Natural Compounds for SIRT1-Mediated Oxidative Stress and Neuroinflammation in Stroke: A Potential Therapeutic Target in the Future

Figure 1

The signal pathway of SIRT1-mediated antioxidation in stroke. The picture shows the signal pathway of SIRT1-mediated antioxidation in stroke. In response to oxidative stress after stroke, SIRT1 mainly mediates four molecular modifications, including Nrf2, FOXO, PGC-1α, and MAPT. By deacetylating the major acetylation sites, the level of FOXO, PGC-1α, and Nrf2 is upregulated by SIRT1, while MAPT is downregulated. When the level of FOXO, PGC-1α, and Nrf2 increases, several kinds of antioxidant proteins also correspondingly increase, which further suppress oxidative stress. In addition, the accumulation of abnormal MAPT will be reduced through deacetylating MAPT, thus reducing the damaging effect on cells. Therefore, some drugs or upstream regulators can inhibit oxidative stress by acting on SIRT1, which further exerts neuroprotective effects.