Balion Zbigniev, Ramanauskienė Kristina, Jekabsone Aistė, Majienė Daiva
Laboratory of Pharmaceutical Sciences, Institute of Pharmaceutical Technologies, Lithuanian University of Health Sciences, Sukilėlių ave. 13, LT 50162 Kaunas, Lithuania.
Laboratory of Biochemistry, Neuroscience Institute, Lithuanian University of Health Sciences, Eivenių str. 4, LT-50161 Kaunas, Lithuania.
Antioxidants (Basel). 2020 Dec 12;9(12):1262. doi: 10.3390/antiox9121262.
Mitochondria are both the primary targets and mediators of ischaemic damage in brain cells. Insufficient oxygen causes reactive oxygen species that damage the mitochondria, leading to the loss of functionality and viability of highly energy-demanding neurons. We have recently found that aqueous (AqEP), polyethylene glycol-aqueous (Pg-AqEP) and ethanolic propolis extracts (EEP) can modulate mitochondria and ROS production in C6 cells of astrocytic origin. The aim of this study was to investigate the effect of the extracts on viability, mitochondrial efficiency and superoxide generation, and inflammatory cytokine release in primary rat cerebellar neuronal-glial cell cultures affected by ischaemia (mimicked by hypoxia +/- deoxyglucose). AqEP and Pg-AqEP (15-60 µg/mL of phenolic compounds, or PC) significantly increased neuronal viability in ischaemia-treated cultures, and this was accompanied by a reduction in mitochondrial superoxide levels. Less extended protection against ischaemia-induced superoxide production and death was exhibited by 2 to 4 µg/mL of PC EEP. Both Pg-AqEP and Ag-EP (but not EEP) significantly protected the cultures from hypoxia-induced elevation of TNF-α, IL-1β and IL-6. Only Pg-AqEP (but not AqEP or EEP) prevented hypoxia-induced loss of the mitochondrial basal and ATP-coupled respiration rate, and significantly increased the mitochondrial respiratory capacity. Summarising, the study revealed that hydrophilic propolis extracts might protect brain cells against ischaemic injury by decreasing the level of mitochondrial superoxide and preventing inflammatory cytokines, and, in the case of Pg-AqEP, by protecting mitochondrial function.
线粒体既是脑细胞缺血性损伤的主要靶点,也是其介导因子。氧气不足会产生活性氧,损伤线粒体,导致对能量需求高的神经元功能丧失和活力下降。我们最近发现,水相蜂胶提取物(AqEP)、聚乙二醇 - 水相蜂胶提取物(Pg - AqEP)和乙醇蜂胶提取物(EEP)可调节星形胶质细胞来源的C6细胞中的线粒体和活性氧生成。本研究的目的是探讨这些提取物对受缺血影响的原代大鼠小脑神经元 - 神经胶质细胞培养物(通过缺氧+/-脱氧葡萄糖模拟)的活力、线粒体效率、超氧化物生成及炎性细胞因子释放的影响。AqEP和Pg - AqEP(酚类化合物或PC浓度为15 - 60μg/mL)显著提高了缺血处理培养物中的神经元活力,同时线粒体超氧化物水平降低。2至4μg/mL的PC EEP对缺血诱导的超氧化物生成和细胞死亡的保护作用较弱。Pg - AqEP和Ag - EP(但不是EEP)均显著保护培养物免受缺氧诱导的TNF-α、IL - 1β和IL - 6升高。只有Pg - AqEP(而不是AqEP或EEP)可防止缺氧诱导的线粒体基础呼吸率和ATP偶联呼吸率丧失,并显著提高线粒体呼吸能力。总之,该研究表明,亲水性蜂胶提取物可能通过降低线粒体超氧化物水平和预防炎性细胞因子来保护脑细胞免受缺血性损伤,对于Pg - AqEP而言,还可通过保护线粒体功能来实现。