21 research outputs found

    Выращивание ремонтного молодняка кур при использовании пробиотических препаратов «Бацелл» и «Моноспорин»

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    Применение пробиотических препаратов с первых дней жизни цыплят позволит получить в дальнейшем здоровую птицу с высокой реализацией генетического потенциала

    Release of TXB<sub>2</sub> (stable metabolite of TXA<sub>2</sub>) under non-stimulation (A) or ACh-stimulation (B) in carotid arteries.

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    <p>Control carotid arteries were incubated for 30°C with vehicle (saline) or 1.65×10<sup>7</sup> cells/mL of control or STZ PLTs before this experiment. (B) TXB<sub>2</sub> production in each treated or untreated carotid artery from control or diabetic rats with ACh (10<sup>−6</sup> M) stimulation. Data are means ± SE; n = 5–6. <i>***P</i><0.001 vs. Control+Veh (only ACh-treated carotid arteries from control). ##<i>P<</i>0.01 vs. Control + Control PLTs.</p

    8-isoprostane concentrations in carotid arterial strips from controls treated with control or STZ PLTs, A.

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    <p>Data are means ± SE; n = 5; <i>##P<</i>0.01 vs. +Control PLTs. Effect of the SOD mimetic tempol on the ACh-induced relaxation of carotid arterial rings from controls induced for 30 min with PLTs isolated from control (Control PLTs) and diabetic (STZ PLTs) rats and tempol (10<sup>−4</sup> M), B. Carotid arterial rings were preincubated with each type of PLT (1.65×10<sup>7</sup> cells/mL; 30 min) or each type of PLT along with tempol. Data are means ± SE; n = 4, ***<i>P<</i>0.001 vs. Control veh, ###<i>P<</i>0.001 vs. +Control PLTs, &&<i>P<</i>0.01 or &&&<i>P<</i>0.001 vs. +STZ PLTs/tempol. Quantification of carotid arterial superoxide anion production by measuring the amount of reduced NBT, C. Control carotid arteries were incubated for 30 min at 37°C with 1.65×10<sup>7</sup> cells/mL of Control or STZ PLTs. Data are means ± SE; n = 5; *<i>P<</i>0.05 or **<i>P<</i>0.01 vs. control + Veh.</p

    ACh-induced vasorelaxation of carotid arterial rings from controls induced for 30 min with PLTs isolated from control (Control PLTs) and diabetic (STZ PLTs) rats.

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    <p>(A) 36-weeks old. (B) 52-weesks old. Carotid arterial rings were preincubated with each type of PLT (1.65×10<sup>7</sup> cells/mL+ 30 min). Data are means ± SE; n = 4; **<i>P<</i>0.01, ***<i>P<</i>0.001 vs. control.</p

    Role of PLT activation in the relationship between diabetes and reduced vascular relaxation.

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    <p>Role of PLT activation in the relationship between diabetes and reduced vascular relaxation.</p

    Effect of PLTs on the phosphorylation of Akt and eNOS.

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    <p>(A) Representative Western blots. Single bands at 60 kDa (Akt), 140 kDa (eNOS), and 42 kDa (β-actin) were observed. (B and D) Effect of PLTs isolated from control or diabetic rats (1.65×10<sup>7</sup> cells/mL; 30 min) on ACh-induced Akt phosphorylation (Ser<sup>473</sup>) (B) or eNOS hosphorylation (Ser<sup>1177</sup>) (D). (C) Total Akt and eNOS expression. (E) Total eNOS expression. Data are means ± SE; n = 5–6. *<i>P</i><0.05 or **<i>P<</i>0.01 vs. *+Veh (ACh-stimulated carotid artery from untreated control).</p

    Total eNOS and eNOS dimers/monomers in HUVEC cultured under control PLTs or STZ PLTs stimulation.

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    <p>Western blots for eNOS expression (A) and eNOS dimer/monomer (B) in HUVECs cultured with PLTs (1.65×10<sup>7</sup> cells/mL; 30 min) isolated from control or diabetic rats. Data are means ± SE; n = 6; *<i>P</i><0.05, **<i>P</i><0.01 vs. vehicle, ##<i>P<</i>0.01 vs. +Control PLTs.</p

    Concentration-response curves for endothelium-dependent vasorelaxation elicited by the cumulative application of ACh (A and C) and endothelium-independent relaxation by incremental concentrations of SNP (B and D) in isolated carotid arterial rings.

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    <p>(A) Effects of the NOS inhibitor L-NNA on the ACh-induced relaxation of carotid arterial rings from control and diabetic (STZ-induced) rats. Carotid arterial rings were preincubated with L-NNA (10<sup>−4</sup> M; 30 min). (C and D) Effects of PLTs. ACh-induced (C) and SNP-induced (D) vasorelaxation of carotid arterial rings from controls induced for 30 min with PLTs isolated from control (Control PLTs) and diabetic (STZ PLTs) rats. Carotid arterial rings were preincubated with each type of PLT (1.65×10<sup>7</sup> cells/mL; 30 min). Data are means ± SE; n = 5; <i>***P</i><0.001 vs. Control, <i>##P</i><0.01 or ###<i>P<</i>0.001 vs. Diabetic or +Control PLTs.</p

    Release of NOx under ACh stimulation in carotid arteries.

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    <p>Control carotid arteries were incubated for 30°C with 1.65×10<sup>7</sup> cells/mL of control or STZ PLTs before this experiment. The release of NOx in each treated or untreated carotid artery from control or diabetic rats with ACh (10<sup>−6</sup> M) stimulation. Data are means ± SE; n = 5–6. <i>*P</i><0.05 or <i>***P</i><0.001 vs. Control+Veh (only ACh-treated carotid arteries from control). #<i>P<</i>0.05, ##<i>P<</i>0.01, or ###<i>P<</i>0.001 vs. Control + Control PLTs.</p

    Values of various parameters in diabetic and control rats.

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    <p>Values are means ± SE. Number of determinations is shown within parentheses. **P<0.01, ***P<0.001 vs. Control.</p><p>HDL, High Density Lipoprotein.</p><p>NEFA, non-esterified fatty acid.</p
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