Wu Feng-Juan, Xue Yong, Tang Qing-Juan, Xu Jie, Du Lei, Xue Chang-Hu, Takahashi Koretaro, Wang Yu-Ming
College of Food Science and Engineering, Ocean University of China, Qingdao, Shandong Province, P.R. China.
J Oleo Sci. 2013;62(9):717-27. doi: 10.5650/jos.62.717.
Neurodegenerative disorders are a class of diseases that have been linked to apoptosis induced by elevated levels of reactive oxygen species (ROS). The present study was undertaken to explore the effect of sea cucumber cerebrosides (SCC) and starfish cerebrosides (SFC) on the hydrogen peroxide (H₂O₂) and tert-butyl hydroperoxide (t-BHP)-induced oxidative damage in PC12 cells. Cell viability, the leakage of lactate dehydrogenase (LDH), reactive oxygen species (ROS) level and superoxide dismutase (SOD) activity were determined for their effect on oxidative damage. Quantitative real-time PCR was investigated to analyze the mitochondrial genes expression. These results showed that both SCC and SFC decreased the leakage of LDH and intracellular ROS in a dose-dependent manner. SCC and SFC could also increase the SOD activity compared with the model groups. In H₂O₂ damage model, 400 μg/mL SCC increased the SOD activity by 79%, which was stronger than SFC. The results demonstrated that SCC and SFC exhibited the protective effects, which may be related to their antioxidant action. In addition, SCC and SFC dramatically increased the gene expression of B-cell lymphoma 2 (Bcl-2) but significantly decreased the gene expression of Cytochrome c, caspase9 and caspase3 compared with H₂O₂ or t-BHP treatment. These results suggested that SCC and SFC might exert a protective function against oxidative damage by inhibiting mitochondria-mediated apoptosis pathway. In conclusion, SCC and SFC played an important protective role in H₂O₂ and t-BHP-induced damage of PC12 cells, suggesting that the SCC and SFC may be a potential therapeutic agent against nervous system oxidative damage.
神经退行性疾病是一类与活性氧（ROS）水平升高诱导的细胞凋亡相关的疾病。本研究旨在探讨海参脑苷脂（SCC）和海星脑苷脂（SFC）对过氧化氢（H₂O₂）和叔丁基过氧化氢（t-BHP）诱导的PC12细胞氧化损伤的影响。测定细胞活力、乳酸脱氢酶（LDH）泄漏、活性氧（ROS）水平和超氧化物歧化酶（SOD）活性，以评估它们对氧化损伤的影响。采用定量实时PCR分析线粒体基因表达。结果表明，SCC和SFC均以剂量依赖方式降低LDH泄漏和细胞内ROS水平。与模型组相比，SCC和SFC还可提高SOD活性。在H₂O₂损伤模型中，400μg/mL SCC使SOD活性提高了79%，效果强于SFC。结果表明，SCC和SFC具有保护作用，这可能与其抗氧化作用有关。此外，与H₂O₂或t-BHP处理相比，SCC和SFC显著增加了B细胞淋巴瘤2（Bcl-2）的基因表达，但显著降低了细胞色素c、半胱天冬酶9和半胱天冬酶3的基因表达。这些结果表明，SCC和SFC可能通过抑制线粒体介导的凋亡途径发挥对氧化损伤的保护作用。总之，SCC和SFC在H₂O₂和t-BHP诱导的PC12细胞损伤中发挥了重要的保护作用，提示SCC和SFC可能是对抗神经系统氧化损伤的潜在治疗剂。
