1，8－桉油素预处理对Aβ25～35诱导大鼠皮层神经元炎症反应的影响

摘要

目的：探讨1，8－桉油素预处理对Aβ25～35诱导原代培养大鼠皮层神经元炎症反应的影响。方法原代培养大鼠皮层神经元，随机分组。采用噻唑蓝（ MTT）还原反应观察神经元损伤；以 Aβ25～35处理24 h 诱导神经元损伤；酶联免疫吸附法（ ELISA ）检测上清液中肿瘤坏死因子（TNF）－α、白介素（IL）－1β及半胱氨酰白三烯（CysLTs）释放水平。结果20μmol／L的 Aβ25～35处理神经元细胞24 h可显著降低神经元活性，增加TNF－α、IL－1β及CysLTs的释放，1，8－桉油素10μmol／L预处理后可明显抑制 Aβ25～35引起的细胞毒性效应，并抑制上述炎症因子及 CysLTs的释放。结论1，8－桉油素对Aβ25～35诱导的神经元损伤具有保护作用，与抑制TNF－α、IL－1β及CysLTs的释放有关。%Objective To investigate the effect of 1,8-cineol against Aβ25~35-induced inflammatory response in rat primary cultured neurons.Methods Rat primary cultured cortical neurons were randomly divided into control , Aβ25~35(20μmol/L), low dose of 1,8-cineol (Aβ25~35 20 μmol/L +1,8-cineol 1 μmol/L),high dose of 1,8-cineol(Aβ25~35 20 μmol/L+1,8-cineol 10 μmol/L) groups.Cell viability was evaluated by 3-(4,5-dimethyl -2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide(MTT) reduction assay.Neuron injury was induced 24hafterAβ25~35treatment.ReleasesofTNF-α,IL-1βandCysLTsinthesupernatantweredeterminedbyELISA.Results 20μmol/Lof Aβ25~35 incubated for 24 h significantly reduced neuronal activity , and increased TNF-α, IL-1βand CysLTs releases.Pretreatment with 1,8-eol obviously inhibited cytotoxicity and decreasedth elevel of abovecytokines and CysL Tsreleases.Conclusions 1,8-cineolhasaprotec-tive effect on Aβ25~35 induced neuron injury , probably relates with inhibition of TNF-α, IL-1βand CysLTs releases .