Cyrendorzhiev D D, Kutina S N, Zubakhin A A
Research Center of Clinical and Experimental Medicine, Siberian Division of the Russian Academy of Medical Sciences, Novosibirsk.
Bull Exp Biol Med. 2000 Jun;129(6):605-7. doi: 10.1007/BF02434890.
Acute toxic hepatitis was modeled in (CBAxC57B1)F1 mice by single injection of 40% CCl(4) in oil. Pretreatment with gadolinium chloride, a selective blocker of Kupffer cells, considerably potentiated damage to hepatocytes leading to generalization of this process, delayed inflammatory infiltration, and inhibited reparative processes. Zymosan administered against the background of gadolinium chloride blockade improved liver resistance to CCl(4)-induced damage, intensified mononuclear infiltration, and accelerated reparative processes.
通过单次注射40%四氯化碳的油溶液，在（CBAxC57B1）F1小鼠中建立急性中毒性肝炎模型。用钆离子氯化物（一种库普弗细胞的选择性阻滞剂）进行预处理，可显著增强对肝细胞的损伤，导致该过程的扩散、炎症浸润延迟，并抑制修复过程。在钆离子氯化物阻断的背景下给予酵母聚糖，可提高肝脏对四氯化碳诱导损伤的抵抗力，增强单核细胞浸润，并加速修复过程。
