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It protects neuronal cells by mitigating oxidative stress, reducing inflammation, and enhancing mitochondrial function, thereby alleviating cerebrovascular injury and slowing the progression of VaD

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The administration of NAC up to 2 h after the brain injury resulted in an improvement in the activity of mitochondrial complexes, enhanced oxidative phosphorylation, and a reduction in the rate of ROS production [11]

In the nucleus, protein phosphatase 2 A (PP2A)-mediated dephosphorylation at serine 298 residue affects the interaction of the nuclear localization signal of HDAC4 and MEF2, finally altering the neuronal activity