(m) rvd - hempressin (α)改善东莨菪碱诱导的HT22细胞氧化应激、凋亡和BDNF/TrkB/Akt通路损伤。

IF 2.9 3区 医学 Q2 NEUROSCIENCES
Neurotoxicity Research Pub Date : 2023-12-01 Epub Date: 2023-11-16 DOI:10.1007/s12640-023-00677-w
Ruisan Zhang, Xinliang He, Jianghong Cheng, Xiaofan Zhang, Chen Han, Yifan Liu, Peng Chen, Yang Wang
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引用次数: 0

摘要

胆碱能系统功能障碍与氧化应激密切相关,并在阿尔茨海默病(AD)中发挥作用。东莨菪碱(scopp)通常用于诱导细胞和动物的胆碱能系统损伤,也会引起氧化应激。我们之前的研究表明肽(m) RVD- hempressin (RVD)通过激活大麻素受体1 (CBR1)逆转scopp对小鼠的记忆损害作用,但其机制尚不清楚。在本研究中,我们发现RVD可以抑制Scop诱导的HT22细胞氧化应激、细胞凋亡、细胞活力降低和突触相关蛋白下调。这种作用与BDNF/TrkB/Akt通路有关,上述RVD的作用可以被CBR1拮抗剂阻断。这些结果表明,RVD可能是一种潜在的候选药物,用于治疗与胆碱能系统损伤和氧化应激相关的疾病,如AD。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

(m) RVD-hemopressin (α) Ameliorated Oxidative Stress, Apoptosis and Damage to the BDNF/TrkB/Akt Pathway Induced by Scopolamine in HT22 Cells.

(m) RVD-hemopressin (α) Ameliorated Oxidative Stress, Apoptosis and Damage to the BDNF/TrkB/Akt Pathway Induced by Scopolamine in HT22 Cells.

Dysfunction in the cholinergic system and oxidative stress are closely related and play roles in Alzheimer's disease (AD). Scopolamine (Scop), which is commonly used to induce cholinergic system damage in cells and animals, also evokes oxidative stress. Our previous study indicated that the peptide (m) RVD-hemopressin (RVD) reversed the memory-impairing effect of Scop in mice by activating cannabinoid receptor 1 (CBR1), but the mechanism was unclear. In this study, we found that RVD inhibited the oxidative stress, apoptosis, decreased cell viability and downregulation of synapse-associated proteins induced by Scop in HT22 cells. The effect was associated with the BDNF/TrkB/Akt pathway, and the effects of RVD outlined above could be blocked by an antagonist of CBR1. These results suggest that RVD may be a potential drug candidate for disorders associated with damage to the cholinergic system and oxidative stress, such as AD.

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来源期刊
Neurotoxicity Research
Neurotoxicity Research 医学-神经科学
CiteScore
7.70
自引率
5.40%
发文量
164
审稿时长
6-12 weeks
期刊介绍: Neurotoxicity Research is an international, interdisciplinary broad-based journal for reporting both basic and clinical research on classical neurotoxicity effects and mechanisms associated with neurodegeneration, necrosis, neuronal apoptosis, nerve regeneration, neurotrophin mechanisms, and topics related to these themes. Published papers have focused on: NEURODEGENERATION and INJURY Neuropathologies Neuronal apoptosis Neuronal necrosis Neural death processes (anatomical, histochemical, neurochemical) Neurodegenerative Disorders Neural Effects of Substances of Abuse NERVE REGENERATION and RESPONSES TO INJURY Neural Adaptations Neurotrophin mechanisms and actions NEURO(CYTO)TOXICITY PROCESSES and NEUROPROTECTION Excitatory amino acids Neurotoxins, endogenous and synthetic Reactive oxygen (nitrogen) species Neuroprotection by endogenous and exogenous agents Papers on related themes are welcome.
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