Effect of nitric oxide synthase inhibitor aminoguanidine on amino acid contents of ischemic brain in rat
- VernacularTitle:一氧化氮合酶抑制剂氨基胍对脑缺血大鼠脑组织氨基酸含量的影响
- Author:
Huixin ZHANG
;
Jianxin ZHANG
;
Lanfang LI
;
Yonghui LI
;
Chao WANG
- Publication Type:Journal Article
- Keywords:
ischemia;
nitric oxide;
nitric oxide synthase;
aminoguanidine;
amino acid
- From:
Chinese Journal of Pharmacology and Toxicology
2005;19(2):87-92
- CountryChina
- Language:Chinese
-
Abstract:
AIM To investigate the beneficial effect of aminoguanide (AG) on cerebral ischemic injury and the possible mechanism. METHODS The model of focal cerebral ischemia in rat was prepared. Rats were divided into sham-operated group, ischemic group and AG group. Each group was further divided into 3 subgroups (n=6 for each): drugs were administrated at 2, 6 and 12 h after the middle cerebral artery occlusion (MCAO), respectively. AG (100 mg·kg-1, ip) was administrated, 2 times a day, for 3 consecutive days. The changes in infarcted volume and the contents of amino acids were assayed. RESULTS The infarcted volume (15.1±3.4, 18.4±5.1, 25.7±3.5) was much decreased compared with that of ischemic group (23.2±2.9, 28.0±3.9, 37.2±2.9) when AG was administrated at 2, 6 and 12 h after MCAO respectively (%, P<0.05, n=6). The contents of aspartate, glutamate, glycine and GABA in striatum, hippocampus and cortex in ischemic group were significantly increased compared with sham-operated group(P<0.05 or P<0.01, n=6). The contents of glutamate in striatum, hippocampus and cortex were markedly decreased when AG was given at 2, 6 and 12 h after ischemia respectively(P<0.05 or P<0.01, n=6). The contents of aspartate in striatum, hippocampus and cortex were markedly decreased when AG was given at 2 and 6 h, and the contents of aspartate in hippocampus and cortex were decreased when AG was given at 12 h after ischemia (P<0.05 or P<0.01, n=6). The contents of GABA in hippocampus and cortex were increased when AG was given at 2 and 6 h, and the contents of GABA in striatum and cortex were increased when AG was given at 12 h after ischemia(P<0.05 or P<0.01, n=6). Thecontents of glycine were increased in striatum, hippocampus and cortex when AG was given at 2 h, the contents of glycine were increased in cortex when AG was given at 6 h, and the contents of glycine in hippocampus and cortex when AG was given at 12 h after ischemia respectively(P<0.05 or P<0.01, n=6). CONCLUSION AG has beneficial effect on ischemic cerebral injury. The possible mechanism is that AG can decrease the contents of aspartate and glutamate, increase the contents of glycine and GABA.
