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槐角苷通过调节麻醉暴露新生大鼠的LTR-4/NF-κB/PI3K信号通路减轻神经元损伤并改善认知功能改变。

Sophoricoside attenuates neuronal injury and altered cognitive function by regulating the LTR-4/NF-κB/PI3K signalling pathway in anaesthetic-exposed neonatal rats.

作者信息

Yang Lihua, Xu Yucan, Zhang Wei

机构信息

Department of Anesthesiology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China.

出版信息

Arch Med Sci. 2020 Mar 10;20(1):248-254. doi: 10.5114/aoms.2020.93638. eCollection 2024.

Abstract

INTRODUCTION

This study examined the protective effects of sophoricoside on neuronal injury and cognitive dysfunction in anaesthetic-exposed neonatal rats.

MATERIAL AND METHODS

Neuronal injury was induced in rat pups by exposure to isoflurane (0.75%) with 30% oxygen for 6 h on P7. The protective effects of sophoricoside were evaluated by assessing cognitive function using the neurological score and Morris water maze. Neuronal apoptosis was assessed in hippocampus tissue using a TUNEL assay. The cytokine and macrophage inflammatory protein levels were assessed by ELISA. Western blot assays and RT-PCR were performed to assess the expression of NF-κB, TLR-4, Akt, and PI3K proteins in neuronal tissues. Immunohistochemical and histopathological changes were observed in the brain tissues of isoflurane-induced neuronal injury rats.

RESULTS

The sophoricoside treatment improved cognitive and neuronal function in rats exposed to isoflurane. Cytokine and MIP levels in the brain tissues of isoflurane-exposed rats decreased. However, sophoricoside treatment attenuated the expression of TLR-4, PI3K, and Akt protein in the brain tissues of isoflurane-exposed rats. The histopathology improved in the sophoricoside-treated isoflurane-exposed rats.

CONCLUSIONS

Sophoricoside treatment protects against neuronal injury and reduced cognitive function in isoflurane-induced neuronal injury rats by regulating TLR-4 signalling.

摘要

引言

本研究探讨了槐角苷对麻醉暴露新生大鼠神经元损伤和认知功能障碍的保护作用。

材料与方法

在出生后第7天,将幼鼠暴露于含30%氧气的0.75%异氟烷中6小时,诱导神经元损伤。通过神经学评分和莫里斯水迷宫评估认知功能,以评价槐角苷的保护作用。使用TUNEL检测法评估海马组织中的神经元凋亡。通过ELISA评估细胞因子和巨噬细胞炎性蛋白水平。进行蛋白质免疫印迹分析和RT-PCR,以评估神经元组织中NF-κB、TLR-4、Akt和PI3K蛋白的表达。观察异氟烷诱导的神经元损伤大鼠脑组织中的免疫组织化学和组织病理学变化。

结果

槐角苷治疗改善了暴露于异氟烷的大鼠的认知和神经元功能。暴露于异氟烷的大鼠脑组织中的细胞因子和MIP水平降低。然而,槐角苷治疗减弱了暴露于异氟烷的大鼠脑组织中TLR-4、PI3K和Akt蛋白的表达。槐角苷治疗的暴露于异氟烷的大鼠的组织病理学得到改善。

结论

槐角苷治疗通过调节TLR-4信号传导,对异氟烷诱导的神经元损伤大鼠的神经元损伤和认知功能降低具有保护作用。

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