摘要
采用Langendorff非作功非循环式离体心脏灌流技术,造成大鼠心肌缺血和再灌注损伤模型。以组蛋白为底物,通过测定^(32)P由(r-^(32)P)ATP中掺入组蛋白的放射性强度计算蛋白激酶C(protein kinase C,PKC)活性。细胞浆PKC活性,在缺血和再灌注期间与对照组相比均无显著差异。细胞膜PKC活性则随缺血时间的延续依次显著增高,分别为对照组的1.68倍(缺血15分钟)、1.88倍(缺血30分钟)、2.18倍(缺血45分钟)和1.34倍(缺血60分钟);再灌注仅见,缺血15分钟/再灌注15分钟为对照组的1.37倍,但与缺血15分钟组相比无显著差异。提示PKC介导的细胞信息传递功能障碍参与了心肌缺血和再灌注损伤的形成。人参二醇皂甙使缺血45分钟增高的细胞膜PKC活性降低62.5%(P<0.01)。
The change of myocatdial protein kinase C (PKC) activity during ische-mia and reperfusion was studied in isolated Langendorff perfused rat hearts. The enzymeactivity was determined by measuring the incorporation of ^(32)P from (r-^(32)P) ATP intohistone. The cytosolic PKC activity was similar in control, ischemic and reperfused hearts;however, there were significant increases in the membrane PKC activity during ischemia and reperfusion There were 1.68, 1.88, 2.18 and 1.34 fold increases of the membrane PKC activity at 15, 30, 45 and 60 minutes after ischemia respetively Following15 minutes of ischemia, repetfusion of heart only caused 1.37 fold increase in the mem-brane PKC activity, compared with that at 15 minutes after ischemta no siginificant differ-ence was found. These results suggested, that the signal transduction mediated by PKC wasimpaired during the development of ischemic and post-ischemic reperfusion injuty of theheart. Panaxadiol saponin decreased the enhanced membrane PKC avtivity induced by is-chemia by 62.5%.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
1993年第5期565-568,共4页
Chinese Journal of Pathophysiology
基金
中华医学基金会
关键词
蛋白激酶C
心肌
缺血
人参
皂甙类
Protein kinase C
Myocardium
Ischemia
Ginseng
Saponins
