左旋四氢巴马汀在大鼠急性全脑缺血再灌注中对肺组织HO-1及CO的影响

Effects of L-tetrahydropalmatine on Hemeoxygenase-1 in Lung Tissues and Blood Endogenous Carbon Monoxide during Global Cerebral Ischemia-reperfusion in Rats

目的:了解左旋四氢巴马汀(颅痛定)在大鼠急性全脑缺血再灌注损伤时对肺组织HO-1和内源性一氧化碳(CO)的影响。方法:44只SD大鼠中的40只采用四血管阻塞法建立急性全脑缺血再灌注模型,并随机分为脑缺血再灌注组(B组)和颅痛定治疗组(C组)各20只,另4只为假手术组(A组)。脑缺血再灌注2、6、12、24及48 h各时间点,B、C组各取4只和A组的4只于术后2 h时均处死,检测肺组织HO-1和血液中CO含量。结果:术后A组大鼠肺组织无充血或渗出等变化;B、C组肺泡间隔变宽,毛细血管及小静脉充血,有中性粒细胞侵润,但C组明显少于B组。CO及HO-1含量在术后2、6、12及24 h点B、C组与A组比较均提高(P<0.05),且在12 h点达最高峰(P<0.05),其后增幅减小;与B组比较,C组表现更明显(P<0.05),48 h点3组间比较差异无显著性意义。结论:颅痛定可通过升高HO-1的活性使CO增加,从而减轻脑缺血再灌注时肺组织炎症损伤,对肺组织起到保护性的作用。

Objective： To investigate the effects of L-tetrahydropalmatine （Rotundine） on hemeoxygenase-1 （HO- 1） in lung tissues and blood endogenous carbon monoxide （CO） during acute global ischemia-reperfusion in rats. Methods： Acute global ischemia-reperfusion models in 40 SD rats were established by four vessel occlusion method and randomly divided into cerebral ischemia reperfusion group （group B） and Rotundine-treated group （group C） （n=20 in each group）. Four SD rats served as sham-operated group （group A）. At different time points of 2, 6, 12, 24 and 48 h during cerebral ischemia-reperfusion. 4 rats in each group of A, B and C were killed 2 h after operation. The contents of HO-1 and blood CO were determined. Results： There were no congestive and exudative changes postoperatively in group A. In groups B and C, alveolar interval was widened, there were congestion of capillary and small veins and neutrophils infiltration. At time points of 2, 6, 12 and 24 h, CO-1 and HO-1 contents in group C were significantly increased （P〈0.05） as compared with group A, reached the peak at 12 h （P〈0.05）, then their increased amplitude reduced. In comparison to group B, the changes in group C were more significant （P〈0.05）. At 48th h, there was no significant difference among the three groups. Conclusion： Rotundine can alleviate lung inflammatory injury during cerebral ischemia reperfusion and protect lung tissues by increasing HO-1 activity which increases CO activity.