血红素加氧酶-1在中毒性肾损伤中的诱导作用：氯化汞诱导的大鼠急性肾衰竭

Induction of heme oxygenase-1 in toxic renal injury: mercuric chloride-induced acute renal failure in rat.

作者信息

Horikawa S, Ito K, Ikeda S, Shibata T, Ishizuka S, Yano T, Hagiwara K, Ozasa H, Katsuyama I

机构信息

Department of Pathological Biochemistry, Medical Research Institute, Tokyo Medical and Dental University, Japan.

出版信息

Toxicol Lett. 1998 Jan 16;94(1):57-64. doi: 10.1016/s0378-4274(97)00103-3.

DOI:10.1016/s0378-4274(97)00103-3

PMID:9544699

Abstract

It is known that mercuric chloride (HgCl2) is a nephrotoxicant. When HgCl2 (1 mg/kg body weight) was intraperitoneally injected into rats, acute renal failure was induced. Histological changes in the kidneys were exclusively observed in the proximal tubules and the severe necrosis was found as early as 24 h after HgCl2 injection. The heme oxygenase-1 (HO-1) mRNA was strongly and promptly induced at about 2.5 h, the earliest time examined and abruptly decreased after the injection. Whereas the time course of HO-1 protein level was delayed as compared with that of HO-1 mRNA level. The levels of HO-1 mRNA and protein similarly increased with dose-dependent manner. The localization of HO-1 protein was restricted to the tubule cells. These findings suggest the potential involvement of HO-1 induction in the response to HgCl2-induced acute renal injury.

摘要

已知氯化汞（HgCl₂）是一种肾毒物。当将HgCl₂（1毫克/千克体重）腹腔注射到大鼠体内时，会诱发急性肾衰竭。肾脏的组织学变化仅在近端小管中观察到，并且早在注射HgCl₂后24小时就发现了严重坏死。血红素加氧酶-1（HO-1）mRNA在约2.5小时时被强烈且迅速诱导，这是最早检测的时间，注射后迅速下降。而HO-1蛋白水平的时间进程与HO-1 mRNA水平相比有所延迟。HO-1 mRNA和蛋白水平以剂量依赖方式同样增加。HO-1蛋白的定位局限于肾小管细胞。这些发现表明HO-1诱导可能参与了对HgCl₂诱导的急性肾损伤的反应。