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营养对药物诱导的肝损伤的影响:来自高脂肪饮食小鼠模型的见解

Murali Badanthadka¹, Vinitha D'Souza¹, Meghashree Shetty¹

¹Nittte (Deemed to be University), Nitte University Center for Science Education and Research (NUCSER), Paneer Campus, Deralakatte, Mangaluru, Karnataka State, India.

Turkish journal of pharmaceutical sciences

|July 12, 2024

概括

高脂肪饮食 (HFD) 在小鼠中显著减少了乙氨基 (APAP) 诱导的肝损伤. 这表明营养状况可能会影响药物毒性,可能需要在临床环境中调整剂量.

科学领域:

肝毒性和毒理学
营养科学营养科学
药理动力学药理动力学

背景情况:

高脂肪饮食 (HFD) 越来越多地与增加对药物诱导毒性的敏感性有关.
乙氨基 (APAP) 过量服用是药物诱导的肝损伤 (肝毒性) 的常见原因.
了解营养状况对APAP肝毒性的影响,对于临床风险评估至关重要.

研究的目的:

研究高脂肪饮食 (HFD) 对乙氨基 (APAP) 诱导的肝毒性对雌性Balb/C小鼠的影响.
评估HFD对APAP药理动力学和肝损伤标志物的影响.
为了确定营养状况是否影响易受APAP诱导的肝损伤.

主要方法:

雌性Balb/C小鼠在15周内被食正常饮食 (ND) 或HFD.
小鼠接受了一次口服APAP剂量 (300 mg/kg).
肝损伤标志物 (ALT,AST),抗氧化酶,组织病理学和APAP的药理动力学在不同时间点进行了评估.

主要成果:

与ND组相比,HFD显著减少了APAP诱导的肝损伤,AST和ALT水平较低.
抗氧化酶水平在两组之间是可比的,但他的病理学发现了显著的差异.
在HFD小鼠中APAP的药理动力学分析显示了较低的血度,增加的清除率和更大的分布体积.

结论:

高脂肪饮食在Balb/C小鼠中对APAP诱导的肝毒性提供了显著的保护.
这些发现强调了营养状况在调节药物毒性的关键作用.
结果表明,在临床实践中,可能需要根据营养状况进行剂量个性化.

关键词:

乙氨基是一种有高脂肪的饮食.肝脏损伤肝脏损伤是什么?营养营养营养营养药物动力学药物动力学第二阶段的毒性.

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