Objective:

2

To evaluate the effect of baicalin on subarachnoid hemorrhage (SAH) in rats and explore the potential mechanisms.

Methods:

2

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:

2

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:

2

Baicalin reduced SAH-induced EBI

partially via activation of the Nrf2/HO-1 pathway and inhibition of MMP-9 and AQP4.