摘要
观察β—EP对失血性休克早期IL—1活性升高的影响,结果表明,30％失血早期大鼠血浆β—EP与IL—1均明显升高,前者先于后者;给失血大鼠静注β—EP抗血清,该大鼠血浆IL—1活性较失血前尽管仍然升高,但却显著低于失血对照组;将不同剂量的β—EP静注给正常大鼠或与巨噬细胞共同培养,血浆及上清液均呈IL—1活性,且与β—EP有量效关系,β—EP与LPS联合刺激高于两者的单独作用。提示:失血性休克早期β—EP可能是导致IL—1活性升高的重要原因之一,β—EP可直接刺激巨噬细胞分泌IL—1。
It was found that both β - EP and IL-1 in circulation increased remarkably after 30% lost of total blood volume and β-EP changed much earlier than IL-1 did. Pretreatment with anti -β -EP resulted in significant decrease in plasma IL-1 activity in shock rat, while β - EP potentiated plasma IL-1 activity in normal rat. When β -EP was cultured in vitro with macrophage, it enhanced the release of IL-1 by macrophages. There existed a dose dependent relation between β -EP and IL-1. The result suggested that β-EP may be an important factor in enhancing IL-1 activity in the early stage of hemorrhagic shock. β-EP could stimulate macrophage to release IL-1 directly.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
1997年第3期321-324,共4页
Chinese Journal of Pathophysiology
