摘要
瞄准：为了如果在肝的铁免职和胖累积玩，调查，在 dimethylnitrosamine (DMN ) 的一个病原的角色在老鼠导致了肝纤维变性。方法：三十只老鼠与 DMN 被对待在每天做 10 muL/kg 的连续的天， i.p，为 3 连续白天为 4 wk 的每个星期。老鼠(n = 30 ) 在 DMN 的停止以后在第一天(模型组 A ) 和第 21 d (模型组 B ) 被牺牲注射。控制组(n = 10 ) 收到了相等的数量盐。肝纸巾与苏木精与曙红被染色(他) 并且在电子显微镜学下面的马森和普鲁士的蓝试金和 oberserved。浆液丙氨酸 aminotransferase (中高音) 和织物羟脯氨酸(忧郁) 满足的肝被测试。结果：肝纤维变性自动地没逆行，它类似于以前的报告，伴有骨胶原的铁的小叶片的免职显示出的仙子在两个标记特征在 DMN 的停止以后的第一和第 21 d 注射。然而，在 hepatocytes 的胖累积仅仅在第 21 d 发生在 DMN 注射的停止以后。结论：铁免职和胖累积可以在导致 DMN 的老鼠肝纤维变性在病理学的变化起重要作用。这些特征需要的详细机制推进研究。
AIM： To investigate if iron deposition and fat accumulation in the liver play a pathogenetic role in dimethylnitrosamine （DMN）-induced liver fibrosis in rat.
METHODS： Thirty rats were treated with DMN at does consecutive days of 10 μL/kg daily, i.p., for 3 consecutive day each week for 4 wk. Rats （n = 30） were sacrificed on the first day （model group A） and 21st d （model group B） after cessation of DMN injection. The control group （n = 10） received an equivalent amount of saline. Liver tissues were stained with hematoxylin ＆ eosin （HE） and Masson and Prussian blue assay and oberserved under electron microscopy. Serum alanine aminotransferase （ALT）and liver tissue hydroxyproline （Hyp） content were tested.
RESULTS： The liver fibrosis did not automaticallyreverse, which was similar to previous reports, the perilobular deposition of iron accompanied with collagen showed marked characteristics at both the first and 21st d after cessation of DMN injection. However, fat accumulation in hepatocytes occurred only at the 21^st d after cessation of DMN injection.
CONCLUSION： Iron deposition and fat accumulation may play important roles in pathological changes in DMN-induced rat liver fibrosis. The detailed mechanisms of these characteristics need further research.
