炎症反应在脑梗死中的研究进展

脑梗死后,多种机制参与神经损伤,其中炎症反应是梗死后损伤的重要环节,梗死早期、亚急性期、修复期均存有这一重要的病理过程。小胶质细胞和星形胶质细胞在梗死急性期被激活,产生炎症因子白细胞介素（IL）-1β、IL-6、肿瘤坏死因子（TNF）-α,炎症因子作用于其他炎症细胞如内皮细胞、中性粒细胞和淋巴细胞等,产生更多的炎症因子,通过TLR4/核因子-κB、PI3K/Akt等炎症通路,诱导凋亡、加重钙超载、促毒性氨基酸释放、促自由基产生,炎症瀑布造成亚急性期不可逆的神经损害。随着巨噬细胞的激活、小胶质细胞形态功能转变,由产生释放促炎症因子状态转变为促吞噬、促神经保护作用的状态。同时一些促炎症因子如TNF-α、IL-6体现其多效性转为神经保护作用,同时转化生长因子-β1、胰岛素样生长因子-1等促神经细胞增殖修复的因子增多,促进修复。在脑梗死后不同阶段参与的炎症细胞或细胞状态、细胞因子水平及信号通路不同,引起的炎症效应也不相同。本文就脑梗死发生后不同阶段炎症反应的研究现状进行综述。

Progress in understanding role of inflammation in pathogenesis of post-ischemia cerebral injury

Many mechanisms are involved in the pathogenesis of cerebral ischemia injury. Inflammation is an important part of post-ischemic injury. This important pathological process exists in each stage. Microglia and astrocytes are activated in the acute stage of ischemia and produce inflammatory factors such as interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)-α. Inflammatory factors act on endothelial cells, neutrophils, and lymphocytes to produce more inflammatory factors, which in turn induce apoptosis, aggravate calcium overload, promote the release of toxic amino acids, and result in the production of free radicals via the TLR4/NF-κB and PI3K/Akt signal pathways. Inflammation cascade causes irreversible neurological damage in the subacute phase. With the activation of macrophages and the transformation of morphology and function of microglia, the body changes from the state of injury to the state of protection. At the same time, some pro-inflammatory factors such as TNF-α and IL-6 exhibit neuroprotective effects. And the factors such as TGF-β1 and IGF-1, which promote the proliferation and repair of nerve cells, increase and promote the repair process. The inflammatory response after cerebral ischemic injury is different in all stages. This paper reviews the progress in understanding the role of inflammation in the pathogenesis of post-ischemia cerebral injury.