Activation of nuclear factor-erythroid 2-related factor 2 (Nrf2) in the basilar artery after subarachnoid hemorrhage in rats.

Cerebral vasospasm plays a pivotal role in the outcome of patients suffering from subarachnoid hemorrhage (SAH). The mechanisms underlying cerebral vasospasm are complex and interrelated. Previous studies that focused on only one of these mechanisms have proved to be ineffective in clinical practice. Therefore, a therapeutic target is desirable that can interrupt the multi-mechanisms underlying cerebral vasospasm. Nuclear factor-erythroid 2-related factor 2 (Nrf2) has been shown to be a key regulator in reducing oxidative stress, inflammatory damage, and accumulation of toxic metabolites, which are all involved in SAH-induced cerebral vasospasm. However, whether Nrf2 is activated in the cerebral artery after SAH hasn't been studied. In the present study, 30 male rats were randomly divided into two groups: control group (n = 15) and SAH group (n = 15). The animals in the SAH group were subjected to injection of autologous blood into the cisterna magna twice on day 0 and day 2 and were killed on day 5. The cross-sectional area of the basilar artery was measured and the nuclear Nrf2 protein level was studied by Western blot, electrophoretic mobility shift assay (EMSA), and immunohistochemical techniques. The expression of nuclear Nrf2 protein was increased remarkably in the SAH group compared with the control group. Immunohistochemical staining demonstrated that high level expression of Nrf2 was present in endothelial and smooth muscle cells; it was located in both the nuclei and cytoplasm. The results of this study indicate that Nrf2 expression is up-regulated in the cerebral artery of rats after experimental SAH.