33 research outputs found

    Renal levels of glutathione and MDA in the experimental groups.

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    <p>(n = 10 each group): SO-P =  sham-operated-placebo; SO-T<sub>3</sub> =  sham-operated, T<sub>3</sub>-treated (100 μg/kg); IR-P =  ischemia-reperfusion, placebo-treated; IR-T<sub>3</sub> =  ischemia-reperfusion, T<sub>3</sub>-treated. Data are means ± SEM. ** p<0.001 <i>versus</i> SO-P group. + p<0.05, ++ p<0.001 <i>versus</i> SO-T<sub>3</sub> group. # p<0.05, ## p<0.001 <i>versus</i> IR-P group.</p

    Representative microphotograph of morphological changes in renal parenchyma of male Wistar rats after 48-reperfusion.

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    <p>Absence of glomerular or tubular injury in kidney sections of rats in SO-P (A) and SO-T3 (B) groups. Rats exposed to bilateral renal ischemia-reperfusion pre-treated with placebo, IR-P (C), show intense acute tubular necrosis (asterisk) with severe detachment of epithelial cells from the basement membrane, loss of brush border, and intratubular casts. The IR-T3 group (D) shows mild tubular necrosis and moderate sloughing of tubular cells (PAS, original magnification ×20).</p

    Glomerular (A) and tubular (B) expression of PARP-1 in the experimental groups.

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    <p>(n = 10 each group): SO-P =  sham-operated-placebo; SO-T<sub>3</sub> =  sham-operated, T<sub>3</sub>-treated (100 μg/kg); IR-P =  ischemia-reperfusion, placebo-treated; IR-T<sub>3</sub> =  ischemia-reperfusion, T<sub>3</sub>-treated. Data are means ± SEM. * p<0.05, ** p<0.001 <i>versus</i> SO-P group.+ p<0.05, ++ p<0.001 <i>versus</i> SO-T<sub>3</sub> group. # p<0.05, ## p<0.001 <i>versus</i> IR-P group.</p

    Variables of renal function.

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    <p>SO-P = sham-operated-placebo; SO-T<sub>3</sub> =  sham-operated, T<sub>3</sub>-treated (100 μg/kg); IR-P =  ischemia-reperfusion, placebo-treated; IR-T<sub>3</sub> =  ischemia-reperfusion, T<sub>3</sub>-treated. Data are means ± SEM, n = 10 each group. * p<0.01, ** p<0.001 compared with the SO-P group. † p<0.01, † † p<0.001 compared with the SO-T<sub>3</sub> group. ‡ p<0.01, ‡ ‡ p<0.001 compared with the IR-P group.</p

    Plasma IL6 levels in the experimental groups.

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    <p>(n = 10 each group): SO-P  =  sham-operated-placebo; SO-T<sub>3</sub> =  sham-operated, T<sub>3</sub>-treated (100 μg/kg); IR-P =  ischemia-reperfusion, placebo-treated; IR-T<sub>3</sub> =  ischemia-reperfusion, T<sub>3</sub>-treated. Data are means ± SEM. ** p<0.001 <i>versus</i> SO-P group. ++ p<0.001 <i>versus</i> SO-T<sub>3</sub> group. # p<0.05, ## p<0.001 <i>versus</i> IR-P group.</p

    Percentage (A) and score (B) of acute tubular necrosis in the experimental groups.

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    <p>(n = 10 each group): SO-P =  sham-operated-placebo; SO-T<sub>3</sub> =  sham-operated, T<sub>3</sub>-treated (100 μg/kg); IR-P =  ischemia-reperfusion, placebo-treated; IR-T<sub>3</sub> =  ischemia-reperfusion, T<sub>3</sub>-treated. Data are means ± SEM. * p<0.05, ** p<0.001 <i>versus</i> SO-P group. + p<0.05, ++ p<0.001 <i>versus</i> SO-T<sub>3</sub> group. # p<0.01 <i>versus</i> IR-P group.</p

    Representative microphotograph of the immunohistochemistry study of PARP-1 expression in renal cortex of male Wistar rats after 48 h of ischemia-reperfusion.

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    <p>Absence of nuclear expression in SO-P (A) and SO-T<sub>3</sub> (B) groups. The IR-P group (C) shows intense nuclear expression (brown deposit) in >80% of tubular cells. The IR-T3 group (D) shows moderate nuclear expression in <20% of tubular cells (micropolymer peroxidase conjugated, original magnification ×20).</p

    Assessment of kidney biopsies and quantification of inflammatory infiltrate in rat control and ischemia/reperfusion groups at different times.

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    <p>Values are expressed as mean ± standard deviation.</p><p>Control: Placebo-treated (SO-P) + sham-operated T<sub>3</sub>- treated (SO- T<sub>3</sub>); I/R-injured placebo-treated (IR-P); I/R-injured T<sub>3</sub>-treated (IR- T<sub>3</sub>) groups. * P<0.05 IR-P vs. Controls; <sup>†</sup> P<0.05 IR- T<sub>3</sub> vs. Controls; Mann Whitney U-test.</p

    Plasma glutathione and MDA levels, and total urinary excretion of hydrogen peroxide and of isoprostanes.

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    <p>(Upper panels) Plasma glutathione and MDA levels, and (lower panels) total urinary excretion of hydrogen peroxide and of isoprostanes in the experimental groups (n = 10 each group),: SO-P  =  sham-operated-placebo; SO-T<sub>3</sub> =  sham-operated, T<sub>3</sub>-treated (100 μg/kg); IR-P =  ischemia-reperfusion, placebo-treated; IR-T<sub>3</sub> =  ischemia-reperfusion, T<sub>3</sub>-treated. Data are means ± SEM. * p<0.05, ** p<0.001 <i>versus</i> SO-P group. + p<0.01, ++ p<0.001 <i>versus</i> SO-T<sub>3</sub> group. # p<0.05, ## p<0.001 <i>versus</i> IR-P group.</p

    AIQ administration inhibits inflammatory response in CIA.

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    <p>DBA1 mice with established CIA were injected i.p. either with PBS (control) or with AIQ (1.5 mg/kg) on day 25 post-immunization. Systemic and local expression of inflammatory mediators was assayed in protein extracts from joints (A) and sera (B) isolated at day 35 post-immunization. A paw from an unimmunized mouse was analyzed simultaneously for assessment of the basal response. n = 3–4 mice/group. *p<0.001 versus controls.</p
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