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Catalpol, a potent antioxidant and free radical scavenger acting through the ERK1/2 signaling pathway, has also been shown to positively affect NG2 glia (pre-myelinating oligodendrocytes) after oxidative stress (Cai et al., Mitochondrial Dysfunction The ischemia-induced excitotoxicity results in mitochondrial malfunctioning due to the damage to mitochondrial proteins, membranes, and DNA, thus impairing the ability of mitochondria to synthesize ATP and carry out their wide range of metabolic functions (Rama and Garca, 2016)