脑出血具有极高的致残率及死亡率，亟需探寻有效的防治措施。我们前期的研究发现：与野生型小鼠相比，组蛋白去乙酰化酶（histone deacetylase, HDAC）6基因敲除小鼠脑出血后脑水肿明显变小，神经功能损伤明显减轻，血肿周围脑组织神经元凋亡明显减少。然而，导致以上表型变化的具体机制目前尚不清楚。. 过氧化物还原酶（peroxiredoxin, Prx）2可以通过氧化还原反应降低氧化应激引起的细胞凋亡，乙酰化修饰的Prx2蛋白其抗氧化应激能力明显提高。前期研究亦发现HDAC6能够降低Prx2的乙酰化修饰水平。因此，我们提出假设：HDAC6通过降低Prx2乙酰化修饰而加重脑出血后神经元凋亡。本项目拟应用基因工程小鼠，以脑出血后相关表型为切入点，从整体、细胞、分子和基因水平阐明HDAC6在脑出血发生发展中的作用及其可能机制。本研究结果将为脑出血后的神经保护治疗提供新靶点。

Stroke is one of the leading causes of death worldwide. Cerebral hemorrhage is a severe form of stroke subtype, more likely to result in death or major disability than cerebral infarction or subarachnoid hemorrhage. Our previous data suggested that histone deacetylase 6(HDAC6) gene deficient mouse exhibited significantly decreased brain edema, functional impairments and neuron apoptosis when compared with wide type mouse after cerebral hemorrhage. The mechanisms by which HDAC6 knockout mouse showed reduced lesion volume, functional impairments and neuron apoptosis after cerebral hemorrhage remain unclear...Peroxiredoxin(Prx) 2 exerts a protective role in oxidative stress-induced neuronal cell death. The anti-oxidant effects of Prx2 are significantly enhanced when Prx2 is acetylated modification. Our previous data indicated that HDAC6 can target Prx2 and reduce the acetylated level of Prx2. Based on the above data, we made the assumption that the functional impairments and neuronal apoptosis after cerebral hemorrhage may be attributed to reduced acetylated level of Prx2 which is regulated by HDAC6. So we chose to focus on this pathway for our investigation, and we intend to clarify the possible mechanisms by which HDAC6 deficiency reduces brain edema, functional impairments and neuronal apoptosis after cerebral hemorrhage. This study may offer a novel target for effectively neuroprotective treatments after cerebral hemorrhage.