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DHEA Treatment Effects on Redox Environment in Skeletal Muscle of Young and Aged Healthy Rats

机译:DHEA治疗效果对年轻和老年健康大鼠骨骼肌中氧化还原环境的影响

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Background: Dehydroepiandrosterone (DHEA) is an important precursor of active steroidhormone, produced abundantly by the adrenal cortex with an age-dependent pattern.Objective: We investigated whether chronic DHEA administration impacts on redox status and onAkt protein activation in skeletal muscle during the aging process (3 and 24 months-old rats).Methods: Rats received one weekly dose/5 weeks of DHEA (10 mg/kg) or vehicle. Gastrocnemiusmuscle was removed to evaluate glutathione system, hydrogen peroxide, antioxidant enzymes, andexpression of Akt kinase protein.Results: In the 3-months-old rats DHEA induced an increase in hydrogen peroxide when comparedboth to its control (276%) and the 24-months-old DHEA group (485%). Moreover, in the 24-months-old rats DHEA caused an increase in GSSG (41 and 28%), a decrease in reduced-GSH (55and 51%), and a more oxidized redox status (reduction in GSH/GSSG ratio, 47 and 65 %) whencompared to 3-month-old DHEA and to 24-months-old control groups, respectively. Both oldergroups had increased G6PDH (2.7 fold) and GST (1.7 fold) activities when compared to youngergroups, independently of any DHEA treatment. However, there was no modulation of Akt protein(phosphorylated/total isoform).Conclusion: The results show that chronic DHEA administration to 3 and 24-months-old rats maynot present positive effects regarding the redox environment in skeletal muscle without modulationof pro-survival Akt kinase. Due to the large-scale self-administration of DHEA as an “anti-aging”dietary supplement, it is crucial to investigate its molecular mechanisms over oxidative stressinducedrelated diseases.
机译:背景:脱氢哌啶(DHEA)是活性甾体激素的重要前兆,其肾上腺皮质与年龄依赖的模式大规模生产。药物:在老化过程中,研究了慢性DHEA给药是否对氧化还原状态和OnaKT蛋白激活的影响(3和24个月大鼠)。方法:大鼠每周一次剂量/ 5周的DHEA(10mg / kg)或载体。除去胃肠血清血管以评估谷胱甘肽系统,过氧化氢,抗氧化酶,Akt激酶蛋白的表达。结果:在3个月大的大鼠中,DHEA与其对照时(276%)和24-几个月的DHEA集团(485%)。此外,在24个月大的大鼠DHEA中导致GSSG(41和28%)的增加,降低降低(551%)和更氧化的氧化还原状态(降低GSH / GSSG比率,47 65%)分别与3个月历史的DHEA和24个月历史的对照组。与年轻群组相比,两种较大较大的较大较大的G6PDH(2.7倍)和GST(1.7倍)活动。然而,没有调节Akt蛋白质(磷酸化/总同种型)。结论:结果表明,慢性DHEA给予3和24个月大的大鼠可能存在关于骨骼肌中氧化还原环境的积极作用,而不会调节Pro-survival akt激酶。由于DHEA的大规模自我施用作为“抗衰老”膳食补充剂,研究其在氧化应激疾病的分子机制至关重要。

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