann-pick C1-like 1 (NPC1L1), acyl-
CoA-cholesterol acyltransferase 2 (ACAT2), microsomal triacylglycerol transport protein (MTP), and up-regulation of ATPbinding
cassette transporter such as subfamily G member 5 and 8 (ABCG5/8) transporters. The mechanisms underlying the
cholesterol-lowering activity of phlorizin were mediated most likely by increasing the sterol excretion and decreasing the
cholesterol absorption and synthesis.

Key words: phlorizin, hamsters, small intestine, serum lipid, gene expression