低氧条件下大鼠大脑皮质星形胶质细胞中IL-1β和CD44的表达及其意义
发布时间：2018-07-29 12:20
【摘要】：中枢神经系统的损伤和大脑疾病产生是由于大脑内细胞的损伤和死亡所造成的,而缺血后的脑损伤通常伴随着炎症反应的发生并介导继发性的脑损伤。缺血早期白细胞的侵润和大脑水肿的形成都是由炎症反应所诱导的。而且,大脑中的细胞包括星形胶质细胞、小胶质细胞以及内皮细胞在缺血的刺激下被激活而成为反应性的细胞。大多数的炎症反应都是由一些炎性细胞因子所介导的。IL-1β作为一类重要的炎症前细胞因子,在脑缺血的损伤中有着重要的作用。在早期的损伤过程中已经发现IL-1β的表达对于脑梗塞的形成有着直接的关系。CD44是作为透明质酸(HA)的受体在细胞增殖和肿瘤的形成及转移有重要作用的一类细胞粘附分子家族,除此之外,CD44和HA的相互作用还参与许多炎症疾病的发生。最近在脑缺血模型中发现,CD44表达的升高可能会通过介导炎症而参与缺血后的损伤。星形胶质细胞作为脑内数量最多的一类细胞,在神经系统中发挥着重要的作用,而且在不同的病理条件下它的功能也是完全不同的。因此,我们想了解的是:它在缺氧状态下对IL-1β和CD44的表达有没有改变?细胞外基质的代谢是否受到低氧条件的调控而介导炎症的发生?如果有,这些改变和变化的意义是什么?为了探讨这些问题,本文对星形胶质细胞进行了体外培养的实验研究。 通过体外分离培养新生大鼠星形胶质细胞,低氧培养20min,建立缺氧缺糖模型,缺氧后复氧1h,3h,6h,12h,24h,利用免疫荧光双标和RT-PCR及Western blot的方法观察和检测IL-1β和CD44,CD44v6及Ⅱ型透明质酸合酶(HAS-2)在复氧不同时间的表达,并以正常的星形胶质细胞作为对照。结果显示:同正常培养的细胞相比,在转录水平,低氧复氧后星形胶质细胞的IL-1β,CD44,CD44v6及HAS-2 mRNA表达明显升高;在蛋白水平,IL-1β在缺氧复氧后6h表达有明显的升高,CD44在缺氧复氧后表达量的变化有时问依赖性趋势升高。我们的结果表明了在星形胶质细胞缺氧缺糖后IL-1β和CD44及其配体的差异性表达,暗示了在损伤过程中IL-1β可能会和CD44相互作用来介导缺血后损伤,此外细胞外基质的改变也可能会促进缺血损伤后炎症的发生的重要因素。
[Abstract]:Central nervous system (CNS) injury and brain disease are caused by the injury and death of brain cells, and the ischemic brain damage is usually accompanied by inflammation and mediates the secondary brain damage. Leukocyte infiltration and cerebral edema are induced by inflammation at the early stage of ischemia. Moreover, cells in the brain include astrocytes, microglia and endothelial cells activated by ischemia to become reactive cells. Most inflammatory responses are mediated by some inflammatory cytokines. IL-1 尾, as an important preinflammatory cytokine, plays an important role in cerebral ischemia injury. It has been found that the expression of IL-1 尾 is directly related to the formation of cerebral infarction in the early stage of injury. CD44 is a kind of cell adhesion molecule family which plays an important role in cell proliferation and tumor formation and metastasis as a receptor of hyaluronic acid (HA). In addition, the interaction of CD 44 and HA is involved in many inflammatory diseases. Recently, it was found that the increased expression of CD44 may play a role in ischemic injury by mediating inflammation in cerebral ischemia model. Astrocytes, as the most abundant cells in the brain, play an important role in the nervous system, and their functions are completely different under different pathological conditions. So what we want to know is: does it change the expression of IL-1 尾 and CD44 in anoxic state? Is the metabolism of extracellular matrix mediated by inflammation due to hypoxia? If so, what is the meaning of these changes and changes? In order to investigate these problems, astrocytes were cultured in vitro. The astrocytes of newborn rats were isolated and cultured in vitro and cultured in hypoxia for 20 min. The model of hypoxia and glucose deficiency was established. The expression of IL-1 尾, CD44v6 and type 鈪，
本文编号：2152656
[Abstract]:Central nervous system (CNS) injury and brain disease are caused by the injury and death of brain cells, and the ischemic brain damage is usually accompanied by inflammation and mediates the secondary brain damage. Leukocyte infiltration and cerebral edema are induced by inflammation at the early stage of ischemia. Moreover, cells in the brain include astrocytes, microglia and endothelial cells activated by ischemia to become reactive cells. Most inflammatory responses are mediated by some inflammatory cytokines. IL-1 尾, as an important preinflammatory cytokine, plays an important role in cerebral ischemia injury. It has been found that the expression of IL-1 尾 is directly related to the formation of cerebral infarction in the early stage of injury. CD44 is a kind of cell adhesion molecule family which plays an important role in cell proliferation and tumor formation and metastasis as a receptor of hyaluronic acid (HA). In addition, the interaction of CD 44 and HA is involved in many inflammatory diseases. Recently, it was found that the increased expression of CD44 may play a role in ischemic injury by mediating inflammation in cerebral ischemia model. Astrocytes, as the most abundant cells in the brain, play an important role in the nervous system, and their functions are completely different under different pathological conditions. So what we want to know is: does it change the expression of IL-1 尾 and CD44 in anoxic state? Is the metabolism of extracellular matrix mediated by inflammation due to hypoxia? If so, what is the meaning of these changes and changes? In order to investigate these problems, astrocytes were cultured in vitro. The astrocytes of newborn rats were isolated and cultured in vitro and cultured in hypoxia for 20 min. The model of hypoxia and glucose deficiency was established. The expression of IL-1 尾, CD44v6 and type 鈪，
本文编号：2152656
本文链接：https://www.wllwen.com/yixuelunwen/binglixuelunwen/2152656.html
最近更新
教材专著
