<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>The protocol of experimental grouping and treatments: (a) protocol used in investigating whether the mitochondrial JNK/Sab/Src/ROS signaling pathway is activated in H9c2 cells after H/R and (b) protocol used in investigating the role of F<sub>2</sub> in H9c2 cells after H/R.</div>

Oxidative Medicine and Cellular Longevity

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Figure 1

Figure 1: <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 1 | 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 