芝麻素对氧糖剥夺损伤大鼠皮质神经元的作用及机制  

EFFECT OF SESAMIN ON CORTICAL NEURON INJURY INDUCED BY OXYGEN-GLUCOSE DEPRIVATION IN RATS AND RELATED MECHANISM

作　　者：陈淑君 何佳林 万芪 CHEN Shujun;HE Jialin;WAN Qi(Institute of Neuroregeneration&Neurorehabilitation,Qing-dao University,Qingdao 266071,China)

机构地区：[1]青岛大学神经再生与康复研究院,山东青岛266071

出　　处：《青岛大学学报（医学版）》2023年第6期791-795,共5页Journal of Qingdao University(Medical Sciences)

基　　金：国家自然科学基金资助项目(82071385)。

摘　　要：目的探讨芝麻素(SSM)是否通过磷脂酰肌醇3激酶(PI3K)/蛋白激酶B(Akt)/核因子-红细胞样2相关因子2(Nrf2)信号通路对氧糖剥夺(OGD)损伤的大鼠皮质神经元发挥神经保护作用。方法原代培养SD大鼠大脑皮质神经元8 d后,构建体外脑缺血模型。采用CCK-8法检测不同浓度SSM对神经元存活率的影响,采用免疫印迹法检测最适作用浓度SSM处理后磷酸化丝氨酸/苏氨酸激酶(p-Akt)、Akt、Nrf2、血红素氧化酶-1(HO-1)蛋白表达水平。结果与Control组相比,OGD组神经元存活率下降,不同浓度的SSM处理均可增加OGD损伤后神经元的存活率(F=35.93,P<0.01),以25μmol/L的SSM作用最明显。各组氧化应激相关蛋白p-Akt、Nrf2、HO-1表达差异有统计学意义(F=23.47~32.21,P<0.01)。与OGD组相比,OGD+SSM组p-Akt、Nrf2、HO-1蛋白表达量均显著上调(P<0.05);与OGD+SSM组相比,OGD+SSM+LY294002组p-Akt、Nrf2、HO-1蛋白上调均被抑制(P<0.05)。各组Akt比较差异无显著性(P>0.05)。结论SSM通过激活PI3K/Akt/Nrf2信号通路,提高OGD损伤后神经元的存活率,发挥神经保护作用。Objective To investigate whether sesamin(SSM)exerts a neuroprotective effect on rat cortical neurons with oxygen-glucose deprivation(OGD)injury through the phosphatidylinositol 3-kinase(PI3K)/protein kinase B(Akt)/nuclear factor-erythroid 2-related factor 2(Nrf2)signaling pathway.Methods Primary cortical neurons of Sprague-Dawley rats were cultured for 8 days to construct an in vitro model of cerebral ischemia.CCK-8 assay was used to observe the effect of different concentrations of SSM on the viability of neurons,and Western blotting was used to measure the protein expression levels of phosphorylated Akt(p-Akt),Akt,Nrf2,and heme oxygenase-1(HO-1)after treatment with the optimal concentration of SSM.Results Compared with the Control group,the OGD group had a significant reduction in the viability of neurons,and SSM treatment at different concentrations could increase the viability of neurons after OGD injury(F=35.93,P<0.01),with the most obvious effect at the concentration of 25μmol/L.There were significant differences between groups in the expression levels of the oxidative stress-rela-ted proteins p-Akt,Nrf2,and HO-1(F=23.47-32.21,P<0.01).Compared with the OGD group,the OGD+SSM group had significantly upregulated protein expression of p-Akt,Nrf2,and HO-1(P<0.05),and compared with the OGD+SSM group,the OGD+SSM+LY294002 group had inhibited upregulation of p-Akt,Nrf2,and HO-1 proteins(P<0.05).There was no significant difference in Akt between groups(P>0.05).Conclusion SSM plays a neuroprotective role by activating the PI3K/Akt/Nrf2 signaling pathway and increasing the viability of neurons after OGD injury.

关 键 词：芝麻脂素 大脑皮质 神经元 脑缺血 神经保护 

分 类 号：R338.2[医药卫生—人体生理学]