Neuroglobin (Ngb) overexpression is considered as an intrinsic neuroprotective response. Therefore, exogenous Ngb increased in brain tissues has become a promising therapeutic strategy for neurological diseases. Previous studies demonstrated that transactivator of transcription (TAT) protein transduction domain was able to mediate synthetic Ngb entrance into neurons, and then protected brain from hypoxia-ischemic injury. However, the role of recombinant Ngb on early brain injury following subarachnoid hemorrhage (SAH) has not been elucidated. The objectives of this study were to investigate the expression of endogenous Ngb in brain using a rabbit model of SAH, and to verify whether TAT-Ngb fusion protein could be delivered into brain parenchyma, as well as to explore the neuroprotective effect of Ngb and its possible mechanisms. We found that Ngb expressions were up regulated in the transcript and protein levels in a similar time dependent manner after SAH as compared to the sham group. Moreover, TAT-Ngb fusion protein was successfully generated and transferred into brain neurons. Compared with the saline- and Ngb-treated group, neuronal viabilities and neurological outcomes were significantly improved 72 h post-SAH in the TAT-Ngb-treated group. Likewise, anti-apoptotic Bcl-2 protein was also elevated obviously. Conversely, pro-apoptotic factors including caspase 3, caspase 9 and Bax were greatly decreased after TAT-Ngb treatment. Our results suggest that Ngb plays a neuroprotective effect in rabbits suffering from SAH possibly through inhibiting the SAH-induced activation of mitochondria apoptotic pathway. Furthermore, TAT-mediated Ngb delivery into brain may be a promising therapeutic approach.

神经球蛋白（Ngb）的过度表达被认为是一种内在的神经保护反应。因此，脑组织中外源性Ngb的增加已成为神经疾病的一种有前途的治疗策略。先前的研究表明，转录反式激活因子（TAT）蛋白转导域能够介导合成Ngb进入神经元，然后保护大脑免受缺氧缺血性损伤的侵害。但是，尚未阐明重组Ngb在蛛网膜下腔出血（SAH）后早期脑损伤中的作用。本研究的目的是使用SAH兔模型研究内源性Ngb在脑中的表达，并验证TAT-Ngb融合蛋白是否可以传递到脑实质中，并探讨Ngb的神经保护作用及其对脑实质的保护作用。可能的机制。我们发现，与假手术组相比，SAH后Ngb表达在转录和蛋白质水平上调的时间相似。此外，TAT-Ngb融合蛋白已成功生成并转移到脑神经元中。与盐水和Ngb治疗组相比，TAT-Ngb治疗组SAH后72小时的神经元活力和神经系统结局显着改善。同样，抗凋亡的Bcl-2蛋白也明显升高。相反，TAT-Ngb处理后促凋亡因子包括caspase 3，caspase 9和Bax大大降低。我们的结果表明，Ngb可能通过抑制SAH诱导的线粒体凋亡途径的活化而对SAH兔产生神经保护作用。此外，