School of Life Science, Sichuan University, Chengdu, Sichuan 610065, China.
Biotechnology and Nuclear Technology Research Institute, Sichuan Academy of Agricultural Sciences, Chengdu 610061, China.
Biomed Pharmacother. 2016 Oct;83:569-576. doi: 10.1016/j.biopha.2016.07.016. Epub 2016 Jul 25.
Oxidative stress played an essential role in neuronal cell injury through several apoptotic mechanisms associated with many neurodegenerative diseases. Reducing oxidative stress through antioxidants might be a possible strategy that could retard the disease's progression. In order to investigate the neuroprotective role of MIP (the crude polysaccharide extracted from the fruiting bodies of Morchella importuna), the antioxidative activity of MIP against the HO-induced cytotoxicity and the underlying preventative mechanisms in rat pheochromocytoma (PC12) cells were illustrated. It was shown that MIP could considerably enhance the viability of PC12 cells exposure to HO and increased the activities of antioxidant enzyme like CAT, GSH-Px and SOD. It also reduced the content of malondialdehyde MDA and caspase-3 activation. In addition, MIP inhibited cell apoptosis via down-regulation of the NF-κB pathway and the p38-JNK pathway as well as activating of the extracellular signal-regulated kinase (ERK). Accordingly, MIP can be used as a promising neuroprotective compound for nervous diseases treatment.
氧化应激通过与许多神经退行性疾病相关的几种凋亡机制在神经元细胞损伤中发挥重要作用。通过抗氧化剂减少氧化应激可能是一种可以延缓疾病进展的可行策略。为了研究 MIP(从进口羊肚菌子实体中提取的粗多糖)的神经保护作用,本文阐述了 MIP 对 HO 诱导的细胞毒性的抗氧化活性及其在大鼠嗜铬细胞瘤(PC12)细胞中的潜在预防机制。结果表明,MIP 可显著提高暴露于 HO 的 PC12 细胞的活力,并提高 CAT、GSH-Px 和 SOD 等抗氧化酶的活性。它还降低了丙二醛 MDA 和 caspase-3 激活的含量。此外,MIP 通过下调 NF-κB 途径和 p38-JNK 途径以及激活细胞外信号调节激酶(ERK)来抑制细胞凋亡。因此,MIP 可用作治疗神经疾病的有前途的神经保护化合物。