| First Author | Li T | Year | 2014 |
| Journal | Brain Res | Volume | 1558 |
| Pages | 90-9 | PubMed ID | 24576487 |
| Mgi Jnum | J:215513 | Mgi Id | MGI:5605466 |
| Doi | 10.1016/j.brainres.2014.02.036 | Citation | Li T, et al. (2014) Genetic elimination of Nrf2 aggravates secondary complications except for vasospasm after experimental subarachnoid hemorrhage in mice. Brain Res 1558:90-9 |
| abstractText | Nuclear factor erythroid 2-related factor 2 (Nrf2) is a key endogenous protective regulator in the body. This study aimed to explore the role of Nrf2 in subarachnoid hemorrhage (SAH)-induced secondary complications. Wild type (WT) and Nrf2 knockout (KO) mice were subjected to experimental SAH by injecting fresh autologous blood into pre-chiasmatic cistern. The absence of Nrf2 function in mice resulted in exacerbated brain injury with increased brain edema, blood-brain barrier (BBB) disruption, neural apoptosis, and severe neurological deficits at 24h after SAH. Moreover, cerebral vasospasm was severe at 24h after SAH, but not significantly different between WT and Nrf2 KO mice after SAH. Meanwhile, Molondialdehyde (MDA) was increased and GSH/GSSG ratio was decreased in Nrf2 KO mice after SAH. Furthermore, higher expression of TNF-alpha and IL-1beta was also found after SAH in Nrf2 KO mice. In conclusion, our results revealed that Nrf2 plays an important role in attenuating SAH-induced secondary complications by regulating excessive oxidative stress and inflammatory response. |
