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More specifically, the researchers posited that the peptide may have enhanced the expression of Ki-67 and CD98hc that are less intensively synthesized during cell aging. Epithalon also seemed to inhibit the activity of Caspase-3, a crucial enzyme believed to facilitate apoptosis (programmed cell death)
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Small-animal studies describe loss or activation of nitric oxiderelated pathways following peptide exposure, potentially contributing to vascular resilience under stress (1)
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