中国神经再生研究(英文版)

中国神经再生研究(英文版) ›› 2017, Vol. 12 ›› Issue (1): 96-102.doi: 10.4103/1673-5374.198992

• 原著:脑损伤修复保护与再生 • 上一篇    下一篇

抑制脑缺血再灌注损伤诱导的细胞凋亡：山奈酚3-0-芸香糖苷与JAK2/STAT3通路

  

  • 收稿日期:2016-10-22 出版日期:2017-01-15 发布日期:2017-01-15
  • 基金资助:

    中国教育部自然科学基金项目（14zb0152）；西南医科大学的联合研究计划（14jc0120）。

Inhibition of cerebral ischemia/reperfusion injuryinduced apoptosis: nicotiflorin and JAK2/STAT3 pathway

Guang-qiang Hu1, Xi Du2, Yong-jie Li3, Xiao-qing Gao4, Bi-qiong Chen2, Lu Yu2   

  1. 1 Department of Anatomy, Southwest Medical University, Luzhou, Sichuan Province, China; 
    2 Department of Chemistry, Southwest Medical University, Luzhou, Sichuan Province, China; 
    3 Drug Discovery Research Center, Southwest Medical University, Luzhou, Sichuan Province, China; 
    4 Department of Anatomy and Neurobiology, Southwest Medical University, Luzhou, Sichuan Province, China
  • Received:2016-10-22 Online:2017-01-15 Published:2017-01-15
  • Contact: Guang-qiang Hu or Lu Yu, hgq863@sina.com or yulu863@sina.com.
  • Supported by:

    This study was mainly supported by the National Science Foundation of Education Department of Sichuan Province of China, No. 14ZB0152; the Joint Research Program of Luzhou and Luzhou Medical College, No. 14JC0120.

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摘要：

山奈酚3-0-芸香糖苷是从红花中提取的一种黄酮类化合物，以往研究显示其具有脑保护作用，但机制不明确。实验拟揭示山奈酚3-0-芸香糖苷调节JAK2/STAT3通路保护脑缺血再灌注诱导的凋亡的作用途径。通过建立大脑中动脉闭塞脑缺血/再灌注损伤大鼠模型，尾静脉注射山奈酚3-0-芸香糖苷10 mg/kg，以TUNEL法与苏木精-伊红染色法评估脑组织神经元凋亡，用免疫组织化学染色检测缺血侧脑皮质组织Bcl-2、Bax的免疫反应，Western blot检测缺血侧脑皮质组织p-JAK2、p-STAT3、Bcl-2、Bax和Caspase-3蛋白的表达。结果显示山奈酚3-0-芸香糖苷可减轻缺血再灌注损伤大鼠大脑皮质神经元损伤并抑制细胞凋亡，明显下调缺血侧脑皮质脑组织p-JAK2和p-STAT3、Caspase-3及Bax蛋白表达，使Bax免疫反应下降，并上调Bcl-2蛋白表达及免疫反应。说明山奈酚3-0-芸香糖苷抑制JAK2/STAT3通路，发挥了减少脑缺血再灌注损伤诱导的神经元凋亡的作用。

ORCID:0000-0002-8873-9138 (Lu Yu)

Abstract:

Nicotiflorin is a flavonoid extracted from Carthamus tinctorius. Previous studies have shown its cerebral protective effect, but the mechanism is undefined. In this study, we aimed to determine whether nicotiflorin protects against cerebral ischemia/reperfusion injury-induced apoptosis through the JAK2/STAT3 pathway. The cerebral ischemia/reperfusion injury model was established by middle cerebral artery occlusion/reperfusion. Nicotiflorin (10 mg/kg) was administered by tail vein injection. Neuronal apoptosis was examined by hematoxylin-eosin staining andterminal deoxynucleotidyl transferase dUTP nick end labeling assay. Bcl-2 and Bax expression levels in ischemic cerebral cortex were examined by immunohistochemial staining. Additionally, p-JAK2, p-STAT3, Bcl-2, Bax, and caspase-3 levels in ischemic cerebral cortex were examined by western blot assay. Our results show that nicotiflorin alters the shape and structure of injured neurons, decreases the number of apoptotic neurons, down-regulates expression of p-JAK2, p-STAT3, caspase-3, and Bax, decreases the immune response of Bax, and up-regulates expression of Bcl-2 protein and the immune response. These results suggest that nicotiflorin protects against cerebral ischemia/reperfusion injury-induced apoptosis via the JAK2/STAT3 pathway.

Key words: nerve regeneration, brain injury, nicotiflorin, ischemic stroke, cerebral ischemia/reperfusion injury, treatment, cell apoptosis, terminal deoxynucleotidyl transferase dUTP nick end labeling, JAK2/STAT3 pathway, Bcl-2, Bax, caspase-3, neural regeneration