Abstract: Objective　To investigate the neuroprotective effect of dexmedetomidine (DEX) on preeclampsia rats, based on the nuclear factor-κB (NF-κB)/intercellular adhesion molecule-1 (ICAM-1) pathway. Methods　SD pregnant rats were randomly divided into the control group, the model group, the low-, middle- and high-dose DEX groups, with 10 rats in each group. Except for the sham operation group, the other groups were intraperitoneally injected with homocysteine (Hcy, 200 mg/kg) daily and subcutaneously injected with monosodium glutamate (MSG, 1 g/kg) on the back every other day to prepare the preeclampsia model. During the 10th day to the 20th day of pregnancy, the low-, middle- and high-dose DEX groups were intraperitoneally injected 7.5, 15.0 and 30.0 μg/kg of DEX for 10 days. Neurological function score was used to evaluate the behavioral defects of rats. Enzyme-linked immunosorbent assay (ELISA) was used to detect the S100B and ferritin in cerebrospinal fluid, the expression levels of brain tissue inflammatory factors interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6). TUNEL staining was used to detect the apoptosis of brain tissue. Western blot assay was used to detect the expression levels of NF-κB/ICAM-1 pathway related proteins in brain tissue. Results　Compared with those in the control group, the apoptosis of brain tissue was serious, the neurological function score, S100B and ferritin in cerebrospinal fluid, contents of IL-1β, TNF-α, IL-6 in brain tissue, protein expression levels of p-NF-κB/NF-κB and ICAM-1 were significantly higher in the model group (P＜0.05). Compared with those in the model group, the proportion of apoptotic cells was less in the low-, medium-, and high-dose DEX groups, the neurological function score, S100B and ferritin in cerebrospinal fluid, contents of IL-1β, TNF-α, IL-6 in brain tissue, protein expression levels of p-NF-κB/NF-κB and ICAM-1 were significantly lower (P＜0.05). There was a dose-dependent relationship between the DEX groups. Conclusion　DEX has a therapeutic effect on nerve cells, and its mechanism may be related to the inhibition of the NF-κB/ICAM-1 signal activation, the inflammatory factor release and the apoptosis of brain nerve cells.

Key words: NF-kappa B, intercellular adhesion molecule-1, dexmedetomidine, neuroprotection, preeclampsia