胶质母细胞瘤（GBM）是最常见和最具侵袭性的原发性脑肿瘤。GBM包含一小部分被认为在治疗抵抗、肿瘤浸润和复发中起关键作用的胶质瘤干细胞（GSCs），因此被视为重要的治疗靶点。最近的临床研究表明，手术麻醉药选择，特别是异丙酚，在肿瘤切除后影响肿瘤对治疗的反应和患者预后。在本研究中，我们研究了异丙酚对GSCs抗肿瘤效应的分子机制以及其与小胶质细胞的相互作用。异丙酚对GSCs的自我更新、间质标记物表达和迁移呈剂量依赖性的抑制作用，并使其对替莫唑胺（TMZ）和放射线敏感。高浓度的异丙酚导致细胞死亡程度较大，这是通过微流控芯片技术证明的。异丙酚增加了胶质母细胞瘤中作为肿瘤抑制因子的长链非编码RNA BDNF-AS的表达，而沉默该长链非编码RNA部分削弱了异丙酚的效应。异丙酚还通过胞外囊泡和BDNF-AS的传递抑制了促肿瘤的GSC-小胶质细胞相互作用。总之，异丙酚对GSCs具有抗肿瘤效应，使这些细胞对放射线和TMZ敏感，并通过胞外囊泡传递BDNF-AS来抑制其与小胶质细胞的促肿瘤相互作用。

Glioblastoma (GBM) is the most common and aggressive primary brain tumor. GBM contains a small subpopulation of glioma stem cells (GSCs) that are implicated in treatment resistance, tumor infiltration, and recurrence, and are thereby considered important therapeutic targets. Recent clinical studies have suggested that the choice of general anesthetic (GA), particularly propofol, during tumor resection, affects subsequent tumor response to treatments and patient prognosis. In this study, we investigated the molecular mechanisms underlying propofol's anti-tumor effects on GSCs and their interaction with microglia cells. Propofol exerted a dose-dependent inhibitory effect on the self-renewal, expression of mesenchymal markers, and migration of GSCs and sensitized them to both temozolomide (TMZ) and radiation. At higher concentrations, propofol induced a large degree of cell death, as demonstrated using microfluid chip technology. Propofol increased the expression of the lncRNA BDNF-AS, which acts as a tumor suppressor in GBM, and silencing of this lncRNA partially abrogated propofol's effects. Propofol also inhibited the pro-tumorigenic GSC-microglia crosstalk via extracellular vesicles (EVs) and delivery of BDNF-AS. In conclusion, propofol exerted anti-tumor effects on GSCs, sensitized these cells to radiation and TMZ, and inhibited their pro-tumorigenic interactions with microglia via transfer of BDNF-AS by EVs.