Effect of aminoguanidine on TNF-?, IL-1? and neuronal apoptosis after focal cerebral ischemic injury in rats
- VernacularTitle:氨基胍对大鼠局灶性脑缺血损伤后TNF-?、IL-1?及细胞凋亡的作用
- Author:
Jianxin ZHANG
;
Lanfang LI
;
Huixin ZHANG
;
Yonghui LI
- Publication Type:Journal Article
- Keywords:
Aminoguanidine;
Brain ischemia;
Tumor necrosis factor;
Interleukin-1;
Apoptosis
- From:
Chinese Journal of Pathophysiology
2000;0(11):-
- CountryChina
- Language:Chinese
-
Abstract:
AIM: To evaluate the effect of aminoguanidine (AG) on inflammatory factors and neuronal apoptosis after focal cerebral ischemic injury in rats and the possible mechanism of protective effect of AG against cerebral ischemic injury. METHODS: Thirty male SD rats (weighing 250 g-280 g) were randomly divided into three groups: (1) sham operated group (SH group, n=10), (2) ischemic groups (IS group, n=10), (3) AG group (n=10). In AG group, AG at dose of 100 mg?kg-1 was given intraperitoneally twice a day for 3 consecutive days. In IS group, normal saline was given instead of AG. Focal cerebral ischemia was produced by middle cerebral artery occlusion (MCAO) for 12 h. A nylon thread with rounded tip was inserted into left internal carotid artery cranially until resistance was felt. The distance from bifurcation of common carotid artery to the tip of the thread was about 18-19 mm. Focal cerebral ischemia was confirmed by left Horner's syndrome and right side hemiplegia. In SH group, the carotid artery was exposed but no thread was inserted. The expression of tumor necrosis factor-?(TNF-?) was determined by immunochemistry and the content of interleulin-1?(IL-1?) was measured by radioimmunoassay. The expressions of Bcl-2 and Bax protein were detected by flow cytometry. RESULTS: The expression of TNF-? and the content of IL-1? were markedly increased after MCAO. Significantly increased DNA fragmentation, the indication of apoptosis, was detected after MCAO. The expression of TNF-? and the content of IL-1? were significantly lower in AG group than those in IS group. The percentage of apoptosis cells and expression of Bax protein were markedly lower in AG group than those in IS group but still significantly higher than those in SH group. The expression of Bcl-2 protein was markedly higher in AG group than that in IS group. No significant difference in the expression of Bcl-2 protein between IS and SH group was observed. CONCLUSION: AG inhibits the increase in the expression of TNF-? and the content of IL-1?, and protects neurons from apoptosis induced by focal cerebral ischemia through increasing the Bcl-2 protein expression and inhibiting the Bax protein expression.
