Mechanisms and therapeutic implications of RTA 408, an activator of Nrf2, in subarachnoid hemorrhage-induced delayed cerebral vasospasm and secondary brain injury.

ABSTRACT:

Objectives

More and more evidence suggests oxidative stress and inflammation contribute importantly to subarachnoid hemorrhage (SAH)-induced cerebral vasospasm and secondary brain injury. Recent evidence indicates Nuclear factor (erythroid-derived 2)-like 2 (Nrf2) increases the expression of antioxidant genes and decreases the expression of pro-inflammatory genes. This study examines the effects of an activator of Nfr2, RTA 408, on SAH-induced cerebral vasospasm and possible mechanism underlying its effect in a two-hemorrhage rodent model of SAH.

Methods

We randomly assigned 60 Sprague-Dawley male rats (350 to 420g) to five groups twelve rats each: one control group (no SAH), one untreated SAH only group and three RTA-408 treatment groups (SAH+ RTA 408 0.5 mg/kg/day, SAH+RTA

SUBMITTER: Tsai TH 

PROVIDER: S-EPMC7535038 | biostudies-literature | 2020

REPOSITORIES: biostudies-literature