随着急诊取栓的发展，血管再通基础上的区域性亚低温对缺血性脑卒中的脑保护作用逐渐受到关注。虽然多项研究表明亚低温能够干预缺血性脑损伤后的多个病理环节，然而其对缺血性损伤的始动环节—能量代谢障碍的作用仍知之甚少。近期，线粒体跨细胞转移的神经保护研究取得重大进展，且我们前期通过预实验发现，血管再通基础上的区域性亚低温能够上调线粒体跨细胞转移的调控通路CD38-cADPR-Ca2+。因此我们推测亚低温通过作用于CD38-cADPR-Ca2+通路，促进线粒体跨细胞转移，发挥脑保护作用。本研究拟通过在体和离体实验，构建慢病毒载体干预CD38的表达，采用分子生物学技术，从线粒体跨细胞转移这一微观现象出发，检测星形胶质细胞和神经元间能量传递及其关键调控机制，研究CD38-cADPR-Ca2+通路介导的线粒体跨细胞转移在亚低温脑保护中的作用机制。本课题将从新的视角为亚低温用于取栓后的患者提供基础理论依据。

With the development of mechanical thrombectomy, the neuroprotection of regional hypothermia on the basis of vascular recanalization in patients with acute ischemic stroke have drawn more and more attention. Although many studies have shown that hypothermia play a neuroprotective role in multiple pathological in ischemic brain damage, little is known about the role it plays in energy metabolism. Recently years, significant progress has been made in the neuroprotective mechnism of transfer of mitochondrial cross cells, and we found that the regional hypothermia on the basis of vascular recanalization can increase the regulation of the CD38-cADPR-Ca2+ pathway which was a regulator of transfer of mitochondrial across cells. Therefore, we hypothesized that mild hypothermia could promote the transfer of mitochondria across cells and play a protective role by acting on the CD38-cADPR-Ca2+ pathway. In this study, the CD38 is intervened by adenovirus vector in vivo and in vitro experiments, and the molecular biology was used to detect the energy transfer between astrocytes and neurons and its key regulatory mechanisms of CD38-cADPR-Ca2+ pathway from the microscopic phenomenon of mitochondrial transfer. The results of this study can clarify the theoretical basis of hypothermia for patients after mechanical thrombectomy from a new perspective.