Cai Jianmei, Kang Zhimin, Liu Wen Wu, Luo Xu, Qiang Sun, Zhang John H, Ohta Shigeo, Sun Xuejun, Xu Weigang, Tao Hengyi, Li Runping
Department of Diving Medicine, Faculty of Naval Medicine, Second Military Medical University, Shanghai 200433, PR China.
Neurosci Lett. 2008 Aug 22;441(2):167-72. doi: 10.1016/j.neulet.2008.05.077. Epub 2008 May 24.
Hypoxia-ischemia (HI) brain injury is a major cause of neuronal cell death especially apoptosis in the perinatal period. This study was designated to examine the effect of hydrogen therapy on apoptosis in an established neonatal HI rat pup model. Seven-day-old rat pups were subjected to left common carotid artery ligation and then 90 min hypoxia (8% oxygen at 37 degrees C). Immediately after HI insult, pups were placed into a chamber filled with 2% H2 for 30 min, 60 min, or 120 min, respectively. 24 h after 2% H2 therapy, the pups were decapitated and brain injury was assessed by 2,3,5-triphenyltetrazoliumchloride (TTC), Nissl, and TUNEL staining, as well as caspase-3, caspase-12 activities in the cortex and hippocampus. H2 treatment in a duration-dependent manner significantly reduced the number of positive TUNEL cells and suppressed caspase-3 and -12 activities. These results indicated H2 administration after HI appeared to provide brain protection via inhibition of neuronal apoptosis.
缺氧缺血性(HI)脑损伤是围生期神经元细胞死亡尤其是凋亡的主要原因。本研究旨在探讨氢疗法对已建立的新生HI大鼠幼崽模型中细胞凋亡的影响。7日龄大鼠幼崽接受左颈总动脉结扎,然后进行90分钟的缺氧(37℃下8%氧气)。HI损伤后,幼崽立即分别置于充满2%氢气的舱内30分钟、60分钟或120分钟。2%氢气治疗24小时后,将幼崽断头,通过2,3,5-氯化三苯基四氮唑(TTC)、尼氏染色和TUNEL染色以及皮质和海马体中半胱天冬酶-3、半胱天冬酶-12的活性评估脑损伤。氢气治疗以时间依赖性方式显著减少TUNEL阳性细胞数量,并抑制半胱天冬酶-3和-12的活性。这些结果表明,HI后给予氢气似乎通过抑制神经元凋亡提供脑保护。