Protective effect 3,4-dihydroxyphenylethanol in subarachnoid hemorrhage provoked oxidative neuropathy.

Clinical studies have indicated that early brain injury (EBI) following subarachnoid hemorrhage (SAH) is associated with fatal outcomes. Oxidative stress and brain edema are the characteristic pathological events in occurrence EBI following SAH. The present study aimed to examine the effect of 3,4-dihydroxyphenylethanol (DOPET) against SAH-induced EBI, and to demonstrate whether the effect is associated with its potent free radical scavenging property. SAH was induced in rats using an endovascular perforation technique, and 24 h later the rats displayed diminished neurological scores and brain edema. Furthermore, elevated malondialdehyde (an index of lipid peroxidation) and depleted levels of antioxidants were observed in the rat cerebral cortex tissue. Quantitative polymerase chain reaction analysis indicated the upregulated mRNA expression of the apoptotic markers caspase-3 and -9 in the cerebral cortex. Furthermore, the protein expression levels of the proinflammatory cytokines tumor necrosis factor-α, interleukin (IL)-1β and IL-6 were significantly upregulated in SAH-induced rats. By constrast, treatment with DOPET significantly attenuated EBI by reducing brain edema, elevation of antioxidant status, inhibition of apoptosis and inflammation. In this context, DOPET may be a potent agent in the treatment of EBI following SAH, as a result of its free radical scavenging capacity.