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首页> 外文期刊>Journal of neuroendocrinology >Temporospatial effects of acyl‐ghrelin on activation of astrocytes after ischaemic brain injury
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Temporospatial effects of acyl‐ghrelin on activation of astrocytes after ischaemic brain injury

机译：酰基甘油蛋白在缺血性脑损伤后激活星形胶质细胞的瞬间作用

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Abstract The protective mechanisms of astrocyte signalling are based on the release of neurotrophic factors and the clearing of toxic substances in the early stages of cerebral ischaemia. However, astrocytes are also responsible for the detrimental effects that occur during the later stages of ischaemia, in which glial scars are formed, thereby impeding neural recovery. Acyl‐ghrelin has been found to be neuroprotective after stroke, although the influence of acyl‐ghrelin on astrocytes after ischaemic injury is yet to be clarified. In the present study, we used permanent middle cerebral arterial occlusion to establish a brain ischaemia model in vivo, as well as oxygen and glucose deprivation ( OGD ) to mimic ischaemic insults in vitro. We found that acyl‐ghrelin injection significantly increased the number of activated astrocytes in the peri‐infarct area at day 3 after brain ischaemia and decreased the number of activated astrocytes after day 9. Moreover, the expression of fibroblast growth factor 2 ( FGF 2) in the ischaemic hemisphere increased markedly after day 3, and i.c.v. injection of SU 5402, an inhibitor of FGF 2 signalling, abolished the suppression effects of acyl‐ghrelin on astrocyte activation in the peri‐infarct region during the later stages of ischaemia. The results from in vitro studies also showed the dual effect of acyl‐ghrelin on astrocyte viability. Acyl‐ghrelin increased the viability of uninjured astrocytes in an indirect way by stimulating the secretion from OGD ‐injured astrocytes. It also inhibited the astrocyte viability in the presence of FGF 2 in a dose‐dependent manner. Furthermore, the expression of acyl‐ghrelin receptors on astrocytes was increased after acyl‐ghrelin and FGF 2 co‐treatment. In conclusion, acyl‐ghrelin promoted astrocyte activation in the early stages of ischaemia but suppressed the activation in later stages of ischaemic injury. These later effects were likely to be triggered by the increased expression of endogenous FGF 2 after brain ischaemia.
机译：摘要星形胶质细胞信号传导的保护机制是基于神经营养因子的释放和脑缺血早期阶段的有毒物质的清除。然而，星形胶质细胞也负责在缺血症的后期阶段发生的不利影响，其中形成胶质疤痕，从而阻碍神经恢复。已经发现酰基-Ghrelin卒中后是神经保护的，尽管酰基-Ghrelin对缺血性损伤后的星形胶质细胞的影响尚未澄清。在本研究中，我们使用永久性中脑动脉闭塞，在体内建立脑缺血模型，以及氧气和葡萄糖剥夺（OGD）以模仿体外缺血性损伤。我们发现亚氨基酚素注射在脑缺血后第3天显着增加了Peri-Infarct区域的活性星形胶质细胞的数量，并在第9天后降低了活性星形胶质细胞的数量。此外，成纤维细胞生长因子2的表达（FGF 2）在第3天之后，缺血半球显着增加，和ICV注射SU 5402，FGF 2信号传导的抑制剂，废除了丙基-Ghrelin对缺血后的后梗塞区域的星形细胞活化的抑制作用。来自体外研究的结果还显示了酰基-Ghrelin对星形胶质细胞活力的双重作用。 Acyl-Ghrelin通过刺激来自OGD-Inuced星形胶质细胞的分泌来增加未加注的星形胶质细胞的活力。它还以剂量依赖性方式在FGF 2存在下抑制星形胶质细胞的活力。此外，在酰基-Ghrelin和FGF 2合作后，在星形胶质细胞上增加了酰基-Ghrelin受体的表达。总之，酰基-Ghrelin促进了缺血性早期阶段的星形胶质细胞活化，但在缺血性损伤的后期阶段抑制了激活。这些后来的效果可能被脑缺血后内源性FGF 2的表达增加来引发。

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