脑缺血是一种脑血管疾病,其症状是由大脑的血液或氧气供应不足引起的。当脑缺血后血液供应恢复时,可能会发生继发性脑损伤,称为脑缺血再灌注损伤(CIRI)。在这个过程中,Janus激酶/信号转导和转录激活因子(JAK/STAT)信号通路发挥着重要作用。它介导神经炎症,参与生理活动的调节,如细胞增殖,分化,和凋亡。CIRI之后,M1小胶质细胞被受损组织激活并募集。M1小胶质细胞通过JAK/STAT通路产生炎症因子,最终导致细胞凋亡。同时,JAK2/STAT3信号通路和脂质运载蛋白2和caspase-3的表达增加。在通路中,磷酸化JAK2和磷酸化STAT3功效化2。它们不仅促进神经元的增殖,还通过进一步作用于Notch信号通路影响神经干细胞的分化方向。最近,中医(TCM)是CIRI的关键参与者,通过JAK2、STAT3、STAT1及其磷酸化。因此,本文就JAK/STAT信号通路及其与CIRI的关系以及中医药对该通路的影响作一综述。旨在为今后中医药治疗CIRI分子机制的临床研究提供依据。
Cerebral ischemia is a cerebrovascular disease with symptoms caused by insufficient blood or oxygen supply to the brain. When blood supplied is restored after cerebral ischemia, secondary brain injury may occur, which is called cerebral ischemia-reperfusion injury (CIRI). In this process, the Janus kinase/signal transducer and activator of transcription (JAK/STAT) signaling pathway plays an important role. It mediates neuroinflammation and participates in the regulation of physiological activities, such as cell proliferation, differentiation, and apoptosis. After CIRI, M1 microglia is activated and recruited by the damaged tissue. The inflammatory factors are produced by M1 microglia through the JAK/STAT pathway, eventually leading to cell apoptosis. Meanwhile, the JAK2/STAT3 signaling pathway and the expression of lipocalin-2 and caspase-3 could increase. In the pathway, phosphorylated JAK2 and phosphorylated STAT3 function of 2 ways. They not only promote the proliferation of neurons, but also affect the differentiation direction of neural stem cells by further acting on the Notch signaling pathway. Recently, traditional Chinese medicine (TCM) is a key player in CIRI, through JAK2, STAT3, STAT1 and their phosphorylation. Therefore, the
review focuses on the JAK/STAT signaling pathway and its relationship with CIRI as well as the influence of the TCM on this pathway. It is aimed at providing the basis for future clinical research on the molecular mechanism of TCM in the treatment of CIRI.