摘要
缺血预处理诱发迟发性保护作用发生于预处理后 2 4~ 72 h。腺苷和 NO可能是两种独立的保护作用启动因子。通过激活 PKC酶、酪氨酸激酶和 p38MAP酶 ,促使 HSP 2 7、Mn- SOD等蛋白合成及磷酸化 ,最终发生迟发性保护效应。 KATP是缺血预处理迟发性保护作用的重要中心环节 。
The delayed protection evoked by ischemia preconditioning occured in 24~72 hours after preconditioning. Adenosine and NO appeared to be independent triggers of the delayed preconditioning response. The phosphorylation of HSP 27 and Mn SOD was likely to induce the delayed protective response through the PKC, tyrosine kinases and p38 MAP kinase activation. Although many studies suggested pivotal involvement of K ATP channel opening during the index ischemic insult, it's not known about related mechanism.
出处
《疾病控制杂志》
2003年第4期335-337,共3页
Chinese Journal of Disease Control and Prevention