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Research published in journals including the Journal of Neurochemistry and Brain Research has examined the molecular mechanisms underlying these effects with Semax-induced upregulation of BDNF, NGF, and TrkB identified as key mediators of the observed neuroprotection, alongside modulation of the inflammatory cytokine cascade in peri-infarct brain tissue

Data are all represented as a scatter dot plot with centerline as mean, except for percentages quantifications, which are represented as histogram bars

Under normal metabolic conditions, reactive oxygen species (ROS) maintain cellular homeostasis and signaling [137]