在HepG2细胞系中阿里尔碳化合物受体 (AhR) - 独立的阿米奥达龙 (AMD) 毒性

Konrad A Szychowski1, Bartosz Skóra1, Tomasz Piechowiak2

  • 1Department of Biotechnology and Cell Biology, Medical College, University of Information Technology and Management in Rzeszow, Rzeszow, Poland.

概括

阿米奥达龙 (AMD) 激活了基碳化合物受体 (AhR) 并促进了药物代谢,但这种受体不会引起AMD诱导的肝损伤. 其他机制可能导致AMD肝毒性.

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