Deng Kewei, Li Yanling, Xiao Mi, Wang Fanghui, Zhou Ping, Zhang Wei, Heep Axel, Li Xiaoquan
Department of Neonatology, Northwest Women's and Children's Hospital, Xi'an 710061, PR China.
Department of Neonatology, Qujiang Maternity Hospital, Xi'an 710060, PR China.
Int J Biol Macromol. 2020 May 4;158:562-568. doi: 10.1016/j.ijbiomac.2020.04.122.
Neonatal hypoxic-ischemic encephalopathy (HIE) is a complex condition that remains the leading cause of mortality and morbidity among infants. Polysaccharide has been reported to possess diverse biological activities, however, the neuro-protective activity of polysaccharide isolated from Lycium ruthenicum remains unknown so far. However, the role of Lycium ruthenicum polysaccharide 3 (LRP3) in HIE has not been evaluated. Herein, we investigated the effect of LRP3 on oxygen-glucose deprivation/reoxygenation (OGD/R)-induced primary cortical neurons. Our results demonstrated that LRP3 significantly improved the cell viability of OGD/R-induced cortical neurons. The OGD/R-caused increase in ROS production and decrease in the activities of anti-oxidative enzymes including catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GPx) were mitigated by LRP3. Besides, the caspase-3 activity in OGD/R-induced cortical neurons was markedly decreased after LRP3 treatment. The increased bax expression and decreased bcl-2 expression caused by OGD/R stimulation were alleviated by pretreatment with LRP3. In addition, LRP3 significantly induced the expressions of nuclear factor erythroid 2-related factor (Nrf2) and heme oxygenase-1 (HO-1) in OGD/R-induced cortical neurons. However, inhibition of Nrf2/HO-1 signaling pathway through transfection with siRNA targeting Nrf2 reversed the protective effects of LRP3. In conclusion, LRP3 exerts a neuroprotective effect against OGD/R-induced neuronal injury in rat primary cortical neurons.
新生儿缺氧缺血性脑病(HIE)是一种复杂的病症,仍然是婴儿死亡和发病的主要原因。据报道,多糖具有多种生物活性,然而,迄今为止,从黑果枸杞中分离出的多糖的神经保护活性尚不清楚。然而,黑果枸杞多糖3(LRP3)在HIE中的作用尚未得到评估。在此,我们研究了LRP3对氧糖剥夺/复氧(OGD/R)诱导的原代皮层神经元的影响。我们的结果表明,LRP3显著提高了OGD/R诱导的皮层神经元的细胞活力。LRP3减轻了OGD/R导致的活性氧生成增加以及包括过氧化氢酶(CAT)、超氧化物歧化酶(SOD)和谷胱甘肽过氧化物酶(GPx)在内的抗氧化酶活性降低。此外,LRP3处理后,OGD/R诱导的皮层神经元中的半胱天冬酶-3活性显著降低。LRP3预处理减轻了OGD/R刺激引起的bax表达增加和bcl-2表达降低。此外,LRP3显著诱导了OGD/R诱导的皮层神经元中核因子红细胞2相关因子(Nrf2)和血红素加氧酶-1(HO-1)的表达。然而,通过转染靶向Nrf2的小干扰RNA抑制Nrf2/HO-1信号通路可逆转LRP3的保护作用。总之,LRP3对OGD/R诱导的大鼠原代皮层神经元损伤具有神经保护作用。