AI总结:以上论文列表主要围绕麻醉药物(如异氟烷、七氟烷等)对神经认知功能的影响展开研究,涉及多个层面的医学机制和实验模型。整体来看,这些研究聚焦于以下关键领域:1. **麻醉诱导的神经炎症与认知障碍**:多篇论文探讨了异氟烷和七氟烷等麻醉剂通过诱导神经炎症反应,影响幼年和成年小鼠的认知功能。研究表明,麻醉可能通过激活小胶质细胞、引发神经炎症或干扰神经元信号传导,导致短期或长期的认知损害。2. **神经发育与干细胞损伤**:部分研究关注麻醉药物对神经干细胞的损伤作用,发现其可能导致神经干细胞的丢失以及神经发生减少,尤其是在幼龄动物模型中更为显著。这种损伤可能与麻醉引起的氧化应激、线粒体功能障碍及凋亡途径激活相关。3. **信号通路与分子机制**:研究深入分析了BDNF/TrkB信号通路、NMDAR/Ca/calpain通路及其他相关分子机制在麻醉诱导的认知障碍中的作用。例如,某些论文指出,麻醉可能通过调节这些信号通路,影响突触可塑性和记忆形成。4. **年龄相关差异**:多篇论文强调了年龄因素对麻醉效应的影响。幼龄动物更容易受到麻醉诱导的认知损害,而老年动物则表现出不同的病理特征,如神经炎症加重或神经退行性变化加速。5. **保护性策略与干预措施**:部分研究探索了潜在的保护性干预措施,如使用抗氧化剂、抗炎药物或其他神经保护剂来减轻麻醉诱导的认知损害。此外,还涉及特定受体(如α7尼古丁乙酰胆碱受体)作为潜在治疗靶点的讨论。6. **行为学与电生理学评估**:实验设计通常结合行为学测试(如学习记忆任务)与电生理学方法(如tau磷酸化水平检测),以全面评估麻醉对神经功能的长期影响。综上所述,这些论文揭示了麻醉药物在不同年龄段对神经系统的影响机制,并为开发有效的预防和干预策略提供了重要的科学依据。研究结果不仅有助于优化临床麻醉方案,也为理解麻醉相关的神经毒性效应奠定了理论基础。
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共1篇 平均IF=12.4 (12.4-12.4)更多分析
  • 1区Q1影响因子: 12.4
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    1. Healthful aging mediated by inhibition of oxidative stress.
    期刊:Ageing research reviews
    日期:2020-10-19
    DOI :10.1016/j.arr.2020.101194
    The progressive increase in lifespan over the past century carries with it some adversity related to the accompanying burden of debilitating diseases prevalent in the older population. This review focuses on oxidative stress as a major mechanism limiting longevity in general, and healthful aging, in particular. Accordingly, the first goal of this review is to discuss the role of oxidative stress in limiting longevity, and compare healthful aging and its mechanisms in different longevity models. Secondly, we discuss common signaling pathways involved in protection against oxidative stress in aging and in the associated diseases of aging, e.g., neurological, cardiovascular and metabolic diseases, and cancer. Much of the literature has focused on murine models of longevity, which will be discussed first, followed by a comparison with human models of longevity and their relationship to oxidative stress protection. Finally, we discuss the extent to which the different longevity models exhibit the healthful aging features through physiological protective mechanisms related to exercise tolerance and increased β-adrenergic signaling and also protection against diabetes and other metabolic diseases, obesity, cancer, neurological diseases, aging-induced cardiomyopathy, cardiac stress and osteoporosis.
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