Investigation of the Protective Role of N-Acetylcysteine Against Amikacin-Induced Systemic Toxicity and Anxiety Behavior in Mice

This dataset confirm the results of our findings that Amikacin-treated mice showed clear anxiety-like behavior, including reduced time in the light area, an effect was improved by NAC. Amikacin altered liver function markers such increasing the levels of alanine transferase and aspartate transferase. NAC attenuated these changes indicating hepatoprotective effects. Metabolic markers such as lactate dehydrogenase, and uric acid were increased after amikacin treatments. Amikacin caused marked increase in inflammatory cytokines and chemokines, including IL-6, TNF-α, IL-12p70, IL-22, CXCL10 and CCL7. NAC lowered IL-6, IL-12p70, IL-22, and CXCL10 indicating potential effects of NAC in reducing the systemic inflammatory responses associated with amikacin exposure. Principle compartment and heatmap analysis of serum biochemistry and inflammatory profiles revealed a clear segregation between amikacin compared to other three groups.本数据集验证了我们的研究结论：经阿米卡星（Amikacin）处理的小鼠可表现出明确的焦虑样行为，具体体现为明区停留时间缩短，而NAC可改善该行为学效应。阿米卡星会改变肝功能标志物水平，例如使丙氨酸转氨酶（alanine transferase）与天冬氨酸转氨酶（aspartate transferase）的含量升高，NAC可缓解上述肝功能指标变化，提示其具有肝保护作用。经阿米卡星处理后，乳酸脱氢酶（lactate dehydrogenase）、尿酸（uric acid）等代谢标志物水平均出现显著升高。阿米卡星可显著上调促炎细胞因子与趋化因子的表达水平，包括IL-6、TNF-α、IL-12p70、IL-22、CXCL10以及CCL7。NAC可降低IL-6、IL-12p70、IL-22与CXCL10的水平，表明其可缓解阿米卡星暴露相关的全身炎症反应。对血清生化指标与炎症因子谱进行主成分与热图分析后可见，阿米卡星组与其余三组呈现清晰的聚类分离。