KININOGEN AND KININ IN EXPERIMENTAL SPINAL-CORD INJURY

被引：39

作者：

XU, J

HSU, CY

JUNKER, H

CHAO, S

HOGAN, EL

CHAO, J

机构：

[1] BAYLOR COLL MED, DIV RESTORAT NEUROL & HUMAN NEUROBIOL, 1 BAYLOR PLAZA, S815, HOUSTON, TX 77030 USA

[2] MED UNIV S CAROLINA, DEPT NEUROL, CHARLESTON, SC 29425 USA

[3] MED UNIV S CAROLINA, DEPT BIOCHEM & MOLEC BIOL, CHARLESTON, SC 29425 USA

来源：

JOURNAL OF NEUROCHEMISTRY | 1991年 / 57卷 / 03期

关键词：

BRADYKININ; T-KININ; T-KININOGEN; RAT;

D O I：

10.1111/j.1471-4159.1991.tb08246.x

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Activation of the kallikrein-kinin system has been implicated in the pathogenesis of vasogenic brain edema and posttraumatic vascular injury. We determined the levels of kininogen and kinin in an experimental spinal cord injury model in the rat. Kininogen content in traumatized cord segments increased in a time-dependent manner. Western blot analysis showed that the kininogen in traumatized cord comigrates with 68K low-molecular-weight kininogen or T-kininogen. Trypsin treatment of the kininogen in traumatized cord released both bradykinin and T-kinin, which were separated by HPLC and quantified with a kinin radioimmunoassay. Endogenous kinin levels in the frozen spinal cord also increased up to 40-fold 2 h after injury as compared with controls. The results demonstrate an increased accumulation of kininogen and its conversion to vasoactive kinins in experimental spinal cord injury.

引用

页码：975 / 980

页数：6

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