18 research outputs found

    Serum insulin levels during IPGTT (in ng/ml).

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    <p>Comparison of insulin levels in IUGR and normal groups from 3 to 15 weeks of age. Data are means ± SE from 4 animals from each group at each age.</p><p>*<i>P</i><0.05 vs. control rats.</p

    Pancreas weights (A) and pancreas weight/body weight (B) of IUGR and control rats from birth to 15 weeks of age.

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    <p>Values are the means ± SE from each group. *** <i>P</i><0.001, ** <i>P</i><0.01, * <i>P</i><0.05 vs. control rats.</p

    Comparison of GSIS test of islets in vitro from 3 to 15 weeks of age in IUGR and normal groups.

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    <p>Values are the means ± SE from 4 animals from each group. ** <i>P</i><0.01 vs. control rats.</p

    Serum glucose levels during ITT (in mmol/l).

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    <p>Comparison of glucose levels in IUGR and normal groups from newborn to 15 weeks of age. Data are means ± SE from 5 to 7 animals from each group at each age.</p><p>*<i>P</i><0.05 vs. control rats.</p

    Choline Plasmalogens Isolated from Swine Liver Inhibit Hepatoma Cell Proliferation Associated with Caveolin-1/Akt Signaling

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    <div><p>Plasmalogens play multiple roles in the structures of biological membranes, cell membrane lipid homeostasis and human diseases. We report the isolation and identification of choline plasmalogens (ChoPlas) from swine liver by high performance thin layer chromatography (HPTLC) and high performance liquid chromatography (HPLC)/MS. The growth and viability of hepatoma cells (CBRH7919, HepG2 and SMMC7721) was determined following ChoPlas treatment comparing with that of human normal immortal cell lines (HL7702). Result indicated that ChoPlas inhibited hepatoma cell proliferation with an optimal concentration and time of 25 μmol/L and 24 h. To better understand the mechanism of the ChoPlas-induced inhibition of hepatoma cell proliferation, Caveolin-1 and PI3K/Akt pathway signals, including total Akt, phospho-Akt(pAkt) and Bcl-2 expression in CBRH7919 cells, were determined by western blot. ChoPlas treatment increased Caveolin-1 expression and reduced the expression of phospho-Akt (pAkt) and Bcl-2, downstream targets of the PI3K/Akt pathway. Further cell cycle analysis showed that ChoPlas treatment induced G<sub>1</sub> and G<sub>1</sub>/S phase transition cell cycle arrest. The expression of essential cell cycle regulatory proteins involved in the G<sub>1</sub> and G<sub>1</sub>/S phase transitions, cyclin D, CDK4, cyclin E and CDK2, were also analyzed by western blot. ChoPlas reduced CDK4, cyclin E and CDK2 expression. Taken together, the results indicate that swine liver-derived natural ChoPlas inhibits hepatoma cell proliferation associated with Caveolin-1 and PI3K/Akt signals. </p> </div

    Effect of ChoPlas on Caveolin-1.

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    <p>CBRH7919 cells were treated with 25 μmol/L ChoPlas for 24 h and then harvested. (A)Total protein was extracted and then blotted with caveolin-1antibody; (B) Graph depicting the semi-quantization of caveolin-1expression computed using Image J software. Data are presented as the mean±S.D(n=3).</p

    Hypothesized model for the proliferation inhibition mechanism of ChoPlas on hepatoma cells.

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    <p>Exogenous natural ChoPlas activates caveolin-1, affecting PI3K/Akt pathway signals and decreasing cell cycle regulatory proteins and Bcl-2 expression. </p
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