| First Author | Sun G | Year | 2022 |
| Journal | Neurosci Lett | Volume | 770 |
| Pages | 136400 | PubMed ID | 34923041 |
| Mgi Jnum | J:321035 | Mgi Id | MGI:6867786 |
| Doi | 10.1016/j.neulet.2021.136400 | Citation | Sun G, et al. (2022) Nrf2 loss of function exacerbates endoplasmic reticulum stress-induced apoptosis in TBI mice. Neurosci Lett 770:136400 |
| abstractText | Nuclear factor erythroid 2-related factor 2 (Nrf2) plays an important role in neuroprotection and recover. Our studies have showed that endoplasmic reticulum (ER) stress-induced apoptosis aggravates secondary damage following traumatic brain injury (TBI). Whether Nrf2 involved in ER stress and ER stress-mediated apoptosis is not clearly investigated. This present study explored the effect of Nrf2 knockout on ER stress and ER stress-induced apoptosis in TBI mice. A lateral fluid percussion injury (FPI)model of TBI was built based on Nrf2 knockout (Nrf2((-/-))) mice and wild-type (Nrf2((+/+))) mice, and the expressions of marker proteins of ER stress and ER stress-induced apoptosis were checked at 24 h following TBI. We found that Nrf2((-/-)) mice presented more severe neurological deficit, brain edema and neuronal cell apoptosis compared with Nrf2((+/+)) mice. And, the TBI Nrf2((-/-)) mice were significantly increased expression of marker proteins of ER stress and ER stress-induced apoptotic pathway including glucose regulated protein (GRP78), protein kinase RNA-like ER kinase (PERK), inositol requiring enzyme (IRE1), activating transcription factor 6 (ATF6), C/EBP homologous protein (CHOP), caspase-12 and caspase-3, compared with that in WT mice. These results suggest that Nrf2 could ameliorate TBI-induced second brain injury partly through ER stress signal pathway. |
