丁苯酞对急性重度一氧化碳中毒大鼠神经元凋亡相关因子表达的影响  

Effects of dl-3-n-butylphthalide on expression of apoptosis-related factors in rats with acute severe carbon monoxide poisoning

作　　者：洪诸权[1] 王杰华[1] 李国前[1] 杨小霞[1] 潘莹[1] 

机构地区：[1]福建医科大学附属泉州第一医院神经内科,福建泉州362000

出　　处：《中国临床药理学杂志》2016年第8期717-719,共3页The Chinese Journal of Clinical Pharmacology

基　　金：2014年泉州市卫生科研基金资助项目

摘　　要：目的研究丁苯酞(NBP)对急性重度一氧化碳(CO)中毒大鼠脑组织中凋亡相关因子B细胞淋巴瘤基因-2(Bcl-2)和Bcl-2相关X蛋白(Bax)表达的影响。方法按照体重将大鼠随机分为正常组、模型组、实验组。用CO染毒法制作大鼠急性重度CO中毒模型。实验组于CO中毒后予以80 mg·kg^(-1)丁苯酞连续灌胃7 d,qd。各组大鼠在治疗完毕后,取脑组织皮层区,用免疫组织化学法、RT-PCR法和免疫印迹法检测脑组织中Bcl-2和Bax的表达。结果正常组大鼠脑组织中Bcl-2和Bax的阳性细胞数分别为(4.23±0.71),(5.03±0.71),显示mRNA和蛋白呈低水平表达。模型组大鼠脑组织中Bcl-2和Bax的阳性细胞数分别为(22.62±4.39),(38.65±7.54),mRNA和蛋白表达水平较正常组显著增多;予以丁苯酞治疗后,实验组大鼠脑组织中Bcl-2和的Bax阳性细胞数为(35.13±6.69),(27.36±5.57),表明Bcl-2的mRNA和蛋白表达水平较模型组显蓍上调而Bax的mRNA和蛋白表达水平较模型组显著下调(均P<0.05)。结论丁苯酞对急性重度CO中毒大鼠有神经保护作用,其机制可能与促进Bcl-2的表达、抑制Bax的表达有关。Objective To investigate the effects of dl-3-n-butylphthalide（NBP） on the expression of B-cell lymphoma-2（Bcl-2）and Bcl-2 associated X protein（Bax） in the rat brain tissue after acute severe carbon monoxide（CO） poisoning. Methods Rats were randomly assigned into three groups： normal group,CO-exposed group（model group） and NBP（test group）. The acute severe carbon monoxide poisoning model was made by the ischiropoulos method. The rats in the test group were lavaged with 80 mg · kg^-1NBP after making a model.The levels of Bcl-2 and Bax expression were measured by immunohistochemistry,RT-PCR and Western blot. Results Bcl-2 and Bax have low level of expression in normal group. After acute severe carbon monoxide poisoning,the expression of Bcl-2 and Bax positive cells were（22. 62 ± 4. 39）,（38. 65 ± 7. 54）,indicating that mRNA and protein increased significantly in rats. Compared with model group,in rats of test group,the expression of Bcl-2 positive cells was（35. 13 ± 6. 69）,the mRNA and protein were up regulated（P〈0. 05）,while the expression of Bax positive cells was（27. 36 ± 5. 57）,mRNA and protein were downregulated（P〈0. 05）. Conclusion NBP can relieve the brain damage partly by regulatng Bcl-2 and Bax synthesis in brain.

关 键 词：丁苯酞 一氧化碳中毒 B细胞淋巴瘤基因-2 Bcl-2相关X蛋白 

分 类 号：R972[医药卫生—药品]