Effects of oxidative stress on white matter damage in rats model of chronic cerebral hypoperfusion
10.3760/cma.j.issn.1671-8925.2010.03.007
- VernacularTitle:氧化应激在慢性缺血性脑白质损伤中的作用
- Author:
Han-Xing LIU
1
;
Jun-Jian ZHANG
;
Li XIONG
;
Hui LIU
;
Lei ZHANG
Author Information
1. 武汉大学中南医院
- Keywords:
Chronic cerebral ischemia;
White matter lesions;
Oxidative stress
- From:
Chinese Journal of Neuromedicine
2010;9(3):245-249
- CountryChina
- Language:Chinese
-
Abstract:
Objective To clarify the participation of oxidative stress in the white matter lesions induced by chronic cerebral hypoperfusion in the rats.Methods Chronic cerebral ischemia models were established by permanent occlusion of bilateral common carotid arteries(2-VO)in male Wistar rats.The rats were assigned to 5 groups(n=6):those with chronic cerebral ischemia for 3 and 7 d,3 and 6 weeks,and those given sham operation.We examined the activities of superoxide dismutase(SOD)and catalase(CAT),the giutathione(GSH)content and the changes of malondialdehyde(MDA)level and HNE modified protein in the white matter of rats.Results The MDA level of the hypoperfused rats was significantly increased 3 weeks after the operation as compared with that of the sham-operated rats with a further increase at 6 weeks(P<0.05).The HNE modified protein level in the hypoperfused rats was gradually and significantly increased from 3 d to 6 weeks after the operation as compared with that of the sham-operated rats(P<0.05).SOD activity of the hypoperfused rats was significantly decreased 3 and 6 weeks after the operation compared with that of the sham-operated rats(P<0.05),while CAT activeity was not altered.Moreover,the GSH content in the hypoperfused rats was gradually and significantly decreased 7 d and 6 weeks after the operation in comparison with that in the sham-operated rats(P<0.05).Conclusion Chronic cerebral ischemia results in increased oxidative damage in the white matter and decreased antioxidant defense capability,which is closely correlative to white matter lesions induced by chronic cerebral ischemia.
