Yamada G, Hama H, Kasuya Y, Masaki T, Goto K
Department of Pharmacology, University of Tsukuba, Ibaraki, Japan.
J Cardiovasc Pharmacol. 1995;26 Suppl 3:S486-90.
We investigated the sources of endothelin-1 (ET-1) detected in the damaged brain tissue of rats after cold injury. ET-1 in the injured sites was increased 1-5 days after the injury. Physiologic observations revealed that breakdown of the blood-brain barrier occurred and that plasma-derived albumin exuded into the brain parenchyma after cold injury. Radiolabeled ET-1, which was injected into the left cardiac ventricle, was detected in the tissue at the injury site, and ET-1-like immunoreactivity was observed in the brain capillaries in the damaged tissues. TGF-beta 1, which is a tissue regeneration factor, potently induced the expression of ET-1 mRNA in cultured astrocytes. These results suggest that ET-1 is produced through a variety of ways in the damaged brain.
我们研究了冷损伤后大鼠受损脑组织中检测到的内皮素 -1(ET-1)的来源。损伤后1 - 5天,损伤部位的ET-1增加。生理学观察显示,血脑屏障发生破坏,冷损伤后血浆来源的白蛋白渗入脑实质。注入左心室的放射性标记ET-1在损伤部位的组织中被检测到,并且在受损组织的脑毛细血管中观察到ET-1样免疫反应性。作为一种组织再生因子的转化生长因子 -β1(TGF-β1)在培养的星形胶质细胞中强烈诱导ET-1 mRNA的表达。这些结果表明,ET-1在受损脑内通过多种方式产生。