妊娠引起的氧化应激和炎症与母体神经元活动或记忆功能受损无关。

IF 2.2 3区 医学 Q3 PHYSIOLOGY
Jessica L Bradshaw, E Nicole Wilson, Jennifer J Gardner, Steve Mabry, Selina M Tucker, Nataliya Rybalchenko, Edward Vera, Styliani Goulopoulou, Rebecca L Cunningham
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引用次数: 0

摘要

妊娠与神经和行为可塑性、全身炎症和氧化应激有关。然而,炎症和氧化应激对孕期母体神经和行为可塑性的影响尚不清楚。我们假设,健康妊娠会短暂降低学习和记忆能力,而这些缺陷与妊娠引起的炎症和氧化应激升高有关。我们使用新物体识别(回忆记忆)、莫里斯水迷宫(空间记忆)和开阔地(焦虑样)行为任务对不同生殖状态的雌性 Sprague-Dawley 大鼠的认知表现进行了测试[非妊娠(空腹)、妊娠(临产)和妊娠后 1-2 个月(初产妇);n = 7-8/ 组]。使用 MILLIPLEX® 磁珠检测法测量血浆和 CA1 促炎细胞因子。血浆氧化应激通过高级氧化蛋白产物(AOPP)检测法进行测量。CA1 氧化应激、神经元活性和细胞凋亡的标记物通过 Western 印迹法进行量化。我们的研究结果表明,与无胎盘大鼠相比,妊娠大鼠的 CA1 氧化应激相关标记物升高(p ≤ 0.017),但妊娠大鼠与初产大鼠的氧化应激相关标记物水平相当。相反,生殖状态并不影响 CA1 炎症细胞因子、神经元活性或细胞凋亡。同样,生殖状态对回忆记忆或空间记忆也没有影响。尽管如此,初产大鼠的空间学习能力受损(p ≤ 0.007),焦虑样行为减少(p ≤ 0.034)。总之,我们的数据表明,母体海马 CA1 受到全身炎症的保护,但容易受到围产期氧化应激的影响。围产期氧化应激升高(如妊娠并发症)可能会导致围产期神经和行为的可塑性。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Pregnancy-induced oxidative stress and inflammation are not associated with impaired maternal neuronal activity or memory function.

Pregnancy is associated with neural and behavioral plasticity, systemic inflammation, and oxidative stress, yet the impact of inflammation and oxidative stress on maternal neural and behavioral plasticity during pregnancy is unclear. We hypothesized that healthy pregnancy transiently reduces learning and memory and these deficits are associated with pregnancy-induced elevations in inflammation and oxidative stress. Cognitive performance was tested with novel object recognition (recollective memory), Morris water maze (spatial memory), and open field (anxiety-like) behavior tasks in female Sprague-Dawley rats of varying reproductive states [nonpregnant (nulliparous), pregnant (near term), and 1-2 mo after pregnancy (primiparous); n = 7 or 8/group]. Plasma and CA1 proinflammatory cytokines were measured with a MILLIPLEX magnetic bead assay. Plasma oxidative stress was measured via advanced oxidation protein products (AOPP) assay. CA1 markers of oxidative stress, neuronal activity, and apoptosis were quantified via Western blot analysis. Our results demonstrate that CA1 oxidative stress-associated markers were elevated in pregnant compared with nulliparous rats (P ≤ 0.017) but there were equivalent levels in pregnant and primiparous rats. In contrast, reproductive state did not impact CA1 inflammatory cytokines, neuronal activity, or apoptosis. Likewise, there was no effect of reproductive state on recollective or spatial memory. Even so, spatial learning was impaired (P ≤ 0.007) whereas anxiety-like behavior (P ≤ 0.034) was reduced in primiparous rats. Overall, our data suggest that maternal hippocampal CA1 is protected from systemic inflammation but vulnerable to peripartum oxidative stress. Peripartum oxidative stress elevations, such as in pregnancy complications, may contribute to peripartum neural and behavioral plasticity.NEW & NOTEWORTHY Healthy pregnancy is associated with elevated maternal systemic and brain oxidative stress. During postpregnancy, brain oxidative stress remains elevated whereas systemic oxidative stress is resolved. This sustained maternal brain oxidative stress is associated with learning impairments and decreased anxiety-like behavior during the postpregnancy period.

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来源期刊
CiteScore
5.30
自引率
3.60%
发文量
145
审稿时长
2 months
期刊介绍: The American Journal of Physiology-Regulatory, Integrative and Comparative Physiology publishes original investigations that illuminate normal or abnormal regulation and integration of physiological mechanisms at all levels of biological organization, ranging from molecules to humans, including clinical investigations. Major areas of emphasis include regulation in genetically modified animals; model organisms; development and tissue plasticity; neurohumoral control of circulation and hypertension; local control of circulation; cardiac and renal integration; thirst and volume, electrolyte homeostasis; glucose homeostasis and energy balance; appetite and obesity; inflammation and cytokines; integrative physiology of pregnancy-parturition-lactation; and thermoregulation and adaptations to exercise and environmental stress.
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