Research Paper Volume 13, Issue 17 pp 21345—21363

Up-regulation of circARF3 reduces blood-brain barrier damage in rat subarachnoid hemorrhage model via miR-31-5p/MyD88/NF-κB axis


Figure 7. The mechanistic diagram. Microglia become activated and released overproduced inflammatory mediators, which then induced BBB damage and neuronal apoptosis. Forced overexpression of circARF3 attenuates BBB destruction, neuronal apoptosis in SAH rats by regulating the miR-31-5p-activated MyD88-NF-κB pathway in microglia.