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核因子-κB调节产前应激诱导的子代大鼠认知障碍。

NF-kappaB regulates prenatal stress-induced cognitive impairment in offspring rats.

作者信息

Li Hui, Li Xia, Jia Ning, Cai Qing, Bai Zhuanli, Chen Rui, Song Tianbao, Zhu Zhongliang, Liu Jiankang

机构信息

Xi'an Jiaotong University.

出版信息

Behav Neurosci. 2008 Apr;122(2):331-9. doi: 10.1037/0735-7044.122.2.331.

Abstract

The study was designed to investigate whether nuclear factor of kappa B (NF-kappaB) plays regulating role in prenatal stress-induced cognitive impairment and oxidative damage in offspring rats. The authors used a rat model to study plasma levels of corticosterone and oxidative DNA damage (8-OH-dG), protein expression of P65/p50 NF-kappaB, and cognitive function in female and male offspring rats in middle pregnant stage and later pregnant stage. Prenatal stress affected the capability of learning and memory in the offspring, especially in later stage stressed female offspring. The levels of corticosterone and 8-OH-dG were enhanced in response to stress. Both middle and later stage stresses induced a significant decrease in P65 expression and a significant increase in P50 expression in female offspring. In addition, later stage stress induced a significant decrease in P50 expression in male offspring. These results suggest that NF-kappaB complex may be acting in a positive regulatory fashion in prenatal stress-induced cognitive impairment and that oxidative DNA damage may exacerbate the activation of NF-kappaB.

摘要

本研究旨在探讨核因子κB(NF-κB)是否在产前应激诱导的子代大鼠认知障碍和氧化损伤中发挥调节作用。作者使用大鼠模型研究妊娠中期和后期子代大鼠血浆皮质酮水平、氧化性DNA损伤(8-羟基脱氧鸟苷,8-OH-dG)、P65/p50 NF-κB蛋白表达及认知功能。产前应激影响子代的学习和记忆能力,尤其是后期应激的雌性子代。应激反应导致皮质酮和8-OH-dG水平升高。妊娠中期和后期应激均导致雌性子代P65表达显著降低,P50表达显著升高。此外,后期应激导致雄性子代P50表达显著降低。这些结果表明,NF-κB复合物可能在产前应激诱导的认知障碍中发挥正向调节作用,且氧化性DNA损伤可能加剧NF-κB的激活。

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