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使用 3D 人肝类器官预测药物诱导的磷脂沉积症。

Use of 3D Human Liver Organoids to Predict Drug-Induced Phospholipidosis.

机构信息

Department of Medical Science, Asan Medical Institute of Convergence Science and Technology, Asan Medical Center, University of Ulsan College of Medicine, Seoul 05505, Korea.

Department of Pathology, University of Ulsan College of Medicine, Asan Medical Center, Seoul 05505, Korea.

出版信息

Int J Mol Sci. 2020 Apr 23;21(8):2982. doi: 10.3390/ijms21082982.

Abstract

Drug-induced phospholipidosis (PL) is a storage disorder caused by the formation of phospholipid-drug complexes in lysosomes. Because of the diversity of PL between species, human cell-based assays have been used to predict drug-induced PL in humans. We established three-dimensional (3D) human liver organoids as described previously and investigated their liver characteristics through multiple analyses. Drug-induced PL was initiated in these organoids and in monolayer HepG2 cultures, and cellular changes were systemically examined. Organoids that underwent differentiation showed characteristics of hepatocytes rather than HepG2 cells. The organoids also survived under PL-inducing drug conditions for 48 h and maintained a more stable albumin secretion level than the HepG2 cells. More cytoplasmic vacuoles were observed in organoids and HepG2 cells treated with more potent PL-induced drugs, but to a greater extent in organoids than in HepG2 cells. Lysosome-associated membrane protein 2, a marker of lysosome membranes, showed a stronger immunohistochemical signal in the organoids. PL-distinctive lamellar bodies were observed only in amiodarone-treated organoids by transmission electron microscopy. Human liver organoids are thus more sensitive to drug-induced PL and less affected by cytotoxicity than HepG2 cells. Since PL is a chronic condition, these results indicate that organoids better reflect metabolite-mediated hepatotoxicity in vivo and could be a valuable system for evaluating the phospholipidogenic effects of different compounds during drug development.

摘要

药物诱导的磷脂病(PL)是一种由溶酶体中磷脂-药物复合物形成引起的储存障碍。由于物种间 PL 的多样性,已使用基于人类细胞的测定法来预测人类的药物诱导 PL。我们按照先前的描述建立了三维(3D)人肝类器官,并通过多种分析方法研究了它们的肝脏特征。这些类器官和单层 HepG2 培养物中启动了药物诱导的 PL,系统地检查了细胞变化。分化后的类器官表现出肝细胞的特征,而不是 HepG2 细胞。类器官在诱导 PL 的药物条件下也能存活 48 小时,并保持比 HepG2 细胞更稳定的白蛋白分泌水平。在接受更有效的 PL 诱导药物处理的类器官和 HepG2 细胞中观察到更多的细胞质空泡,但类器官中的空泡比 HepG2 细胞中的空泡更多。溶酶体相关膜蛋白 2(LAMP2)是溶酶体膜的标志物,在类器官中的免疫组织化学信号更强。透射电子显微镜仅在胺碘酮处理的类器官中观察到 PL 特有的板层小体。因此,人肝类器官对药物诱导的 PL 更敏感,比 HepG2 细胞受细胞毒性的影响更小。由于 PL 是一种慢性疾病,这些结果表明类器官更好地反映了体内代谢物介导的肝毒性,并且可能是在药物开发过程中评估不同化合物磷脂生成作用的有价值系统。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/20fd/7216064/f9181ad6d1dc/ijms-21-02982-g001.jpg

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