妊娠期糖尿病大鼠暴露于低温会引起后代大脑的氧化变化

Rizwan Sharief, Afreen Mahaboob, P. MahaboobBasha
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摘要

背景:产前压力是独特的,由于一系列的问题,可以影响胚胎/胎儿从受孕开始。妊娠期糖尿病是孕妇关注的问题,其中葡萄糖耐受不良伴持续高血糖是妊娠期的威胁因素。目的:如果多种应激源对宫内生活造成影响,而胎盘在妊娠期间成为交感神经张力增加的目标,则可能存在功能脆弱性,这可能有助于产后生活的发病机制。研究后代大脑区域差异可能有助于了解产前应激诱导的抗氧化屏障变化和促进氧化应激。材料和方法:本研究评估了暴露于妊娠糖尿病(链脲佐菌素诱导)和冷应激(15°C和20°C)的大鼠后代离散脑区氧化应激指数的变化。结果:研究结果明确了冷应激在脑隔间内引起更高程度氧化应激的参与,如抗氧化酶的减少,即超氧化物歧化酶、过氧化氢酶、谷胱甘肽过氧化物酶、谷胱甘肽s -转移酶和谷胱甘肽,以及丙二醛浓度的增加。结果强调,由于自由基的产生增加,应激源的协同作用。与20°C的暴露相比,15°C的冷应激通过消耗糖尿病受试者的抗氧化酶而引起加重作用。结论:研究结果证明冷应激对妊娠期胎儿是一个重要的刺激,并可触发氧化应激,尤其是糖尿病患者,并可能造成不利影响。这些变化在一定程度上解释了产前压力受试者更容易出现功能障碍,包括记忆和认知过程的缺陷。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Consequential exposure to hypothermia in gestational diabetic rats induces oxidative changes in the brain of offspring
Background: Prenatal stress is unique due to range of problems and can affect the embryo/fetus beginning with conception. Gestational diabetes mellitus is the concern for expectant-mothers wherein glucose intolerance with consistent hyperglycemia is a threatening factor during pregnancy. Objectives: In the event of multiple stressors posing their effects on intrauterine life and placenta being the target of increased sympathetic tone during gestation, there is a possibility of functional vulnerabilities that may contribute to the pathogenesis in post-natal life. Studying brain regional discrepancies in offspring might help to know the prenatal stress-induced variation in the antioxidant barrier and promoted oxidative stress. Materials and Methods: The changes occurring in oxidative stress indices in discrete brain regions of rat offspring born as a consequential exposure to gestational diabetes (streptozotocin induction) and cold stress (15 and 20°C) are assessed in this study. Results: The findings specify the involvement of cold-stress provoked induction of higher degree oxidative stress within brain compartments as evidenced by a decrease in antioxidant enzymes, namely, superoxide dismutase, catalase, glutathione peroxidase, glutathione S-transferase, and GSH as well as increase in the concentration of malondialdehyde. Results highlight the synergistic actions of stressors due to the increased generation of free radicals. Cold stress at 15°C found to cause exacerbatory actions by depleting antioxidant enzymes in diabetic subjects than the exposures made at 20°C. Conclusion: The findings prove that cold stress is a crucial stimulus to a fetus during gestation and acts as a trigger of oxidative stress especially in diabetic subjects and can pose an adverse impact. These changes could partly explain the increased vulnerability of prenatally stressed subjects to functional disorders including deficits in memory and cognitive processes in later life.
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