<i>N</i>-n-Butyl Haloperidol Iodide Ameliorates Oxidative Stress in Mitochondria Induced by Hypoxia/Reoxygenation through the Mitochondrial c-Jun N-Terminal Kinase/Sab/Src/Reactive Oxygen Species Pathway in H9c2 Cells

<div>Model of the JNK/Sab/Src/ROS signaling pathway and the role of F<sub>2</sub> in H9c2 cells during H/R. H/R causes oxidative stress in mitochondria by activating JNK, which binds to mitochondrial outer membrane Sab protein, leading to inactivation of mitochondrial p-Src and increasing mitochondrial ROS production in H9c2 cells. F<sub>2</sub> could inhibit H/R-induced JNK activation and ameliorate dephosphorylation of Src and reduce the mitochondrial ROS level.</div>

Oxidative Medicine and Cellular Longevity

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Figure 9

Figure 9: <i>N</i>-n-Butyl Haloperidol Iodide Ameliorates Oxidative Stress in Mitochondria Induced by Hypoxia/Reoxygenation through the Mitochondrial c-Jun N-Terminal Kinase/Sab/Src/Reactive Oxygen Species Pathway in H9c2 Cells 

Figure 9 | N-n-Butyl Haloperidol Iodide Ameliorates Oxidative Stress in Mitochondria Induced by Hypoxia/Reoxygenation through the Mitochondrial c-Jun N-Terminal Kinase/Sab/Src/Reactive Oxygen Species Pathway in H9c2 Cells 