M V Shvedova, Ya D Anfinogenova, I A Schepetkin, D N Atochin
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引用次数: 0
Abstract
The article reviews the literature regarding the role of c-Jun-N-terminal kinases (JNK) and its inhibitors in brain damage in the settings of ischemia and reperfusion injury. The implication of JNK in signaling mechanisms involved in ischemia-reperfusion-induced cerebral injury are discussed. Described effects associated with JNK inhibition using synthetic and natural substances in experimental models of ischemic and reperfusion injury of the brain. Results of experimental studies demonstrated that JNK represent promising therapeutic targets for brain protection against ischemic stroke. However, multiple physiologic functions of various JNK family members do not allow for the systemic use of non-specific JNK inhibitors for therapeutic purposes. The authors conclude that the continuous search for selective inhibitors of JNK3 remains an important task.
本文综述了c- jun - n末端激酶(JNK)及其抑制剂在缺血再灌注损伤脑损伤中的作用。本文讨论了JNK在脑缺血再灌注损伤信号机制中的作用。描述了在脑缺血和再灌注损伤的实验模型中使用合成和天然物质抑制JNK的相关作用。实验研究结果表明，JNK代表了对缺血性脑卒中的脑保护有希望的治疗靶点。然而，各种JNK家族成员的多种生理功能不允许全身使用非特异性JNK抑制剂用于治疗目的。作者得出结论，持续寻找JNK3的选择性抑制剂仍然是一项重要的任务。
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