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Furthermore, studies on HDAC6 have shown that inhibiting HDAC6 can protect mice from experimental stroke-induced brain injury by regulating oxidative stress through activation of the NRF2/HO-1 pathway [66]

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Support for the hypothesis that neuroprotection occurs through increasing cystine/cysteine availability is provided by experiments demonstrating the loss of this effect following BSO treatment or cystine depletion [250]