13 research outputs found

    Cholesterol metabolism associated gene and protein expressions.

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    <p>Representative Western blot and group data depicting LDLR protein and mRNA abundance (A), cyp7α-1 protein and mRNA abundance (B) in livers, ABCG5 protein and mRNA abundance(C), ABCG8 protein and mRNA abundance(D), NPC1L1 protein and mRNA abundance(E) in intestines of hamsters. N = 8 per group. # P<0.05 compared with Control group, *P<0.05 compared with Simvastatin group.</p

    Effect of APS on fractional cholesterol absorption and cholesterol synthesis rates in hamsters.

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    <p>Values are means±SD of 8 animals per group.</p>#<p>P<0.05 compared with Control group,</p><p>*P<0.05 compared with Simvastatin group.</p

    Relationships between plasma lipids and intestinal cholesterol absorption.

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    <p>Intestinal cholesterol absorption rates are significantly correlated with the plasma LDL-C (A) and TC (B) levels, respectively.</p

    Changes of plasma lipids in response to APS and simvastatin treatments.

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    <p>APS and simvastatin significantly lowered total cholesterol (TC), triglycerides (TG), high-density lipoprotein –cholesterol (HDL-C) and low-density lipoprotein-cholesterol (LDL-C) concentrations compared to the control. # P<0.05 compared with control group.</p

    Effect of APS and simvastatin on fecal excrection of bile acids and neutral sterol.

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    <p>The daily total bile acids and neutral sterols were measured and expressed per 100 g body weight (BW). Values are means±SDs of 8 animals per group.</p>#<p>P<0.05 compared with Control group,</p><p>*P<0.05 compared with Simvastatin group.</p

    HE staining of liver tissue from different groups (Original magnification, Ă—200).

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    <p>A: control group; B: APS group; C: Simvastatin group. Livers of APS and Simvastatin group show mild fatty degeneration. In contrast, livers of control rats showed severe fatty degeneration, extensive hepatocytes hypertrophy, oedema, and vacuolization of the hepatocyte cytoplasm.</p
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