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低效的溶酶体降解是多种脑部疾病发展的中心环节，但其具体机制及参与的细胞种类仍不清楚。既往研究显示，星形胶质细胞大量吞噬死亡的细胞，但将这些吞噬的物质储存在细胞内而不是进行降解。本研究对星形胶质细胞降解消化功能减弱的原因进行研究，并探索增强星形胶质细胞降解消化功能的方法。结果显示，长期存在于吞噬泡周围的肌动环阻碍了溶酶体的吞噬溶解作用。此外，Rab27a 蛋白可以通过Nox2减少溶酶体的酸化，而星形胶质细胞高表达 Rab27a 蛋白，阻碍抗原呈递。本研究还发现，Nox2与星形胶质细胞摄取的物质共定位，且表达主要组织相容性复合体 II，提示这可能影响星形胶质细胞内的抗原呈递。使用酸化纳米粒子对星形胶质细胞溶酶体进行长时间的酸化处理，能增加星形胶质细胞对所摄取物质和死亡细胞的消化。但随着酸化时间的延长，星形胶质细胞的消化能力再次回复到较低水平，提示随着酸化作用的增强，细胞的对抗酸化的通路也相应增强了。“,”Inefficient lysosomal degradation is central in the development of various brain disorders, but the un-derlying mechanisms and the involvement of different cell types remains elusive. We have previously shown that astrocytes effectively engulf dead cells, but then store, rather than degrade the ingested material. In the present study we identify reasons for the slow digestion and ways to accelerate degradation in primary astrocytes. Our re-sults show that actin-rings surround the phagosomes for long periods of time, which physically inhibit the pha-go-lysosome fusion. Furthermore, astrocytes express high levels of Rab27a, a protein known to reduce the acidity of lysosomes by Nox2 recruitment, in order to preserve antigens for presentation. We found that Nox2 colocalizes with the ingested material, indicating that it may influence antigen processing also in astrocytes, as they express MHC class II. By inducing long-time acidification of astrocytic lysosomes using acidic nanoparticles, we could increase the digestion of astrocyte-ingested, dead cells. The degradation was, however, normalized over time, in-dicating that inhibitory pathways are up-regulated in response to the enhanced acidification.