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甲对老鼠CKD诱导的认知功能障碍的神经保护作用:CBS和Nrf2/HO-1通路的作用

Zeinab Hamidizad^1,2, Mehri Kadkhodaee³, Farzaneh Kianian³

¹Electrophysiology Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran.

Neuromolecular medicine

|January 8, 2025

概括

氧化 (NO) 有效治疗老鼠慢性病 (CKD) 引起的认知缺陷和神经元损伤. 这些好处取决于囊氨酸β合成酶 (CBS) 活性和硫化 (H2S) 水平.

科学领域:

神经科学是一个神经科学.
腎臟病學 (nephrology) 是一種醫學專業.
生物化学生化学

背景情况:

慢性病 (CKD) 与认知障碍和痴呆症有关.
尿素毒素,氧化应激和炎症是CKD相关神经系统疾病的关键媒介.
氧化 (NO) 在神经元信号传递和细胞内通路中起着至关重要的作用.

研究的目的:

研究NO在缓解与CKD相关的认知缺陷方面的治疗潜力.
探索核因子-红色素因子2相关因子2 (Nrf2) /血氧酶-1 (HO-1) 途径和囊氨酸β-合成酶 (CBS) 在NO的影响中的参与.

主要方法:

建立了一种CKD (5/6腎切除术) 的老鼠模型.
这些组包括假药,CKD,CKD + NO捐赠体 (SNP) 和CKD + SNP + CBS抑制剂 (AOAA).
用行为测试评估认知功能; 生物化学和组织学分析评估神经元损伤和通路活动.

主要成果:

慢性结核病的老鼠表现出显著的认知衰退,增加了血液尿素 (BUN) 和血清肌素 (sCr),以及神经元损伤.
慢性瘤还降低了海马和前额叶皮层中的Nrf2/HO-1通路活性.
SNP治疗改善了认知功能,减少了神经元损伤,并恢复了Nrf2/HO-1活性,但这些效应被CBS抑制剂消除了.

结论:

氧化 (NO) 在改善慢性瘤的认知障碍和神经元损伤方面表现出显著的有效性.
的神经保护作用取决于氨酸β合成酶 (CBS) 的活性和内源硫化 (H2S) 的产生.
针对NO-CBS-H2S轴可能提供一种新的治疗策略,用于治疗慢性病患者的神经并发症.

关键词:

这是CBS的活动.慢性脏疾病慢性脏疾病认知障碍认知障碍是一种认知障碍.酸尼特罗普鲁化 Nrf2/HO-1信号通路的使用情况

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