《中国康复理论与实践》

《中国康复理论与实践》 ›› 2019, Vol. 25 ›› Issue (12): 1418-1424.doi: 10.3969/j.issn.1006-9771.2019.12.010

• 基础研究 • 上一篇    下一篇

丰富环境对缺氧缺血性脑损伤新生大鼠海马神经元凋亡及脑源性神经营养因子/酪氨酸蛋白激酶受体信号通路的影响

赵彬1, 唐强1, 朱路文1, 王艳1, 梁碧莹2   

  1. 1.黑龙江中医药大学附属第二医院，黑龙江哈尔滨市 150001
    2.黑龙江中医药大学，黑龙江哈尔滨市 150040
  • 收稿日期:2019-07-24 修回日期:2019-09-21 出版日期:2019-12-25 发布日期:2019-12-26
  • 通讯作者: 唐强，E-mail: tangqiang1963@163.com E-mail:tangqiang1963@163.com
  • 作者简介:赵彬(1982-)，男，汉族，黑龙江大庆市人，博士研究生，副主任医师，主要研究方向：神经系统疾病的中医康复基础与临床研究。
  • 基金资助:
    1.国家自然科学基金项目(No. 81674077)；2.黑龙江中医药大学校基金项目(No. 201506)

Effects of Enriched Environment on Apoptosis and Brain-derived Neurotrophic Factor /Tyrosine Kinase Receptor B Signaling Pathway in Hippocampal Neurons of Neonatal Rats with Hypoxic-ischemic Brain Damage

ZHAO Bin1, TANG Qiang1, ZHU Lu-wen1, WANG Yan1, LIANG Bi-ying2   

  1. 1.The Second Hospital, Heilongjiang University of Chinese Medicine, Harbin, Heilongjiang 150001, China
    2.Heilongjiang University of Chinese Medicine, Harbin, Heilongjiang 150040, China
  • Received:2019-07-24 Revised:2019-09-21 Published:2019-12-25 Online:2019-12-26
  • Contact: TANG Qiang, E-mail: tangqiang1963@163.com E-mail:tangqiang1963@163.com
  • Supported by:
    Supported by National Natural Science Foundation of China (No. 81674077) and Heilongjiang University of Traditional Chinese Medicine Fund (No. 201506)

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摘要： 目的 探讨丰富环境对缺血缺氧性脑损伤新生大鼠海马神经元凋亡及脑源性神经营养因子(BDNF)/酪氨酸蛋白激酶受体(TrkB)信号通路的影响。 方法 将48只7日龄Wistar大鼠幼仔，随机分成假手术组、模型组和丰富环境组，每组再分为14 d和28 d两个亚组，每个亚组8只。采用Rice方法制作缺氧缺血性脑损伤模型。模型组和假手术组不进行处理，丰富环境组在造模24 h后应用丰富环境进行刺激。造模后14 d和28 d，采用TUNEL法和双重免疫荧光染色法检测海马区神经元凋亡水平；采用免疫组化染色法检测海马区BDNF、TrkB蛋白表达情况。 结果 造模后14 d、28 d，与假手术组比较，模型组海马区TUNEL阳性细胞数、双标记阳性细胞数以及海马BDNF和TrkB阳性细胞数显著增加(t > 27.214, P < 0.001)，丰富环境组TUNEL阳性细胞数、双标记阳性细胞数显著少于模型组(t > 12.687, P < 0.001)，丰富环境组造模后28 d海马BDNF和TrkB阳性细胞数显著高于模型组(t > 137.998, P < 0.001)。 结论 丰富环境刺激可以降低缺血缺氧性脑损伤新生大鼠海马神经元凋亡，上调BDNF、TrkB蛋白表达。

关键词: 缺血缺氧性脑损伤, 丰富环境, 脑源性神经营养因子, 酪氨酸蛋白激酶受体, 细胞凋亡, 大鼠

Abstract: Objective To investigate the effects of enriched environment on hippocampal neuronal apoptosis and brain-derived neurotrophic factor (BDNF)/tyrosine kinase receptor B (TrkB) signaling pathway in neonatal rats with hypoxic-ischemic brain damage. Methods Forty-eight newborn Wistar rats aged seven days were randomly divided into sham operation group, model group and enriched environment group, each group was divided in to 14 days group and 28 days group, with eight in each subgroup. The model was established with the Rice method. The sham operation group and the model group did not receive any intervention, and the enriched environment group received enriched environment stimulation 24 hours after modeling. Fourteen days and 28 days after modeling, the levels of neuronal apoptosis in hippocampus were detected by TUNEL and double immunofluorescence staining; BDNF and TrkB proteins in hippocampus were detected by immunohistochemical staining. Results Fourteen days and 28 days after modeling, the numbers of TUNEL positive cells, double immunofluorescence positive cells, BDNF and TrkB positive cells were significantly more in the model group than in the sham operation group (t > 27.214, P < 0.001), while the numbers of TUNEL positive cells, double immunofluorescence positive cells were significantly less in the enriched environment group than in the model group (t > 12.687, P < 0.001); and the number of BDNF and TrkB positive cells were significantly more in the enriched environment group than in the model group 28 days after modeling (t > 137.998, P < 0.001). Conclusion Enriched environmental stimulation could reduce the apoptosis of hippocampal neurons, and up-regulate the expression of BDNF and TrkB proteins in the neonatal rats with hypoxic-ischemic brain damage.

Key words: hypoxic-ischemic brain damage, enriched environment, brain-derived neurotrophic factor, tyrosine kinase receptor B, apoptosis, rats

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