关键词: 葛根素, 七氟烷, 阿尔兹海默病 , 凋亡, 氧化应激

Abstract: Objective To observe the effect of puerarin on the injury of H4 human neuroglioma cells induced by sevoflurane. Methods H4 human neuroglioma cells were cultured in vitro and divided into 4 groups: control group; sevoflurane group (cells were treated with 4.1% sevoflurane for 6 h); puerarin (cells were cultured only with 100 μmol/L puerarin for 6 h); sevoflurane+puerarin group (cells were pre-treated with 100 μM puerarin for 1 h before the expose to sevoflurane for 6 h). CCK8 assay was used to detect the cell viability. Cell apoptosis was detected by caspase 3 activity kit and flow cytometry. The production of reactive oxygen (ROS) was tested by probe DCFH-DA. Spectrophotometry was used to evaluate the malondialdehyde (MDA) and superoxide dismutase (SOD). Western blot was used to assess expression of BACE1. Results Compared with control group, cell viability of sevoflurane group was significantly decreased(p＜0.01), apoptosis and the expression of BACE1 was obviously increased (p＜0.01), the level of ROS and MDA was significant increased (p＜0.01) while the activities of SOD was significantly depressed(p＜0.01). However, the puerarin observably attenuated these changes (p＜0.01). Conclusion Puerarin protected H4 human neuroglioma cells against apoptosis and oxidative stress and attenuated the expression of BACE1 induced by sevoflurane, suggesting that it may be new strategy for prevention of Alzheimer’s disease caused by inhalation anesthetics.

Key words: Puerarin, sevoflurane, Alzheimer’s disease, apoptosis, oxidative stress