5 research outputs found

    Comparison of Soluble Aβ42/40 by the CG extracts on Tg mice brain.

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    <p>The cerebral Aβ42(A) and Aβ40 (B) load was quantitated by capturing antigen such as Amyloid beta 42 and/or Amyloid beta 40 mediated Enzyme-Linked Immunosorbent Assay (ELISA) kit (Invitrogen, CA) using brain lysates (i.e., total brain lysate of hippocampus and neocortex area) from the EA-CG-treated or vehicle (PBS)-treated Tg (Mo/Hu APPswe PS1dE9) mice. The cerebral Aβ42 concentrations in the EA-CG-treated mice were significantly reduced compared to the vehicle-treated controls (**P < 0.01). The values shown were the means ± S.E.M. (n = 10 per group).</p

    Comparison of the amyloid burden in the Tg brains by the CG extracts.

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    <p>(A) The amyloid plaques were identified by immunohistochemistry (IH) and H&E counterstaining. The CG extract-treated (EA-CG fraction) and control Tg brain sections were formalin fixed and subjected to immunohistochemistry with the 6E10 antibody that interacts with the Aβ1–16 epitope (monoclonal antibody) in the hippocampus (a, control; b, EA-CG treated) and cortex (e, control; f, EA-CG-treated). Concomitant with the IH staining, other hippocampal (n = 6) (c, vehicle; d, EA-CG-treated) and cortical (n = 6) (g, vehicle; h, EA-CG-treated) sections from the Mo/Hu APPswe PS1dE9 mice were subjected to H&E counterstaining. The scale bar indicates 200 μm (a through h). The amyloid load (% of stained area) as a quantitation result was decreased by the CG extracts (B. hippocampus area; C. cortex area). The area in the hippocampus (D, vehicle alone vs. EA-CG) and cortex (E, vehicle alone vs. EA-CG) was quantified by comparing the morphometric analysis of the Thioflavin-S-stained area between the vehicle-treated vs. EA-CG-treated Mo/Hu APPswe PS1dE9 brain sections. The values (%) shown were the means ± S.E.M. *p < 0.05, Tg vs. Tg+EA-CG.</p

    Effect of CG extracts on liver toxicity using aspartate/alanine aminotransferase activity in Tg mice.

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    <p>The Mo/Hu APPswe PS1dE9 mice were fed with or without EA-CG (50 mg/kg BW) for 6 months. The brain were isolated from the EA-CG treated and control (PBS) groups (n = 3 mice per each group). After the brain was divided in half, we tested the gene expression profile of the inflammatory cytokines IL-1α (A) and IFN-γ (B) as markers of the cellular response by semi-quantitative RT-PCR. The fold change was presented after normalization to the housekeeping gene β-actin). *p < 0.05; n.s. mean not significant. The levels of Aspartate aminotransferase activity (AST, Units/L) and Alanine aminotransferase activity (ALT, Units/L)) were measured in the sera by centrifugation after obtain mice blood from each group, and then the relative value (U/L) of ALT (C) or AST (D) as hepatotoxicity markers were measured and presented after comparison to the controls (PBS groups), according to the manufacturer’s instructions. The values were presented as the means ± S.E.M (n = 3 mice per each group). n.s. mean not significant.</p

    Effect of Centipedegrass (CG) extract on humoral immune response in APP/PS1 transgenic (Tg) mice.

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    <p>The CG ethylacetate (EA-CG) fraction contains five flavoglycosides, including Maysin and other phytochemicals, as described in a previous study [<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0169509#pone.0169509.ref020" target="_blank">20</a>]. Mouse sera were isolated from the EA-CG-treated and control Tg animal subjects (Mo/Hu APPswe PS1dE9) after feeding with admixture in diet food for 6 months (n = 10 mice per each group; all male and 10 weeks old mice). (A, B) To measure the beta amyloid dependent antibody response, using a sandwich ELISA, quantitation was performed utilize the Aβ1–42 synthetic peptide as the coating antigen and HRP-conjugated secondary IgG or IgM as a secondary antibody. Immunoglobulin IgG (A) and Immunoglobulin IgM (B), markers of an immune response against the EA-CG extract, were measured by ELISA, which was described in detail in the Materials and Methods. The values were presented as the means ± S.E.M. *p < 0.05 means statistically significant.</p

    Assessment workflow of novel Anti-AD effectiveness using Maysin and its flavonoid derivative compounds on APP/PS1 AD mice model.

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    <p>Complication of traumatic brain injury is associated with inflammation and neural cell death from induction of Aβ 42/40 formation likely due to unfolded cerebral plaque or fibril form which results from genetic alteration in APPswe and PSEN1dE9 in the 85Dbo/J mice model for Experimental AD study. Experimental design for treatment and sampling procedure as the objectives in animal model to understand anti-AD of Maysin flavonoid with respect to prevention and/or prophylactic effect against Aβ40/42 mediated neuronal-toxicity and functional delineation as the assessment workflow in animal study are presented.</p