目的 探讨神经干细胞来源外泌体（NSC⁃Exos）对脑缺血再灌注损伤大鼠星形胶质细胞TGF⁃β1 信号转导及炎症因子的影响。方法 40 只 SD 大鼠随机分为 Sham 组、MCAO 组、PBS 组和 NSC⁃Exos 组。建 立 MCAO 模型，侧脑室注射 NSC⁃Exos，3 d 后检测大鼠神经功能缺陷评分，取脑进行相对梗死体积测定、组 织病理学、IL⁃6、IL⁃1β、TGF⁃β1 蛋白表达检测，以及 MAP⁃2 和外泌体标记探针 PKH26 共定位检测。结果 NSC⁃Exos 干预降低损伤大鼠神经功能缺陷评分和脑梗死体积（P < 0.05），大鼠海马 CA3 区神经元数量增 加，GFAP 阳性细胞表达率和神经元细胞凋亡指数降低（P < 0.05），蛋白 IL⁃6、IL⁃1β 表达下降，而 TGF⁃β1 表 达增加（P < 0.05）；PKH26 和 MAP⁃2 双阳性细胞在海马 CA3 区表达。结论 NSC⁃Exos 可能通过影响星形 胶质细胞 TGF⁃β1 信号转导，抑制星形胶质细胞增生与炎症因子 IL⁃6、IL⁃1β 的表达，通过增强 TGF⁃β1 的表 达来修复脑损伤。 

Objective To investigate the effects of neural stem cell⁃derived exosomes（NSC⁃Exos）on TGF⁃ β1 signal transduction and inflammatory factors in astrocytes during cerebral ischemia ⁃ reperfusion injury in rats. Methods 40 SD rats were randomly divided into Sham group，MCAO group，PBS group and NSC ⁃Exos group. The rat model of MCAO was established. NSC⁃Exos was injected into right lateral ventricle. After 3 days，the neural deficit score was performed，and the brain was taken for relative infarct volume determined，histopathology and expression detection of IL⁃6，IL⁃1β，and TGF⁃β1 protein respectively. The colocalization of MAP⁃2 and exosome⁃ labeled probe PKH26 was detected. Results NSC ⁃Exos intervention could reduce the neurological deficit score and cerebral infarction volume（P < 0.05），increase the number of neurons，reduce the expression rate of GFAP positive cells and neuronal apoptosis index（P < 0.05），and decrease the expression of protein IL⁃6 and IL⁃1β. TGF⁃ β1 expression was increased（P < 0.05）. PKH26 and MAP ⁃2 positive cells were colocalized in CA3 region of hippocampus. Conclusions NSC⁃Exos may inhibit TGF⁃β1 signaling in astrocytes and repair brain injury by reducing astrogliosis and expression of inflammatory factors while enhancing the expression of TGF⁃β1.