丝裂素活化蛋白激酶参与去甲肾上腺素预处理的保护作用

目的:探讨丝裂素活化蛋白激酶(P38MAPK,P38)是否参与去甲肾上腺素预处理的延迟保护作用。方法:18只大鼠随机分成三组:(1)缺血／再灌注(I／R)组;(2)NE预处理组;(3)SB203580(P38的特异性抑制剂)+NE预处理组。于预处理后24 h对心脏进行较长时间缺血再灌注,观察其心肌梗塞范围、LDH释放。结果:与未预处理组的心肌组织比较,于NE预处理后24 h I／R所致的心梗范围缩小,血浆LDH活性降低(P均<0.01)。用SB203580抑制P38磷酸化时,则消除了预处理后的延迟保护作用,上述心肌损伤指标接近单纯缺血／再灌注组(P>0.05)。结论:去甲肾上腺素预处理有使心肌减少缺血／再灌注损伤的延迟保护作用,P38参与了这种保护作用。

Role of P38MAPK on the cardiae delayed protection induced by norepinephrine preconditioning for ischemia/reperfusion injury in rats

Objective: To investigate the role of P38MAPK (P38) on the cardiac delayed protection induced by nore-pinephrine preconditioning (NE - P) for ischemiareperfusion (IR) injury in rats. Methods: Eighteen rats were randomly assigned to three groups: (1) ischemic -reperfusion (IR) group; (2) NE -P group: Six rats received injection of norepinephrine prior to 30 min of ischemia followed by 120 min of reperfusion; (3) SB203580 (inhibitor of P38) -NE group: Six rats received SB203580 10 min prior to NE administration. The activity of P38was detected after NE administration. At the end of reperfusion, the myocardial infarct size, LDH level were detected. Results: Compared with IR group the infarct size, LDH level respectively significantly reduced in NE -P group after NE -P 24 h (P<0. 05). The protective effects of NE completely abolished by SB203580. Conclusion: NE preconditioning can protect the heart reducing myocardial infarct size in rats; P38perticipates this cardio-protective effect.