Figure 5.

The potential molecular mechanism of natural compounds on TBI. These natural compounds can activate the expression of Nrf2 and facilitate Nrf2’s translocation from the cytosol to the nuclear, thus, inhibiting oxidative stress and protecting from neuronal apoptosis. Tannic acid positively regulates the protein expression of PGC-1α, thereby activating the Nrf2/ARE pathway. Instead, aicalin and wogonin increase the level of phosphorylated AKT and PI3K and activates Nrf2, which translocates into the nucleus to increase its downstream effectors’ production, which are responsible for anti-apoptosis and anti-oxidative effects, thus realizing the repair of TBI. The image was created using the image bank of Servier Medical Art (Available online: http://smart.servier.com/, accessed on 15 November 2022), licensed under a Creative Commons Attribution 3.0 Unported License (Available online: https://creativecommons.org/licenses/by/3.0/, accessed on 15 November 2022). Traumatic brain injury: TBI; nuclear factor E2-related factor 2: Nrf2; antioxidant response element: ARE; small muscleaponeurotic fibrosarcoma: sMAF; Kelch-like erythroid cell-derived protein with CNC homology-associated protein 1: Keap1; β-transducing repeat-containing protein: β-TrCP; Cullin 3: CUL3; RING-box protein 1: RBX1; PTEN Induced Kinase 1: PINK1; peroxisome proliferator–activated receptor gamma co-activator 1 alpha: PGC-1α; Phosphoinositide 3-kinases: PI3Ks.