Park Hee Ra, Lee Heeeun, Park Hwayong, Jeon Jong Wook, Cho Won-Kyung, Ma Jin Yeul
Korean Medicine (KM)-Application Center, Korea Institute of Oriental Medicine (KIOM), 70, Cheomdan-ro, Dong-gu, Daegu, 701-300, South Korea.
BMC Complement Altern Med. 2015 Jun 9;15:171. doi: 10.1186/s12906-015-0679-3.
Oxidative stress is involved in neuronal cell death and mitochondrial dysfunction in neurodegenerative diseases. Liriope platyphylla (LP) has been suggested to have anti-inflammation, anti-bacterial, and anti-cancer effects. However, whether LP exerts neuroprotective effects on neuronal cells is unknown.
The present study was performed to investigate the neuroprotective effects of LP extract (LPE) against hydrogen peroxide (H2O2)-induced injury in human neuroblastoma cells SH-SY5Y. To test neuroprotective effects of LPE, we performed cell viability assay, flow cytometry analysis and western blot analysis. In addition, mitochondrial membrane potential (MMP) and oxidative stress were performed to evaluate the anti-apoptotic and anti-oxidant effects.
LPE pretreatment conferred significant protection against the H2O2-induced decrease of SH-SY5Y cell viability. H2O2-induced increases of intracellular oxidative stress and mitochondrial dysfunction were attenuated by LPE pretreatment. Therefore, LPE pretreatment prevented SH-SY5Y cell injury. Treatment with H2O2 significantly induced poly(ADP ribose) polymerase (PARP) and caspase-3 cleavage, which was blocked by LPE. We found that p38 activation was involved in the neuroprotective effects of LPE.
Current findings suggest that LPE exerts neuroprotective effects against H2O2-induced apoptotic cell death by modulating p38 activation in SH-SY5Y cells. Therefore, LPE has potential anti-apoptotic effects that may be neuroprotective in neurodegenerative diseases and aging-related dementia.
氧化应激参与神经退行性疾病中的神经元细胞死亡和线粒体功能障碍。阔叶山麦冬(LP)已被证明具有抗炎、抗菌和抗癌作用。然而,LP是否对神经元细胞具有神经保护作用尚不清楚。
本研究旨在探讨LP提取物(LPE)对过氧化氢(H2O2)诱导的人神经母细胞瘤细胞SH-SY5Y损伤的神经保护作用。为了测试LPE的神经保护作用,我们进行了细胞活力测定、流式细胞术分析和蛋白质印迹分析。此外,还检测了线粒体膜电位(MMP)和氧化应激,以评估其抗凋亡和抗氧化作用。
LPE预处理可显著保护SH-SY5Y细胞活力免受H2O2诱导的降低。LPE预处理可减轻H2O2诱导的细胞内氧化应激增加和线粒体功能障碍。因此,LPE预处理可预防SH-SY5Y细胞损伤。H2O2处理可显著诱导聚(ADP核糖)聚合酶(PARP)和半胱天冬酶-3的裂解,而LPE可阻断这种裂解。我们发现p38激活参与了LPE的神经保护作用。
目前的研究结果表明,LPE通过调节SH-SY5Y细胞中的p38激活,对H2O2诱导的凋亡细胞死亡发挥神经保护作用。因此,LPE具有潜在的抗凋亡作用,可能对神经退行性疾病和衰老相关痴呆具有神经保护作用。