Protective effects and mechanism of aspirin against cerebral ischemia-reperfusion in rats
- VernacularTitle:阿司匹林抗脑缺血/再灌注损伤的作用及机制
- Author:
Liying QIU
;
Juan YU
;
Chonghong CHEN
- Publication Type:Journal Article
- Keywords:
aspirin;
focal cerebral ischemia-reperfusion injury;
apoptosis;
Bcl-2/Bax;
calcineurin;
adenosine 5′-triphosphate
- From:
Chinese Pharmacological Bulletin
2003;0(08):-
- CountryChina
- Language:Chinese
-
Abstract:
Aim To investigate the protective effects and mechanism of aspirin against focal cerebral ischemia-reperfusion in rats. Methods Right middle cerebral artery was occluded by inserting a thread through internal carotid artery for 2 h, and then reperfused for 72 h. 60 mg?kg -1 dose of aspirin was intragastric administrated at 0 h and 6 h after reperfusion. The brain injured area, the mortality, and cerebral edema were estimated. The apoptotic cells of brain tissue were detected by terminal deoxynucleotidyl transferase mediated dUTP-biotin nick-end labeling (TUNEL) method. Bcl-2 and Bax were detected by immunohistochemical staining method. The activity of calcineurin (CaN) in brain tissue was determined by the inorganic phosphorus method. The content of adenosine 5′-triphosphate (ATP) in brain tissue was separated by capillary electrophoresis. Results By using of aspirin 60 mg?kg -1, all indications were dramatically improved. The injured area of brain [from (10.51?1.12)% to (0.94?0.08)%], the cerebral edema of occluded side [from (82.43?2.0)% to (76.29?0.77)%], and the mortality [from 28% to 0%] were dramatically reduced. In brain tissue of occluded side, 60 mg?kg -1 aspirin helped to reduce the number of apoptotic cells from (26.43?2.0) to (17.53?0.44), increase the ratio of Bcl-2/Bax from (0.61?0.05) to (1.01?0.15), inhibit the activity of CaN from (6.03?1.5) to (3.47?0.96), and improve the ATP level from (10.26?1.02) to (25.65?3.45). Conclusion The neuroprotective effects of aspirin on focal cerebral ischemia-reperfusion injury in rats for 72 h might be attributed to its effects by anti-apoptosis, increasing the ratio of Bcl-2/Bax, inhibiting the activity of CaN, and improving the energy metabolism.
