Without a Hesperetin-only control group, how can you definitively rule out that the observed restoration of SIRT1/Nrf2 pathway components is not due to Hesperetin independently elevating these pathways in a normal physiological state? Could the effects seen in the ADHD/HSP groups be a combination of blocking MSGL’s effects and an inherent, baseline-upgrading action of Hesperetin?
Consequently, wouldn’t it be more accurate to conclude that Hesperetin “prevented the MSGL-induced downregulation” of the SIRT1/Nrf2 pathway, rather than claiming it caused “upregulation”? The current language implies an enhancing effect that the experimental design cannot verify.