9 research outputs found

    AS induces lipolysis in mature adipocytes by activating the phosphorylation and activity of PKA and HSL.

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    <p>Fully differentiated 3T3-L1 adipocytes were incubated in the absence and presence of various concentrations of AS (0, 0.5, 1.5, and 4.5 μM) for 3 h. Immunoblots are representative of seven independent experiments; β-actin served as a loading control. *P < 0.05, **P < 0.01, ***P < 0.001 vs. untreated adipocytes at the same time point.</p

    AS inhibits 3T3-L1 preadipocyte differentiation and fat accumulation.

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    <p>(<b>A</b>) Cell viability was assessed with the MTT assay24 h after AS treatment. (<b>B</b>) Relative lipid content. (<b>C</b>) Inhibition of fat droplet formation by AS. 3T3-L1 cells were seeded and induced to differentiate for 8 days with or without AS in 6-well plates, then stained with Oil Red O and imaged by light microscopy (200×). Values are expressed as mean ± SEM. Significant differences were observed between the untreated and differentiated control cells. *P < 0.05, **P < 0.01, **P < 0.001 vs. AS-treated cells; <sup>#</sup>P < 0.05, <sup>##</sup>P < 0.01, <sup>###</sup>P < 0.001 vs. differentiated control cells.</p

    AS inhibits PPARγ, C/EBPα, HSL, and ATGL expression in adipocytes.

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    <p>Protein levels were assessed by western blotting in 3T3-L1 cells cultured for 0, 2, 4, and 7 days in the presence or absence of 1.5 μM AS during adipogenesis. Immunoblots are representative of five independent experiments; β-actin served as a loading control. *P < 0.05, **P < 0.01, ***P < 0.001 vs. untreated adipocytes at the same time point.</p

    AS extract reduces adipose tissue weight, white adipocyte size and liver accumulation in obese rats.

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    <p>Coefficients of (<b>A</b>) epididymal adipose tissue and (<b>B</b>) liver were calculated after rats had fasted for 12 h at the end of experiment according to the following equation: coefficient = tissue (g/rat)/weight (g/rat). (<b>C</b>) Epididymal adipose tissue and (<b>D</b>) liver were stained with hematoxylin and eosin for histopathological examination. Images were acquired at 400× magnification on a light microscopy. Values are expressed as mean ± SE (n = 6). Significant differences were observed between normal and HFD groups. *P < 0.05, **P < 0.01, ***P < 0.001 vs. normal group; <sup>#</sup>P < 0.05, <sup>##</sup>P < 0.01, <sup>###</sup>P < 0.001 vs. model group.</p

    AS extract reduces HFD-induced obesity in rats.

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    <p>Rats were randomly divided into five groups: normal control, HFD model, and HFD with AS extract (100, 300, or 900 mg/kg). The extract was intragastric administered for 6 weeks. (<b>A</b>) Food intake per rat was recorded six times a week. (<b>B</b>) Food efficiency ratio was calculated as body weight gain divided by food intake. (<b>C</b>) Change in body weight was measured six times a week. (<b>D</b>) Body weight gain measured in a given week was subtracted from the weight in the previous week. Values are expressed as mean ± SE (n = 30). Significant differences were observed between normal and HFD groups. *P < 0.05, **P < 0.01, ***P < 0.001 vs. normal group; <sup>#</sup>P < 0.05, <sup>##</sup>P < 0.01, <sup>###</sup>P < 0.001 vs. model group.</p

    MOESM4 of Enhancement of scutellarin oral delivery efficacy by vitamin B12-modified amphiphilic chitosan derivatives to treat type II diabetes induced-retinopathy

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    Additional file 4. Effects of chronic treatment of Scu or Scu-loaded nanoparticles on body weight and blood-glucose in STZ-induced diabetic rats. (A) The changes of body weight of rats. (B) The changes of blood-glucose in rats. STZ was administrated to the DM group, DM +Chit-DC group, DM + Scu group, DM + Chit-DC-Scu group, and DM + Chit-DC-VB12-Scu group at week 8(n = 8)
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