Abstract: Objective To study the protective effect of dexmedetomidine (DEX) on human neuroblastoma cell line SH-SY5Y under anoxia condition and its specific mechanism. Methods SH-SY5Y cells were divided into control group, anoxia group (treated with final concentration of 1.2 mmol/L CoCl₂ for 24 h) and DEX intervention group (treated with final concentration of 1.2 mmol/L CoCl₂ and 10 μmol/L DEX for 24 h). Cell morphology was observed by microscope; Cell viability and apoptosis were detected by MTT assay, TUNEL staining and annexin V-FITC/PI staining; The expression levels of cleaved caspase-9, cleaved caspase-3, p75^NTR and p-NF-κB proteins were detected by Western blot. Results Compared with control group, the cell size in anoxia group was shrinked(P<0.01). Cell viability was decreased (P<0.01). The apoptosis rate was increased (P<0.01). The expression levels of cleaved caspase-9, cleaved caspase-3, p75^NTR and p-NF-κB proteins was all significantly increased (P<0.01). DEX intervention could significantly alleviate the above changes in anoxia group (P<0.01). Conclusions Alleviation of anoxia-induced SH-SY5Y cell injury is potentially mediatd by inhibiting p75^NTR expression and NF-κB activity.

Key words: dexmedetomidine, SH-SY5Y cell, p75^NTR, anoxia