The effect of naloxone on heme oxygenase-1 expression in focal cerebral ischemia-reperfusion in rats
- Author:
Shui-Xiu ZHOU
1
Author Information
1. Department of Neurology
- Publication Type:Journal Article
- From:
Chinese Journal of Cerebrovascular Diseases
2006;3(9):412-416
- CountryChina
- Language:Chinese
-
Abstract:
Objective: To discuss the expression of heme oxygenase-1 (HO-1) protein around ischemic focus after focal cerebral ischemia-reperfusion in rats and the effect after naloxone intervention. Methods: Forty-five Sprague-Dawley rats were randomly allocated into three groups (n = 15, each): sham operation group, ischemia-reperfusion group, and naloxone group. A focal cerebral ischemia-reperfusion model was built by the suture method for middle cerebral artery occlusion (MCAO) in rats. After the successful reperfusion by inserting and withdrawing sutures, naloxone (3 mg/kg) was injected intraperitoneally into the rats of naloxone group, and isotonic saline was injected intraperitoneally into the rats of sham operation group and ischemia-reperfusion group. The expression of HO-1 was assayed by immunohistochemistry. In situ terminal deoxynucleotidyl transferase (TUNEL) assay was used to observe the numbers of brain apoptosis. Results: The numbers of HO-1 positive cell in the ischemia-reperfusion group were significantly higher than those in the sham operation group with an average of 51.6 ± 10.8 vs 9.8 ± 2.8/high-power field (HP) (P < 0.05). The numbers of HO-1 positive cell around the ischemic foci in the naloxone group were higher than those in the ischemia-reperfusion group averaged 63.5 ± 10.0 vs 51.6 ± 10.8/HP (P < 0.05). The numbers of TUNEL positive cell in the naloxone group were significantly lower than those in the ischemia-reperfusion group (20.5 ± 3.5 vs 29.8 ± 4.0/ HP,), but were higher than those in the sham operation group (4.2 ± 2.0/ HP), and there were significant differences between the groups (P < 0.05). Conclusion: Naloxone may reduce neuronal apoptosis caused by focal cerebral ischemia-reperfusion injury after MCAO, and its mechanism may be associated with the increase of naloxone-induced HO-1 expression.
