Pyridoxal Isonicotinoyl Hydrazone Improves Neurological Recovery by Attenuating Ferroptosis and Inflammation in Cerebral Hemorrhagic Mice

Figure 7

Schematic illustration of the proposed mechanism underlying PIH-mediated protection against ICH. ICH causes ruptured red cells and release of heme, which results in excess iron accumulation. Then excess iron produces ROS through Fenton reaction, which subsequently leads to lipid peroxidation and eventually induces ferroptosis. Iron accumulation and ROS also activate polarization of microglia, leading to the aggravation of inflammatory response. PIH prevents Fenton response through binding iron ions, thereby reduces ROS production, and ultimately inhibits ferroptosis and reduces inflammation. ICH: intracerebral hemorrhage; Hb: hemoglobin; PIH: pyridoxal isonicotinoyl hydrazone; GSH: glutathione; ROS: reactive oxygen species.