脑出血（ICH）是一种极为严重的脑血管病。ICH继发性损伤是造成患者预后不良的重要因素，调节小胶质细胞（MG）向M2型极化对减轻ICH继发性损伤具有重要意义。前期发现miR-21转染的BM-MSCs（miR-21-MSCs）可有效缩小血肿、抑制炎症反应及MMP/TIMP失衡，提示miR-21-MSCs可能通过调节MG向M2型极化发挥保护作用。因此我们提出假说：miR-21-MSCs通过外泌体调控MG向M2型极化相关基因的表达，促进ICH的神经功能恢复。本研究拟从动物、细胞及分子水平明确miR-21-MSCs对ICH后神经炎症的作用；探讨miR-21-MSCs调控MG极化的机制；揭示miR-21-MSCs通过外泌体中的miRNA靶向作用于TLR4及STAT3，减轻MG介导的神经元损伤，最终实现神经保护作用的具体机制。本研究将以外泌体作为切入点，以期为ICH的BM-MSC治疗提供新的理论依据。

Intraerebral hemorrhage (ICH) is a kind of cerebrovascular disease with high disability and high mortality. Secondary injury of ICH is an important factor in the poor prognosis of patients，inducing microglia (MG) to M2 type is very important for reducing secondary injury of ICH. We have found that microRNA-21 overexpressing BM-MSCs (miR-21-MSCs) can effectively reduce hematoma, inhibit inflammation, and improve MMP/TIMP imbalance. These results suggest that miR-21-MSCs protected neurological function though regulating MG to M2 type polarization. Therefore, we propose a hypothesis: miR-21-MSCs regulate the expression of MG to M2-type polarization-related genes through exosomes and improve the neurological recovery of ICH. This study intends to clarify the role of miR-21-MSCs on neuroinflammation in ICH rats from various aspects such as animal, cell and molecular levels; explore the regulatory mechanism of miR-21-MSCs on MG type polarization; reveal miR-21-MSCs derived exosomes present miRNAs to target TLR4 and STAT3, thereby improving MG-mediated neuronal damage after intracerebral hemorrhage, and finally realizing the specific mechanism of neuroprotective effect. This study takes exosomes as a new perspective, with a view to providing a new theoretical basis for BM-MSCs treatment of ICH.