Fig. 10
From: TAK1 mediates neuronal pyroptosis in early brain injury after subarachnoid hemorrhage
Schematic diagram for TAK1-mediated neuronal pyroptosis in EBI following SAH. The p-TAK1 level is upregulated following SAH ictus. Inhibition of TAK1 by OZ treatment reduces ROS production and prevents lysosomal cathepsin B releasing into the cytoplasm. ROS and cathepsin B could activate NLRP3 inflammasome. Blockade of TAK1 mitigates neuronal pyroptosis via inhibition of NLRP3 inflammasome and NF-κB signaling pathway. Treatment with OZ shows remarkable therapeutic effects on EBI following SAH