glutathione sickle cell disease Keap1-Nrf2 Heterodimer: A Therapeutic Target to Ameliorate l glutathione sickle cell l-glutamine,

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163,164,198,199 Breakdown of ion homoeostasis ion gradients, uncontrolled neurotransmitter release, oedema and mitochondrial failure are thus the key mechanisms behind pathophysiology of the ischaemic stroke

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By catalyzing the phosphorylation and degradation of IkB at specific amino acid residues, NFkB can translocate from the cytoplasm to the nucleus and further activate immune mediators such as IL-6 and IL-8 (122)

(PubMed) Huang Z, Rose AH, Hoffmann PR