黄曲霉毒素B1对雄性小鼠空间记忆损伤的影响一氧化氮途径的参与。

IF 2.6 4区医学 Q2 PHARMACOLOGY & PHARMACY

Toxicon Pub Date : 2025-02-01 DOI:10.1016/j.toxicon.2025.108272

Amin Haghighat Naeini , Ehsan Nassireslami , Marjan Shariatpanahi , Mohsen Chamanara , Ali Abdolali , Mehdi Aghsami

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引用次数: 0

摘要

黄曲霉毒素B1是在食物中发现的毒性最大的黄曲霉毒素。海马体中的一氧化氮对学习和记忆至关重要。坏死性上睑下垂在包括神经退行性疾病在内的许多疾病的细胞死亡和病理中起作用。本研究旨在探讨一氧化氮途径和坏死性下垂信号在黄曲霉毒素B1神经毒性中的作用。将35只雄性NMRI小鼠分为5组：对照组、黄曲霉毒素B1、黄曲霉毒素B1+ l -精氨酸、黄曲霉毒素B1+氨基胍、黄曲霉毒素B1+L-NAME。采用Barnes Maze实验评估小鼠的空间记忆，采用western blot检测小鼠脑海马区RIP1、RIP3和MLKL生物标志物的表达。行为测试表明黄曲霉毒素B1引起的记忆损伤明显，L-Name和氨基胍显著改变了记忆损伤。分子检测显示，黄曲霉毒素B1触发RIP1、RIP3和MLKL生物标志物升高，L-Name观察到RIP1、RIP3和MLKL生物标志物明显中和。本研究表明，坏死坏死途径可能是afb1诱导记忆损伤的一个可能机制，而一氧化氮途径可能在改变这些变化中发挥作用。

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Necroptosis signaling in spatial memory impairment caused by Aflatoxin B1 in male mice; involvement of the nitric oxide pathway

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Necroptosis signaling in spatial memory impairment caused by Aflatoxin B1 in male mice; involvement of the nitric oxide pathway

Aflatoxin B1 is the most toxic form of aflatoxins found in food. Nitric oxide in the hippocampus is essential for learning and memory. Necroptosis plays a role in cell death and pathology of many diseases, including neurodegenerative diseases. This study aimed to explore the role of the nitric oxide pathway and necroptosis signaling in Aflatoxin B1 neurotoxicity. A total of 35 male NMRI mice were divided into 5 groups as follows: Control group, Aflatoxin B1, Aflatoxin B1+L-Arginine, Aflatoxin B1+Aminoguanidine, and Aflatoxin B1+L-NAME. The spatial memory of the mice was assessed using the Barnes Maze test, and Western blot was conducted to evaluate the expression of RIP1, RIP3 and MLKL biomarkers in the hippocampus of mice brain. The behavioral tests indicated a significant memory impairment caused by Aflatoxin B1, which was significantly altered by L-Name and Aminoguanidine. The molecular tests showed an elevation of RIP1, RIP3 and MLKL biomarkers triggered by Aflatoxin B1 and a significant neutralization was then observed by L-Name. This study demonstrated that necroptosis pathway could be a possible mechanism of AFB1-induced memory damages and the nitric oxide pathway could play a role in altering these changes.

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来源期刊

Toxicon 医学-毒理学

CiteScore

4.80

自引率

10.70%

发文量

358

审稿时长

68 days

期刊介绍： Toxicon has an open access mirror Toxicon: X, sharing the same aims and scope, editorial team, submission system and rigorous peer review. An introductory offer Toxicon: X - full waiver of the Open Access fee. Toxicon''s "aims and scope" are to publish: -articles containing the results of original research on problems related to toxins derived from animals, plants and microorganisms -papers on novel findings related to the chemical, pharmacological, toxicological, and immunological properties of natural toxins -molecular biological studies of toxins and other genes from poisonous and venomous organisms that advance understanding of the role or function of toxins -clinical observations on poisoning and envenoming where a new therapeutic principle has been proposed or a decidedly superior clinical result has been obtained. -material on the use of toxins as tools in studying biological processes and material on subjects related to venom and antivenom problems. -articles on the translational application of toxins, for example as drugs and insecticides -epidemiological studies on envenoming or poisoning, so long as they highlight a previously unrecognised medical problem or provide insight into the prevention or medical treatment of envenoming or poisoning. Retrospective surveys of hospital records, especially those lacking species identification, will not be considered for publication. Properly designed prospective community-based surveys are strongly encouraged. -articles describing well-known activities of venoms, such as antibacterial, anticancer, and analgesic activities of arachnid venoms, without any attempt to define the mechanism of action or purify the active component, will not be considered for publication in Toxicon. -review articles on problems related to toxinology. To encourage the exchange of ideas, sections of the journal may be devoted to Short Communications, Letters to the Editor and activities of the affiliated societies.