中国神经再生研究(英文版) ›› 2015, Vol. 10 ›› Issue (9): 1471-1476.doi: 10.4103/1673-5374.165519

• 观点:神经损伤修复保护与再生 • 上一篇    下一篇

低氧预适应脑脊髓液对氧糖剥夺神经元的保护

  

  • 收稿日期:2015-07-06 出版日期:2015-09-28 发布日期:2015-09-28
  • 基金资助:

    国家科技支撑计划(2013BAI07B01),山东省自然科学基金项目(ZR2012HQ014,ZR2011HM044),低氧预适应转化医学北京市重点实验室开放研究课题(2015DYSY02)

Cerebrospinal fluid from rats given hypoxic preconditioning protects neurons from oxygen-glucose deprivation-induced injury

Yan-bo Zhang1, Zheng-dong Guo2, Mei-yi Li3, Si-jie Li4, Jing-zhong Niu1, Ming-feng Yang1, Xun-ming Ji4, Guo-wei Lv4   

  1. 1 Department of Neurology, Affiliated Hospital of Taishan Medical University, Taian, Shandong Province, China
    2 Department of Endocrinology, Affiliated Hospital of Taishan Medical University, Taian, Shandong Province, China
    3 Department of Neurology, Shandong Taishan Chronic Disease Hospital, Taian, Shandong Province, China
    4 Hypoxia Medical Institute, Xuanwu Hospital, Capital Medical University, Beijing, China
  • Received:2015-07-06 Online:2015-09-28 Published:2015-09-28
  • Contact: Yan-bo Zhang, M.D., bbnnbn@163.com.
  • Supported by:

    This study was supported by a grant from the National Science and Technology Support Program of China, No. 2013BAI07B01; and the Natural Science Foundation of Shandong Province in China, No. ZR2012HQ014, ZR2011HM044; a grant from the Open Research Project of Beijing Key Laboratory for Hypoxic Preconditioning and Translational Medicine, No. 2015DYSY02.

摘要:

低氧预适应是一种机体内源性保护机制,对缺血缺氧脑损伤具有保护作用,为验证这一机制假说,实验将成年大鼠于低氧环境(8% O2和92% N2)饲养3h后,于正常氧浓度环境下饲养12h,取其脑脊液培养新生大鼠大脑皮质神经元1d,再对神经元进行氧糖剥夺1.5h。结果发现低氧预适应脑脊液能明显减少氧糖剥夺诱导的大脑皮质神经元凋亡,显著提高大脑皮质神经元生存率,上调抑凋亡蛋白Bcl-2表达、下调促凋亡蛋白Bax的表达。结果提示低氧预适应大鼠脑脊液以影响凋亡相关蛋白表达的途径,对新生鼠大脑皮质氧糖剥夺损伤神经元产生保护作用。

关键词: 神经再生, 低氧预适应, 脑脊液, 氧糖剥夺, 神经元, 大脑皮质, 细胞凋亡, Bcl-2/Bax

Abstract:

Hypoxic preconditioning activates endogenous mechanisms that protect against cerebral ischemic and hypoxic injury. To better understand these protective mechanisms, adult rats were housed in a hypoxic environment (8% O2/92% N2) for 3 hours, and then in a normal oxygen environment for 12 hours. Their cerebrospinal fluid was obtained to culture cortical neurons from newborn rats for 1 day, and then the neurons were exposed to oxygen-glucose deprivation for 1.5 hours. The cerebrospinal fluid from rats subjected to hypoxic preconditioning reduced oxygen-glucose deprivation-induced injury, increased survival rate, upregulated Bcl-2 expression and downregulated Bax expression in the cultured cortical neurons, compared with control. These results indicate that cerebrospinal fluid from rats given hypoxic preconditioning protects against oxygen-glucose deprivation-induced injury by affecting apoptosis-related protein expression in neurons from newborn rats.

Key words: nerve regeneration, hypoxic preconditioning, cerebrospinal fluid, cerebral cortex, oxygen- glucose deprivation, neurons, apoptosis, Bcl-2/Bax, neural regeneration