摘要
目的探讨体外缺血再灌注(ischemia-reperfusion,I-R)脑损伤中NF-κB的表达及白藜芦醇苷(polydatin,PD)的保护作用。方法将体外培养7 d的大鼠大脑皮层神经元分为3组:对照组、模型组和PD组。AO/EB及DAPI染色观察细胞凋亡的形态学变化,同时测定再灌注0、6、12、24、48 h细胞凋亡率、Bcl-2/Bax、NF-κB p65的动态变化。结果模型组可见凋亡细胞的特征性变化;与对照组相比,模型组细胞凋亡率、NF-κB p65的表达量随再灌注时间的延长而明显增加(P<0.05),24 h达高峰,随后渐降低,Bcl-2/Bax的高峰点位于6 h,之后降低(P<0.05);PD组细胞凋亡率及NF-κBp65的表达量较模型组均明显降低(P<0.05),Bcl-2/Bax值则明显升高(P<0.05)。结论NF-κB p65的活化参与了体外I-R脑损伤的病理过程,PD可能通过抑制NF-κB p65的表达,上调Bcl-2/Bax值,阻止神经元凋亡,从而减轻I-R脑损伤。
Objective To observe the expression of NF-κB and explore the effect of polydatin （PD） during ischemia-reperfusion （I-R） induced cortical neuron injury in vitro. Methods The cortical neurons from newborn SD rats cultured for 7 d were randomly divided into control group, model group and PD group. The morphological features of neuronal apoptosis were observed with AO/EB and DAPI staining. Apoptosis, Bcl-2/ Bax, and the expressions of NF-κB p65 were determined 0, 6, 12, 24, 48 h after reperfusion. Results Typi- cal morphological changes of neuronal apoptosis were observed in model group. The number of apoptotic cells and the expressions of NF-κB p65 increased with time prolongation after reperfusion （P 〈 0. 05 ）, peaked 24 h after reperfusion, then decreased in model group compared with those in control group, while Bcl-2/Bax ratio peaked 6 h after reperfusion, then decreased （P 〈 0. 05）. The number of apoptotic cells and the expressions of NF-κB p65 were decreased in PD group compared with those in model group with statistical significance （P 〈 0. 05 ）, while Bcl-2/Bax ratio was increased （ P 〈 0.05 ）. Conclusion The activation of NF-s：B p65 participates in cerebral I-R injury. PD protects against in vitro I-R injury by decreasing neuron apoptosis that may be through suppressing NF-κB p65 activation and upregulating Bcl-2/Bax ratio.
出处
《第三军医大学学报》
CAS
CSCD
北大核心
2009年第2期113-116,共4页
Journal of Third Military Medical University
基金
国家自然科学基金(30772362)
重庆市自然科学基金(2005BB5228)~~
