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免疫抑制小鼠中D-半乳糖胺诱导的肝损伤

D-galactosamine-induced liver injury in immunosuppressed mice.

作者信息

Schaff Z, Lapis K, Szendröi M

出版信息

Acta Morphol Hung. 1984;32(1):67-72.

PMID:6087623
Abstract

Thymectomized DBA/2 mice, irradiated with 720 rad/min and reconstituted with syngeneic bone marrow, were treated i.p. with 1 g/kg body weight D-galactosamine-HCl (DGA). Light and electron microscopic changes characteristic of the toxic effect of the agent, such as hepatocellular cytoplasmic inclusions and unicellular necrosis, could be observed but no inflammatory reaction was detectable in the liver. The phagocytic activity of Kupffer cells proved to be unchanged in immunosuppressed animals. Liver regeneration following DGA injury took place in 120 hours exactly as in animals having an intact immune system. The experiments suggested that T-lymphocytes participate in the development of DGA-hepatitis and their absence does not influence the restoration of liver injury. The experimental system described seems to be suitable for separating primary and secondary events and also for studying the role of the immune system in toxic liver injury.

摘要

对经胸腺切除的DBA/2小鼠以720拉德/分钟的剂量进行照射,并用同基因骨髓进行重建,然后腹腔注射1克/千克体重的盐酸D-半乳糖胺(DGA)。可以观察到该药物毒性作用的特征性光镜和电镜变化,如肝细胞胞质内包涵体和单细胞坏死,但在肝脏中未检测到炎症反应。在免疫抑制动物中,库普弗细胞的吞噬活性被证明未发生改变。DGA损伤后的肝脏再生在120小时时发生,与免疫系统完整的动物完全一样。实验表明,T淋巴细胞参与DGA肝炎的发展,缺乏T淋巴细胞并不影响肝损伤的恢复。所描述的实验系统似乎适用于区分原发性和继发性事件,也适用于研究免疫系统在中毒性肝损伤中的作用。

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