基于抑制海马神经元铁凋亡的芦荟大黄素对铜负荷大鼠认知功能的保护作用

Xie Wang, Hong Chen, Nan Shao, Xiaoyan Zhang, Chenye Huang, Xiangjun Li, Juan Zhang, Ze Chang, Le Tang, Daojun Xie
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引用次数: 0

摘要

背景:芦荟大黄素(AE)是一种从传统中药中提取的单体,在临床治疗认知障碍方面具有显著疗效。铁突变(FPT)是细胞程序性死亡的一种特殊形式,在各种认知疾病的病理发展过程中起着至关重要的作用:本研究探讨了 AE 在大鼠威尔逊氏病认知障碍(WDCI)模型中的治疗潜力,并研究了这些效果是否通过沉默信息调节器 1(SIRT1)调节的 FPT 信号通路介导。我们采用了莫里斯水迷宫(MWM)、血红素和伊红(H&E)染色、透射电子显微镜(TEM)、免疫荧光(IF)、氧化应激标记物评估和 FPT 相关蛋白水平测量等技术,评估了 SIRT1 介导的 FPT 的程度和 AE 的疗效:WD铜负荷大鼠模型实验结果显示,MWM、H&E、TEM和IF结果表明AE具有促进学习和记忆功能恢复、改善海马神经元形态损伤和保护细胞膜完整性的潜力。免疫印迹(WB)和酶联免疫吸附(ELISA)分析结果表明,AE 能显著上调 SIRT1、核因子红细胞-2 相关因子 2(Nrf2)、溶质运载家族 7 成员 11(SCL7A11)和谷胱甘肽过氧化物酶 4 的表达、和谷胱甘肽过氧化物酶 4(GPX4)蛋白的表达,同时逆转氧化应激标记物(如丙二醛(MDA)、谷胱甘肽(GSH)、超氧化物歧化酶(SOD)和活性氧(ROS))的表达。因此,我们推测 AE 可通过激活 SIRT1 介导的信号通路来减轻 WD 铜负荷大鼠海马神经元 FPT:这些研究结果表明,AE可通过激活SIRT1介导的FPT减轻WD铜负荷模型大鼠海马神经元损伤,从而为临床治疗WDCI提供了一种有价值的候选中药单体。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Protective Effect of Aloe-emodin on Cognitive Function in Copper-loaded Rats Based on The Inhibition of Hippocampal Neuron Ferroptosis.

Background: Aloe-emodin (AE), a monomer derived from traditional Chinese medicine, has demonstrated remarkable efficacy in the clinical management of cognitive disorders. Ferroptosis (FPT), a specialized form of programmed cell death, plays a critical role in the pathological progression of various cognitive diseases.

Methods: This study explored the therapeutic potential of AE in a rat model of Wilson's disease cognitive impairments (WDCI) and examined whether these effects are mediated through the silencing information regulator 1 (SIRT1)-regulated FPT signaling pathway. Employing techniques, such as the Morris water maze (MWM), Hematoxylin & eosin (H&E) staining, Transmission electron microscopy (TEM), Immunofluorescence (IF), assessments of oxidative stress markers, and measurements of FPT-related protein levels, we evaluated the extent of SIRT1-mediated FPT and the therapeutic efficacy of AE.

Results: The findings from the WD copper-loaded rat model experiments revealed that MWM, H&E, TEM, and IF outcomes indicated AE's potential to promote the restoration of learning and memory functions, ameliorate hippocampal neuronal morphological damage, and preserve cell membrane integrity. Results from western blot (WB) and ELISA analyses demonstrated that AE markedly upregulated the expression of SIRT1, nuclear factor erythroid-2-related factor 2 (Nrf2), solute carrier family 7 member 11 (SCL7A11), and glutathione peroxidase 4 (GPX4) proteins while simultaneously reversing the expression of oxidative stress markers such as malondialdehyde (MDA), glutathione (GSH), and superoxide dismutase (SOD), and reactive oxygen species (ROS). Consequently, we posit that AE may attenuate WD copper-loaded rat model hippocampal neuronal FPT by activating the SIRT1-mediated signaling pathway.

Conclusion: These findings suggested that AE mitigates WD copper-loaded rat model hippocampal neuronal damage through the activation of SIRT1-mediated FPT, thereby presenting a valuable candidate Chinese herbal monomer for the clinical treatment of WDCI.

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