Traumatic brain injury (TBI), a leading cause of morbidity worldwide, induces mechanical, persistent structural, and metabolic abnormalities in neurons and other brain-resident cells. The key pathological features of TBI include neuroinflammation, oxidative stress, excitotoxicity, and mitochondrial dysfunction. These pathological processes persist for a period of time after TBIs. Sirtuins are evolutionarily conserved nicotinamide-adenine dinucleotide (NAD+)-dependent deacetylases and mono-ADP-ribosyl transferases. The mammalian sirtuin family has seven members, referred to as Sirtuin (SIRT) 1-7. Accumulating evidence suggests that SIRT1 and SIRT3 play a neuroprotective role in TBI. Although the evidence is scant, considering the involvement of SIRT2, 4-7 in other brain injury models, they may also intervene in similar pathophysiology in TBI. Neurodegenerative diseases are generally accepted sequelae of TBI. It was found that TBI and neurodegenerative diseases have many similarities and overlaps in pathological features. Besides, sirtuins play some unique roles in some neurodegenerative diseases. Therefore, we propose that sirtuins might be a promising therapeutic target for both TBI and associated neurodegenerative diseases. In this paper, we review the neuroprotective effects of sirtuins on TBI as well as related neurodegeneration and discuss the therapeutic potential of sirtuin modulators.

Background Blue light (400 nm -480 nm), is a main source of eye damage emitted by light-emitting diodes (LEDs). Excessive blue light exposure has been shown to cause damage in cornea. This study aimed to investigate the effects of blue light exposure on phosphatidylinositol 3 kinase (PI3K)/AKT signaling pathway and metabolic abnormalities and tissue damage via PI3K/AKT signaling in human corneal epithelial cells (hCECs) and mice corneal tissues. Method The effects on blue light damage in hCECs were investigated by using qRT-PCR, WB, cell scratch assay, and cell reactive oxygen species (ROS) assay. The effects on blue light damage in vivo were investigated by using corneal fluorescein sodium staining. Result We revealed that blue light exposure caused the promotion of cell apoptosis, the increase of ROS and suppression of cell migration, proliferation and viability through the inhibition of PI3K/AKT/protein 70 kDa S6 Kinase (p70S6K) signaling pathway in hCECs in vitro. Furthermore, blue light exposure also induced the corneal epithelial defects and delayed corneal epithelial wound healing in mice cornea in vivo. Conclusion Collectively, this study suggests that PI3K/AKT signaling pathway may be an important target for the treatment of corneal epithelial damage caused by blue light exposure.