Figure 8From: The role of Nox2-derived ROS in the development of cognitive impairment after sepsis Summary of the main findings. This figure highlights the involvement of Nox2 in brain dysfunction associated to sepsis- associated encephalopathy (SAE) and the long-term consequences. Nox2 activation is inhibited by apocynin, preventing ROS production without affecting microglial activation. Gp91phox gene deletion impairs microglial activation after sepsis.Back to article page