慢性炎症性肺动脉高压大鼠肺动脉蛋白激酶C的活性变化  

Changes of pulmonary artery protein kinase C activity in rats with chronic inflammatory pulmonary hypertension

作　　者：董旭[1] 王钢[2] 王怀良[3] 章新华[3] 宗志宏[4] 邢军[3] 

机构地区：[1]大连医科大学生物化学教研室,辽宁大连116027 [2]大连市友谊医院医务教育部,辽宁大连116001 [3]中国医科大学药学院临床药理教研室,辽宁沈阳110001 [4]中国医科大学生物化学教研室,辽宁沈阳110001

出　　处：《南方医科大学学报》2007年第6期875-877,共3页Journal of Southern Medical University

摘　　要：目的观察慢性炎症性肺动脉高压大鼠在肺动脉高压形成过程中肺动脉蛋白激酶C(PKC)的活性变化。方法建立野百合碱诱导的慢性炎症性肺动脉高压大鼠模型,采用同位素标记的放射活性测定法检测肺动脉高压形成过程中肺动脉蛋白激酶C的活性。结果随着慢性炎症性肺动脉高压的进展,大鼠肺动脉PKC总活性和胞浆PKC活性先是逐渐上升,而后逐渐下降(与对照组相比,P<0.05),但胞膜PKC活性和PKC活性的膜质比持续上升(与对照组相比,P<0.05)。结论PKC活性的上调和PKC的转位活化可能参与了慢性炎症性肺动脉高压的形成过程。Objective To observe the changes in pulmonary artery protein kinase C （PKC） activity in rats with chronic inflammatory pulmonary hypertension （PHT）. Methods Chronic inflammatory PHT was induced in rats with monocrotaline. The PKC activities in the rat pulmonary arteries were measured by radioactive assay during the development of PHT. Results With the development of chronic inflammatory PHT, the total and cytosolic fractions of PKC activity in PHT rat pulmonary arteries increased initially with subsequent decrease （P〈0.05）, but the membranous fraction of PKC activity and the membrane-to-cytosol PKC activity ratio increased continuously （P〈0.05）, Conclusion The up-regulation of PKC activity and the translocation of PKC might be associated with the development of chronic inflammatory PHT in rats.

关 键 词：肺动脉高压 蛋白激酶C 炎症 野百合碱 

分 类 号：R543[医药卫生—心血管疾病]