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大鼠肝脏肉芽肿形成模式反映了亚微米硅颗粒内化机制。

The Pattern of Granuloma Formation in the Liver of Rats as a Reflection of the Mechanism of Internalization of Submicron Silicon Particles.

机构信息

I. P. Pavlov First St. Petersburg State Medical University, Ministry of Health of the Russian Federation, St. Petersburg, Russia.

V. A. Almazov National Medical Research Center, Ministry of Health of the Russian Federation, St. Petersburg, Russia.

出版信息

Bull Exp Biol Med. 2024 Jan;176(3):399-402. doi: 10.1007/s10517-024-06032-z. Epub 2024 Feb 12.

Abstract

A morphological analysis of the liver of Wistar rats was performed 2 months after a single intravenous injection of porous silicon particles of different sizes (60-80, 250-300, and 500-600 nm; 2 mg/ml, 1 ml). Histological, immunohistochemical, and electron microscopic methods showed the development of CD68 granulomas in all experimental groups. Injection of 60-80-nm porous silicon particles led to the formation of single large granulomas (>2000 μm), while 500-600-nm nanoparticles caused the formation of numerous smaller granulomas. The mechanism of involution of granulomas by apoptosis of Kupffer cells and the absence of subsequent connective tissue remodeling of the organ tissue is shown.

摘要

对 Wistar 大鼠进行了肝脏的形态学分析,这些大鼠在单次静脉注射不同大小的多孔硅颗粒(60-80nm、250-300nm 和 500-600nm;2mg/ml,1ml)2 个月后。组织学、免疫组织化学和电子显微镜方法显示,所有实验组均出现 CD68 肉芽肿。注射 60-80nm 多孔硅颗粒导致单个大肉芽肿(>2000μm)的形成,而 500-600nm 纳米颗粒导致许多较小肉芽肿的形成。该研究表明,细胞凋亡是导致肉芽肿退化的机制,而组织的后续结缔组织重塑则不存在。

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