摘要
目的探讨新生大鼠脑白质损害时神经胶质细胞凋亡与内源性胶质细胞源性神经营养因子(GDNF)表达的变化。方法实验组和对照组各45只大鼠分别于缺氧缺血后30 min、1 h、4 h、12 h、1 d、3 d、7 d、14 d及21 d处死,免疫组化(SP)法检测GDNF,TUNEL法测定细胞凋亡。结果新生大鼠脑白质损害时,细胞凋亡在缺氧缺血后3 d达到高峰,与对照组比较,在4 h、12 h、1 d、3 d、7 d均有统计学意义(均P<0.05)。实验组GDNF表达在缺氧缺血后7 d达到高峰,与对照组相比,在3、7、14 d有统计学意义(P<0.05)。结论新生大鼠脑白质损害时,GDNF于细胞凋亡的高峰时间开始表达,与此同时,细胞凋亡逐渐减少。表明在缺氧缺血所致的新生大鼠脑白质损害时,内源性GDNF的表达升高可能通过抑制细胞凋亡来发挥保护作用,并对后期的神经修复起一定作用。
Objective To observe the expression of GDNF protein and apoptosis of neuroglial cells in the neonatal rats with white matter damage (WMD). Methods The neonatal rats (45 in each group) were perfused at 30th min, 1st h, 4th h, 12th h, 1st day, 3rd day, 7th day, 14th day, 21st day of recovery from hypoxia-ischemia (HI). Immunohistochemistry was applied to investigate the changes in the expression of GDNF in periventricular white matter tissues. Apoptotic cells were detected in these tissues by TUNEL. Results In the neonatal rats with WMD, the apoptosis of neuroglial cells reached the peak at 3rd day after HI, demonstrating significant differences at 4th h, 12th h, 1st day, 3rd day and 7th day between experimental group and control group (P〈0.05). There was significant difference in level of GDNF at 3rd, 7th and 14th day between experimental group and control group (P〈0.05). Conclusion In the WMD neonatal rats, GDNF is expressed at the peak of apoptosis while apoptosis decreased, which suggests that in the HI-induced WMD the increasedexpression of endogenous GDNF maybe protect the brain by inhibiting apoptosis and exert some effects on the repair of nerves.
出处
《华中科技大学学报(医学版)》
CAS
CSCD
北大核心
2008年第2期225-228,F0004,共5页
Acta Medicinae Universitatis Scientiae et Technologiae Huazhong
关键词
脑白质损害
脑室周围白质软化
神经营养因子
细胞凋亡
white matter damage
periventricular leukomalacia
glial cell line-derived neurotrophic factor
apoptosis