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Semax reduced the ischemia-associated increase in nitric oxide generation and affected markers of oxidative damage.⁹ These findings suggest that Semax’s proposed neuroprotective profile may involve several cellular processes: Calcium homeostasis Mitochondrial stability Oxidative signaling Responses to excessive glutamate Cellular adaptation to reduced blood flow These studies were conducted in cultured cells or animal ischemia models

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Among them, acyl-ghrelin and desacyl-ghrelin have emerged as the most biologically relevant 121,124