Shvedova M V, Anfinogenova Ya D, Schepetkin I A, Atochin D N
Ross Fiziol Zh Im I M Sechenova. 2017 Mar;103(3):268-83.
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.
本文综述了有关c-Jun氨基末端激酶（JNK）及其抑制剂在缺血再灌注损伤所致脑损伤中作用的文献。讨论了JNK在缺血再灌注诱导的脑损伤相关信号机制中的作用。描述了在脑缺血再灌注损伤实验模型中使用合成和天然物质抑制JNK的相关效应。实验研究结果表明，JNK是脑缺血性卒中脑保护的有前景的治疗靶点。然而，各种JNK家族成员的多种生理功能使得非特异性JNK抑制剂不能用于全身治疗。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任务。
