The promoting effect of hyperbaric oxygen on the proliferation of endogenous neural stem cells in neonatal rats with hypoxic ischemic brain damage
10.3760/cma.j.issn.0254-1424.2009.05.008
- VernacularTitle:高压氧治疗对缺氧缺血性脑损伤新生大鼠内源性神经干细胞增殖的影响
- Author:
Xiaoli WANG
;
Fansong ZHAO
;
Yujia FANG
;
Min XIE
- Publication Type:Journal Article
- Keywords:
Hypoxie-ischemic brain damage;
Hyperbaric oxygen;
Neural stem cellsDOI:10.3760/cma-j.issn.0254-1424.2009.05.008
- From:
Chinese Journal of Physical Medicine and Rehabilitation
2009;31(5):309-312
- CountryChina
- Language:Chinese
-
Abstract:
Objective To study the effect of hyperbaric oxygen (HBO) therapy on changes in the prolifera-tion of endogenous neural stem ceils (NSCs) in neonatal rats after hypoxie ischemic brain damage (HIBD). Meth-ods A total of 150 Sprague-Dawley rats aged 7 d were randomly divided into a normal eontrol group ( CON ), a HIBD group and a HBO treatment group. HBO was administered to the HBO treatment group within 3 h after HIBD at 2 atmospheres, once daily for 7 d. The HIBD model rats were subjected to unilateral carotid artery ligation followed by 2 h of hypoxia (8% O2> ). BrdU/nestin immunofluorescence was used to examine the proliferation of NSCs dynami-cally in the subventricular zone (SVZ) and the dentate gyms (DG) at the 3rd h, 21st h, 3rd d, 7th d and 14th d af-ter HBO therapy. Nestin protein was detected by Western blot analysis at various time points after HIBD. Results In the HIBD rats treated with HBO, proliferation of endogenous NSCs was observed in the SVZ and DG. The prolifer-ating NSCs increased at the 3rd h and 21st h after HBO therapy in the SVZ and DG respectively, peaked at the 7th d after HBO therapy, and decreased by the 14th d after HBO therapy, though their level was still higher than that in the controls. The Western blot analysis showed that nestin protein began to increase at the 21st h after HBO therapy, peaked at the 7th d after HBO therapy, then decreased. Conclusion HBO administered within 3 h after HIBD can promote proliferation of endogenous NSCs in neonatal rats after HIBD.