Stat3 phosphorylation in pathogenesis of chronic cerebral ischemia

许多研究者报道急性缺血性脑卒中患者血清细胞因子水平升高。在细胞因子激活的JAK-STAT通路所涉及的众多分子中，Stat3是最重要的，受到了广泛的关注。我们已经证明Stat3磷酸化与急性脑缺血的神经保护有关。Stat3磷酸化的神经保护作用也得到了其他报道的支持。我们观察到，在局灶性缺血大鼠脑皮层注射高剂量重组LIF后，Stat3磷酸化水平快速增强。我们研究了在较长时间内使用Stat3磷酸化的可能治疗策略，例如在脑缺血后的前2-3个月使用该信号的选择性药理学药物。然而，我们未能证明Stat3磷酸化在慢性脑缺血中的确切作用。这可能是因为Stat3蛋白可以被多种信号激活，包括其他生长因子、细胞因子和氧化应激

An increase in serum cytokine level has been reported in acute ischemic stroke patients by many investigators. Among the various molecules involved in the JAK-STAT pathway activated by cytokine, Stat3 is the most important and has attracted much attention. We have already proven that Stat3 phosphorylation is associated with neuroprotection against acute cerebral ischemia. The neuroprotective effects of Stat3 phosphorylation are also supported by other reports. We observed the rapid enhancement of Stat3 phosphorylation was detected after the injection of high-dose recombinant LIF into the cerebral cortex on the ischemic side in rat focal ischemia. We examined the possible treatment strategy using Stat3 phosphorylation over a longer period, such as the first 2-3 months after cerebral ischemia using selective pharmacological agents of this signaling. However, we failed to prove definitive effects of Stat3 phosphorylation in chronic cerebral ischemia. This reason may be explained that Stat3 protein can be activated by a variety of signals, including other growth factors, cytokines, and oxidative stress