Baicalin Reduces Early Brain Injury after Subarachnoid Hemorrhage in Rats

Objective: To evaluate the effect of baicalin on subarachnoid hemorrhage(SAH) in rats and explore the potential mechanisms. Methods: Sprague-Dawley rats underwent experimental SAH and received treatment with baicalin at 10 or 50 mg/kg after 2 and 12 h of SAH. Neurological scores, brain water content, Evans-blue extravasation, and levels of glutathione peroxidase(GSH-Px), superoxide dismutase(SOD), myeloperoxidase(MPO), and malondialdehyde(MDA) were measured 24 h after SAH. Expression of nuclear factor erythroid-related factor 2(Nrf2), NAD(P)H: quinone oxidoreductase 1(NQO1), matrix metalloproteinase-9(MMP-9), aquaporin 4(AQP4), occludin, and zonulaoccludens-1(ZO-1) were detected in the brain by Western blot. Heme oxygenase-1(HO-1) was detected by quantitative polymerase chain reaction, and tumor necrosis factor-α(TNF-α) and interleukin-1β(IL-1β) were assessed by enzyme-linked immunosorbent assay. Results: Baicalin attenuated EBI 24 h after SAH in rats(P<0.05). Baicalin elevated neurological scores, GSH-Px, SOD, and increased the expression of Nrf2, NQO1, HO-1, occludin, and ZO-1 in SAH rats(P<0.05 or P<0.01). Baicalin reduced MPO, MDA, and the expression of MMP-9, AQP4, TNF-α, and IL-1β(P<0.05 or P<0.01). Conclusion: Baicalin reduced SAH-induced EBI, partially via activation of the Nrf2/HO-1 pathway and inhibition of MMP-9 and AQP4.