The effect of Resveratrol on the Upregulation of Ngb

Abstract

Apoptosis involves a series of biochemical events that leads to the eventual death of the cell. One pathway – intrinsic pathway, involves the fragmentation of mitochondria and the release of pro-apoptotic proteins, such as cytochrome c. A certain globin protein has been shown to be able to protect cells from apoptosis, called Neuroglobin (Ngb). Ngb is a globin haem protein that has been shown to reduce the ferric form of cytochrome c to inhibit apoptosis. In addition, Ngb has been shown to translocate into the mitochondria under stress, where it reacts with cytochrome c. Estradiol (E2) has been shown to greatly upregulate the levels of Ngb and also stimulates the translocation of Ngb into the mitochondria. The upregulation of Ngb has been shown to be mediated via the ER subtype, ERβ. Even though literature covers the effects of E2 and the ERβ agonist DPN (Diartylpropiolnitrile), there is a lack of evidence on the ER agonist, Resveratrol (RES); RES is a phytoestrogen that has been shown to induce mitochondrial biogenesis and abrogate mitochondrial fragmentation, ameliorating apoptosis. The hypothesis of this study is that RES will upregulate Ngb levels as E2 does, and will translocate Ngb into the mitochondria as E2 does. The results of this study showed that Ngb bands could not be detected via western blots, and the mRNA transcript levels in MCF-7 and DLD-1 could not be quantified. The Ngb-GFP fusion protein did not fluoresce and Ngb’s translocation into the mitochondria could not be determined. Ngb overexpression did not inhibit mitochondrial fragmentation and did not induce mitochondrial fusion.