To evaluate the effect of stellate ganglion block (SGB) on vascular cognitive impairment (VCI) in rats.

Forty SPF healthy male Sprague-Dawley rats, aged 4-6 weeks, weighing 200-220 g, were divided into 4 groups (n=10 each) using a random number table method: sham operation group (group Sham), VCI group, right SGB group (group R) and left SGB group (group L). VCI was induced by permanently ligating bilateral common carotid arteries of anesthetized rats.SGB model was established by transection of the left and right cervical sympathetic trunk while establishing the VCI model in group L and group R, respectively.At 8 weeks after establishing VCI model, Morris water maze test was performed to evaluate the spatial learning and memory abilities, serum neuron-specific enolase (NSE) and S100β protein concentrations were determined by enzyme-linked immunosorbent assay, the hippocampal superoxide dismutase (SOD) activity and malondialdehyde (MDA) contents were measured using microplate method, and the expression of peroxisome proliferator-activated receptor gamma coactivator-1α (PGC-1α), NADPH oxidase 1 (NOX1), zonula occludens-1 (ZO-1), and claudin-5 was detected by Western blot.

Compared with group Sham, the escape latency was significantly prolonged, the time of staying at the target quadrant was shortened, the hippocampal MDA content and concentration of serum S100β protein and NSE were increased, hippocampal SOD activity was decreased, the expression of PGC-1α, ZO-1 and claudin-5 was down-regulated, and the expression of NOX1 was up-regulated in group VCI (P<0.05). Compared with group VCI, the escape latency was significantly shortened, the time of staying at the target quadrant was prolonged, the hippocampal MDA content and concentration of serum S100β protein and NSE were decreased, hippocampal SOD activity was increased, the expression of PGC-1α, ZO-1 and claudin-5 was up-regulated, and the expression of NOX1 was down-regulated in group R, and the escape latency was significantly prolonged, the hippocampal SOD activity was increased, the MDA content was decreased, and the expression of NOX1 was down-regulated in group L (P<0.05). Compared with group R, the escape latency was significantly prolonged, the time of staying at the target quadrant was shortened, the hippocampal MDA content and serum NSE concentration were increased, the hippocampal SOD activity was decreased, the expression of PGC-1α and claudin-5 was down-regulated, and the expression of NOX1 was up-regulated in group L (P<0.05).

SGB can alleviate VCI, and left SGB produces better efficacy than right SGB, and the mechanism may be related to inhibiting the oxidative stress responses and reducing the damage to blood brain barrier in rats.

Stellate ganglion; Nerve block; Cognition disorders