21 research outputs found

    A-769662 treatment abrogated joint damage and IL-6 expression in passive K/BxN arthritis.

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    <p>(A) Representative H&E and Safranin O stained sections of ankle joints on day 7 of arthritis induction in DMSO and A-769662-treated mice. Magnification 200x original. Black arrows in H&E stained sections show joint inflammation and white arrows in Safranin O stained sections show cartilage damage that was reduced in A-769662-treated ankles. (B) Histological scores for joint inflammation, erosion and cartilage damage in vehicle and high dose A-769662-treated mice on day 7 after serum transfer. (C) Proteins of joint tissues from naive (n = 3 mice per group) and arthritic mice (n = 5 mice per group) of DMSO and A-769662-treated mice were extracted and analyzed by ELISA for the presence of the indicated cytokines.</p

    A-769662 activated AMPKα and regulated NF-κB and MAPK signaling in BMDMs.

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    <p>BMDMs were cultured in the presence of different concentrations of A-769662 for 2 hours (A), or BMDMs were pre-treated with A-769662 for 2 hours before stimulated with LPS (1 μg/ml) (B). Lysates of BMDMs were prepared and analyzed for the expression of the indicated proteins by Western blot (WB). Semi-quantitative densitometry analysis of Western blots (arbitrary densitometry units) for phosphorylation of indicated proteins normalized to total protein is shown. Results are representative of three independent experiments.</p

    AMPKα1 deficiency mildly increased clinical arthritis in K/BxN arthritis.

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    <p>WT mice and AMPKα1 KO were injected with 100μl serum from adult K/BxN mice on day 0 to induce arthritis. (A) Clinical score and ankle thickness in WT and AMPKα1 deficient animals (n = 5 mice per group) at day 6 after arthritis induction. (B) Proteins of joint tissues from naive (n = 4 mice per group) and arthritic mice (n = 4 mice per group) of WT and AMPKα1 deficient mice were extracted at day 6 after arthritis induction and analyzed by ELISA for the presence of IL-6. (C) Clinical score in WT animals (black circles, n = 6) and AMPKα1 animals (black squares, n = 6). Values are means ± SEM. * = p<0.05; ** = p<0.01.</p

    A-769662 treatment activated AMPK in joints and diminished clinical arthritis in passive K/BxN arthritis.

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    <p>WT mice were injected with 150μl serum from adult K/BxN mice on day 0 to induce arthritis. A-769662 was administrated twice a day from day 0. (A) Proteins of joint tissues from naive and arthritic mice injected with control vehicle (DMSO) and A-769662 (60mg/kg) were extracted and analyzed for phospho-AMPKα, phosphor-ACC, total AMPKα and total ACC by WB. D as DMSO and A as A-796662. Semi-quantitative densitometry analysis of Western blots (arbitrary densitometry units) for phosphorylation of AMPKα and ACC normalized to total AMPKα and ACC respectively is shown. (B) Clinical score at day 7 in mice treated with vehicle, A-769662 at high (60mg/kg) and low dose (30mg/kg) (n = 5 mice per group). (C) Ankle thickness in DMSO-treated animals (black circles, n = 9) and high dose A-769662-treated animals (black squares, n = 5) injected with 150 μl of K/BxN serum on day 0. Values are means ± SEM. * = p<0.05; ** = p<0.01.</p

    AMPK inhibited IL-6 and NO production in BMDMs stimulated with TLR2 and TLR4 agonists.

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    <p>(A,B) BMDMs were pre-treated with A-769662 (100, 250 or 500 μM) for 2 hours before stimulated with LPS (1 μg/ml) and Pam3Cys4 (1 μg/ml) for 18 hours. The conditioned media was subjected to ELISA and Griess reaction for the indicated cytokine and NO release, respectively. (C,D) BMDMs were pre-treated with A-769662 (100 μM) for 2 hours before stimulated with LPS for two hours. RNA was isolated and analyzed for the expression of the indicated genes. (E,F) BMDMs were pre-treated with A-769662 (100 μM) for 2 hours before stimulated with LPS (1 μg/ml) and Pam3Cys4 (1 μg/ml) for 18 hours. The conditioned media was subjected to ELISA for the indicated cytokines. Results are expressed as means ± SEM.* p< 0.05 vs DMSO; ** p<0.01; *** p<0.001 and are representative of four independent experiments.</p

    A-769662 treatment also abrogated joint damage and IL-6 expression in AIA.

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    <p><b>(</b>A) Representative H&E and Safranin O stained sections of knee joints on day 10 of AIA induction in vehicle and A-769662-treated mice, which were treated either at day 0 or day 4 after intraarticular injection of mBSA (n = 5 mice per group). Original magnification 200x. (B) Knee thickness in A-769662-treated mice on day 10 of AIA induction. (C) Sections of knee joints were scored for inflammatory infiltration, bone erosion and cartilage damage. A-769662-treated mice had significantly lower scores than WT. (D) Proteins of joint tissues from naive (n = 3 mice per group) and arthritic mice (n = 5 mice per group) of vehicle and A-769662-treated mice were extracted and analyzed by ELISA for the presence of IL-6. (E) Serum from naive (n = 3 mice per group) and arthritic mice (n = 5 mice per group) of vehicle and A-769662-treated mice was analyzed by ELISA for IL-6. Results are expressed as means ± SEM.* p< 0.05 vs WT mice; ** p<0.01</p
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