Protective effect of DL-3-n-Butylphthalide on radiation injury of rat brain tissue
10.3760/cma.j.issn.0254-5098.2012.03.008
- VernacularTitle:丁苯酞对大鼠脑组织放射性损伤的保护作用
- Author:
Yingzhu CHEN
;
Xianxian ZHANG
;
Lu XIAO
;
Yanhong QI
;
Pu YANG
;
Jinzhong HUANG
;
Shiyao BAO
- Publication Type:Journal Article
- Keywords:
DL-3-n-Butylphthalide;
Ionizing radiation;
Brain injury;
Apoptosis-associated gene;
Malondialdehyde;
Super oxide dismutase
- From:
Chinese Journal of Radiological Medicine and Protection
2012;32(3):255-258
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the protective effect and its mechanism of DL-3-n-Butylphthalide on the brain damage in rats following whole brain irradiation.Methods A total of 120 male Sprague Dawley rats were randomly divided into sham-irradiation group,irradiatien group and DL-3-n-Butylphthalide group.The model of whole-brain irradiatien was established by exposuring rat brain to 4 MeV X-rays with a single-dose of 10 Gy.The rats were intraperitoneally injected with DL-3-n-Butylphthalide at the dosages of 0.3,1.0,and 3.0 mg/kg once a day.The contents of malondialdchyde and super oxide dismutase activity were measured,while the expressions of apoptosis-associated genes and the ultrastructural changes in hippocampus were examined by immunohistnchemisty staining and electron microscope,respectively.Results After irradiation,the content of malondialdehyde and the expression of apoptosis gene bax in rat brain tissue increased while the activity of super oxide dismutase(SOD) and the expression of anti-apoptosis gene bcl-2 decreased.Apoptosis was also observed in the neurons of hippocampus CA1.Compared with irradiation group,the content of malondialdehyde and the expression of bax gene in the DL-3-n-Butylphthalide group wen significantly reduced ( t =-3.89--1.96,2.72-3.48,P ＜ 0.05 ),while the activity of SOD and bcl-2 gene were significantly elevated ( t =2.94-3.76,-3.18--2.08,P ＜ 0.05),and the injury degree of neuron structure in the DL-3-n-Butylphthalide group was slighter than that in the irradiation group.Conclusions DL-3-n-Butylphthalide executes protective effects in a dose-dependent manner againest the radiation injury in rats brain by reducing the induction of malondialdehyde,raising the activity of SOD and inhibiting the generation of apoptosis.
