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铁过载大鼠肝小叶中转铁蛋白受体分布及铁沉积

Transferrin receptor distribution and iron deposition in the hepatic lobule of iron-overloaded rats.

作者信息

Lu J P, Hayashi K

机构信息

Department of Pathology, Shanghai Medical University, China.

出版信息

Pathol Int. 1995 Mar;45(3):202-6. doi: 10.1111/j.1440-1827.1995.tb03443.x.

Abstract

Under the condition of obvious iron-overload, there is a zonal hemosiderin (iron) deposition in hepatic lobules. The deposition is heaviest in the periportal (zone 1) and lightest in the perivenous (zone 3) hepatocytes. However, the mechanism for this pattern of iron deposition is obscure. Hepatic tissues from control, iron-deficient or iron-overloaded Wistar rats were used to study its pathogenesis. Iron-deficiency was induced by a low iron regimen. Iron-overload was produced by repeated intraperitoneal injections of ferric nitrilotriacetate (Fe(3+)-NTA) for 1-4 months. Liver tissues of the rats were immunohistochemically and histochemically stained for transferrin receptor (TfR), transferrin (Tf), ferritin (Ft), and iron. The staining intensity of TfR, Tf and Ft increased in hepatocytes of iron-deficient rats and decreased in that of the iron-overloaded in comparison with the control rats. TfR staining was strong in zone 1, with gradual transition into weak staining in zone 3 hepatocytes of the rat liver. TfR located primarily on the hepatocyte membrane. Tf had both membranous and cytoplasmic distribution. Many hepatocytes in group B had strong cytoplasmic Tf staining. Conversely, only a few hepatocytes had weakly stained cytoplasmic Tf in group C. Hepatocytes and Kupffer cells were Ft positive in control rats. Ft was distributed only in the cytoplasm. The staining intensity of Ft was stronger in zone 3 than in zone 1 hepatocytes of iron-deficient rats. In iron-overloaded rats, the iron deposition was severe in zone 1 and mild in zone 3 hepatocytes.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

在明显铁过载的情况下,肝小叶内存在带状含铁血黄素(铁)沉积。这种沉积在汇管区周围(1区)的肝细胞中最为严重,而在中央静脉周围(3区)的肝细胞中最轻。然而,这种铁沉积模式的机制尚不清楚。使用对照、缺铁或铁过载的Wistar大鼠的肝组织来研究其发病机制。通过低铁饮食诱导缺铁。通过反复腹腔注射次氮基三乙酸铁(Fe(3+)-NTA)1至4个月来产生铁过载。对大鼠的肝组织进行转铁蛋白受体(TfR)、转铁蛋白(Tf)、铁蛋白(Ft)和铁的免疫组织化学和组织化学染色。与对照大鼠相比,缺铁大鼠肝细胞中TfR、Tf和Ft的染色强度增加,而铁过载大鼠肝细胞中的染色强度降低。大鼠肝脏1区TfR染色强,向3区肝细胞逐渐过渡为弱染色。TfR主要位于肝细胞膜上。Tf有膜性和胞质分布。B组许多肝细胞胞质Tf染色强。相反,C组只有少数肝细胞胞质Tf染色弱。对照大鼠的肝细胞和枯否细胞Ft呈阳性。Ft仅分布于细胞质中。缺铁大鼠3区肝细胞中Ft的染色强度强于1区。在铁过载大鼠中,1区肝细胞铁沉积严重,3区肝细胞铁沉积轻度。(摘要截选至250字)

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