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泰莫林-GHaR减轻LPS诱导的认知障碍和微质激活,通过调节内分泌网膜应激应激

Da-Qi Zhang^1,2,3, Xiaoqian Dong¹, Simin Su¹

¹Key Laboratory of Tropical Biological Resources of Ministry of Education, School of Pharmaceutical Sciences, Collaborative Innovation Center of One Health, Hainan University, Haikou, 570228, China.

Probiotics and antimicrobial proteins

|May 11, 2024

概括

泰莫林-GHaR (GHaR) 通过减少神经炎症来缓解认知障碍. GHaR抑制了微质激活和内质网膜应激 (ERS),提供神经保护.

科学领域:

神经科学是一个神经科学.
免疫学免疫学免疫学

背景情况:

由微质细胞驱动的神经炎症是认知障碍的一个关键因素.
细胞内膜网膜应激 (ERS) 和NF-κB信号传递与神经炎症过程有关.

研究的目的:

为了研究临时-GHaR (GHaR) 在改善认知功能方面的潜力.
阐明GHaR对神经炎症和认知障碍的影响的潜在机制.

主要方法:

使用LPS诱导的认知障碍小鼠模型的体内研究.
用BV2微质细胞和神经元细胞进行体外实验.
评估微质激活,ERS,NF-κB通路和炎症性细胞因子分泌 (TNF-α,IL-6).

主要成果:

在小鼠中,GHaR治疗显著缓解了LPS诱导的认知障碍.
GHaR抑制了微质激活,M1两极分化,并减少了TNF-α和IL-6分泌.
在体外和体外模型中,GHaR抑制了ERS和NF-κB信号激活.
GHaR保护神经元细胞免受由LPS激活的微质引起的亡.

结论:

GHaR证明了对LPS诱导的认知障碍的神经保护作用.
GHaR通过逆转微质激活来减轻神经炎症.
GHaR的神经保护机制涉及抑制内细胞网膜应激 (ERS) 信号传递.

关键词:

认知障碍认知障碍是一种认知障碍.微质细胞中的微质细胞神经炎症是一种神经炎症.这是一种Temporin-GHaR.

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