中国神经再生研究(英文版) ›› 2015, Vol. 10 ›› Issue (10): 1617-1621.doi: 10.4103/1673-5374.167760

• 原著:脑损伤修复保护与再生 • 上一篇    下一篇

可抑制鱼藤酮致原代神经元凋亡的京尼平苷作用途径

  

  • 收稿日期:2015-06-28 出版日期:2015-10-28 发布日期:2015-10-28
  • 基金资助:

    山西省科技厅项目(201108106),山西省奖学金(2011-44)

Geniposide prevents rotenone-induced apoptosis in primary cultured neurons

Lin Li1, Juan Zhao1, Ke Liu1, Guang-lai Li2, Yan-qing Han2, Yue-ze Liu2, *   

  1. 1 Key Laboratory of Cellular Physiology, Shanxi Medical University, Taiyuan, Shanxi Province, China
    2 Second Hospital, Shanxi Medical University, Taiyuan, Shanxi Province, China
  • Received:2015-06-28 Online:2015-10-28 Published:2015-10-28
  • Contact: Yue-ze Liu, Ph.D., yuezeliu@163.com.
  • Supported by:

    This research was supported by grants from the Shanxi Science and Technology Department in China, No. 2011081060 and Shanxi Scholarship Council of China, No. 2011-44.

摘要:

从栀子中提取的中药单体京尼平苷是一种新型的胰高血糖素样肽1受体激动剂,研究显示胰高血糖素样肽1具有脑保护作用,但抗神经元凋亡用于治疗神经退行性疾病的机制目前还不清楚,实验拟揭示此问题。首先使用不同浓度的鱼藤酮诱导原代神经元48h,通过细胞形态观察、CCK-8证实及乳酸脱氢酶检测和Western blot分析表明,0.5 nmol/L鱼藤酮诱导可导致正常神经元乳酸脱氢酶释放增加,procaspase-3和Bcl-2表达降低,而cleaved caspase-3表达增加。经京尼平苷预处理减少了乳酸脱氢酶的释放,促进procaspase-3和Bcl-2表达,并抑制cleaved caspase-3表达。证实中药单体京尼平苷能通过抑制培养的原代神经元凋亡蛋白的表达,减轻鱼藤酮导致的原代神经元损伤,作者认为,实验结果说明了京尼平苷能给治疗神经退行性疾病的部分作用途径。

关键词: 神经再生, 京尼平苷, 鱼藤酮, 细胞凋亡, 阿尔茨海默病, caspase-3, Bcl-2

Abstract:

Geniposide, a monomer extracted from gardenia and widely used in Chinese medicine, is a novel agonist at the glucagon-like peptide-1 receptor. This receptor is involved in neuroprotection. In the present study, we sought to identify an anti-apoptotic mechanism for the treatment of neurodegenerative diseases. Primary cultured neurons were treated with different concentrations of rotenone for 48 hours. Morphological observation, cell counting kit-8 assay, lactate dehydrogenase detection and western blot assay demonstrated that 0.5 nM rotenone increased lactate dehydrogenase release, decreased the expression of procaspase-3 and Bcl-2, and increased cleaved caspase-3 expression in normal neurons. All these effects were prevented by geniposide. Our results indicate that geniposide diminished rotenone-induced injury in primary neurons by suppressing apoptosis. This may be one of the molecular mechanisms underlying the efficacy of geniposide in the treatment of neurodegenerative diseases.

Key words: nerve regeneration, geniposide, rotenone, cell apoptosis, Alzheimer’s disease, caspase-3, Bcl-2, neural regeneration