Gallic acid (GA), a plant-derived ubiquitous secondary polyphenol metabolite, can be a useful dietary supplement. This in vitro study’s primary purpose was to assess the anti-aging properties of GA using rat embryonic fibroblast (REF) cells, antidiabetic effects via pancreatic islet cells, and finally, elucidating the molecular mechanisms of this natural compound. REF and islet cells were isolated from fetuses and pancreas of rats, respectively. Then, several senescence-associated molecular and biochemical parameters, along with antidiabetic markers, were investigated. GA caused a significant decrease in the β-galactosidase activity and reduced inflammatory cytokines and oxidative stress markers in REF cells. GA reduced the G0/G1 phase in senescent REF cells that led cells to G2/M. Besides, GA improved the function of the β cells. Flow cytometry and spectrophotometric analysis showed that it reduces apoptosis via inhibiting caspase-9 activity. Taken together, based on the present findings, this polyphenol metabolite at low doses regulates different pathways of senescence and diabetes through its antioxidative stress potential and modulation of mitochondrial complexes activities.

No abstract

Background The rapid-growing population of diabetic patients and the elderly are among the direst challenges that the science of medicine is facing today. Targeting these two challenges can shed light on new means to control and ideally reverse this trend. In this experiment, Vinpocetine’s effect on aged pancreatic beta-cell functions in correlation with oxidative stress was studied. Methods Islet cells were isolated from the pancreas of aged rats and exposed to Vinpocetine, dissolved in acetone and RPMI, for 48 h. Then, senescence-associated molecular parameters, including P16 and P38 gene expressions and β-galactosidase activity, were investigated along with diabetic and inflammation markers. Results Experimental results showed that Vinpocetine could significantly increase aged islets insulin secretion and also make a meaningful reduction in oxidative stress markers. This drug can also decrease expression levels of P16 and P38, the primary genes responsible for the aging pathway. TNF-α, IL-6, and NF-κB expressions were also reduced noticeably after treatment with Vinpocetine. Conclusion The current study showed that Vinpocetine, a derivative of the secondary plant metabolite called Vincamine, could break this vicious cycle of oxidative stress and aging by reducing oxidative stress and inflammation, thus inhibiting cellular aging.