Effect of aminoguanidine on mitochondria injury in focal cerebral ischemia rats
- VernacularTitle:氨基胍对局灶性脑缺血大鼠线粒体损伤的影响
- Author:
Yonghui LI
;
Jianxin ZHANG
;
Huixin ZHANG
;
Lanfang LI
- Publication Type:Journal Article
- Keywords:
cerebral ischemia;
mitochondria;
aminoguanidine;
ultrastructure
- From:
Chinese Pharmacological Bulletin
2003;0(12):-
- CountryChina
- Language:Chinese
-
Abstract:
Aim To examine the effect of selective inducile nitro oxide synthase inhibitor, aminoguanidine(AG), on mitochondria injury in focal cerebral ischemia rats. Methods Rats were randomly devided into sham, ischemia and AG treatment groups. The model of focal cerebral ischemia in rats was prepared with thread embolism. AG was administered respectively at 2,6,12 h after MCAO. Rats were killed and mitochondria of cerebral tissue were isolated with differential centrifugation 3 d after AG treatment. Activities of ATPase, SOD and GSH-Px and contents of NO and MDA in mitochondria were measured. Ultrastructure changes of neuronal mitochondria were examined with electronic microscope after the ischemia and AG treatment. Results The contents of mitochondria NO and MDA markedly increased. The activities of mitochondria ATPase,SOD and GSH-Px markedly decreased in MCAO rats. Compared with ischemia group, the activities of ATPase, SOD and GSH-Px in mitochondria enhanced and the contents of NO and MDA in mitochondria decreased in ischemia 2,6,12 h group administered with AG. The study showed that the neuronal cytoplasm and the mitochondria swelled, the cristae were disrupted, dissolved or disappeared in MCAO rats. AG ameliorated these injuries induced by cerebral ischemia in rats. Conclusion AG can inhibit the production of NO, beneficially improve mitochondria energy pump and ameliorate oxidative injury after cerebra ischemia, and thus effectively protect brain damage induced by focal cerebral ischemia.
