17 research outputs found

    Reactive astrocytes in TLR4m AD mice increase compared to TLR4w AD mice by immunohistochemistry

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    The frozen sections of cerebral cortices from TLR4m (A and B) and TLR4w (C and D) AD mice were stained with anti-GFAP antibody. Scale bars are 50 μm in A and C, and 10 μm in B and D. The middle images (B and D) are a high magnification of the areas indicated by the squares in the top images (A and C). GFAP immunoreactive area percentages of TLR4m and TLR4w AD mice were shown as a bar graph (means ± SE, **P < 0.001) (E). Approximately 15 fields of the cerebral cortex (0.5 to 1 mmeach, using a 10× objective and 1× eyepiece lens) from 4 – 5 coronal brain sections, each separated by more than 240 μm interval, from each mouse were analyzed. TLR4m and TLR4w represent TLR4m and TLR4w AD mice, respectively.<p><b>Copyright information:</b></p><p>Taken from "Toll-like receptor 4-dependent upregulation of cytokines in a transgenic mouse model of Alzheimer's disease"</p><p>http://www.jneuroinflammation.com/content/5/1/23</p><p>Journal of Neuroinflammation 2008;5():23-23.</p><p>Published online 29 May 2008</p><p>PMCID:PMC2430555.</p><p></p

    Levels of GFAP and GAPDH in the cerebral tissue lysates were determined by immunoblotting using anti-GFAP and anti-GAPDH antibodies, respectively

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    The bar graph represents densitometric quantification of GFAP after normalization with GAPDH (means ± SE). GFAP levels in TLR4m AD mice are greater than those in TLR4w AD mice (*P < 0.05). Lane 1 through 4 are tissue lysates from TLR4m AD mice and lane 5 through 7 are from TLR4w AD mice.<p><b>Copyright information:</b></p><p>Taken from "Toll-like receptor 4-dependent upregulation of cytokines in a transgenic mouse model of Alzheimer's disease"</p><p>http://www.jneuroinflammation.com/content/5/1/23</p><p>Journal of Neuroinflammation 2008;5():23-23.</p><p>Published online 29 May 2008</p><p>PMCID:PMC2430555.</p><p></p

    Levels of CD11b and GAPDH in the cerebral tissue lysates were determined by immunoblotting using anti-CD11b and anti-GAPDH antibodies, respectively

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    The bar graph represents densitometric quantification of CD11b after normalization with GAPDH (means ± SE). The mean of CD11b levels in TLR4m AD mice is greater than that in TLR4w AD mice but not statistically significant. Lane 1 through 4 are tissue lysates from TLR4m AD mice and lane 5 through 9 are from TLR4w AD mice.<p><b>Copyright information:</b></p><p>Taken from "Toll-like receptor 4-dependent upregulation of cytokines in a transgenic mouse model of Alzheimer's disease"</p><p>http://www.jneuroinflammation.com/content/5/1/23</p><p>Journal of Neuroinflammation 2008;5():23-23.</p><p>Published online 29 May 2008</p><p>PMCID:PMC2430555.</p><p></p

    Levels of cerebral cytokines and chemokines in TLR4m AD and non-AD mice at the age of 13–15 months

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    Levels of cytokines and chemokines in the cerebral tissue lysates were determined by multiplex cytokine/chemokine array analysis. Hatched and open bars represent levels of cytokines and chemokines in TLR4m AD and non-AD mice, respectively. Mean concentrations ± SE are expressed in picograms per milligram of brain protein. *P < 0.05.<p><b>Copyright information:</b></p><p>Taken from "Toll-like receptor 4-dependent upregulation of cytokines in a transgenic mouse model of Alzheimer's disease"</p><p>http://www.jneuroinflammation.com/content/5/1/23</p><p>Journal of Neuroinflammation 2008;5():23-23.</p><p>Published online 29 May 2008</p><p>PMCID:PMC2430555.</p><p></p

    Levels of cerebral cytokines and chemokines in TLR4w AD and non-AD mice at the age of 13–15 months

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    Levels of cytokines and chemokines in the cerebral tissue lysates were determined by multiplex cytokine/chemokine array analysis. Hatched and open bars represent levels of cytokines and chemokines in TLR4w AD and non-AD mice, respectively. Mean concentrations ± SE are expressed in picograms per milligram of brain protein. *P < 0.05, **P = 0.001.<p><b>Copyright information:</b></p><p>Taken from "Toll-like receptor 4-dependent upregulation of cytokines in a transgenic mouse model of Alzheimer's disease"</p><p>http://www.jneuroinflammation.com/content/5/1/23</p><p>Journal of Neuroinflammation 2008;5():23-23.</p><p>Published online 29 May 2008</p><p>PMCID:PMC2430555.</p><p></p

    Additional file 1: of Rubus crataegifolius Bunge regulates adipogenesis through Akt and inhibits high-fat diet-induced obesity in rats

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    Effects of supplementing RCB on body weight gain, and serum profiles in rats fed a high fat diet for two weeks. (A) Weight gain, (B) serum triglyceride level, and (C) total cholesterol level. The values are expressed as the mean ± SD. The bars showing different letters indicate significant differences among each group of bars, according to Duncan’s test; *p < 0.05. (ZIP 90 kb

    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

    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
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