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

发布时间：2018-10-11 18:40

【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P0.05)。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。
[Abstract]:Objective to investigate the effects of butyphthalide (NBP) on the expression of apoptosis-related factor B cell lymphoma gene 2 (Bcl-2) and Bcl-2 related X protein (Bax) in the brain of rats with acute severe carbon monoxide (CO) poisoning. Methods according to body weight, rats were randomly divided into normal group, model group and experimental group. The acute severe CO poisoning model of rats was made by CO poisoning. The experimental group was given 80 mg kg~ (-1) butyphthalide by gastric perfusion for 7 days after CO poisoning. After treatment, the expression of Bcl-2 and Bax in brain tissue was detected by immunohistochemistry, RT-PCR and Western blotting. Results the number of Bcl-2 and Bax positive cells in brain tissue of normal rats was (4.23 卤0.71), (5.03 卤0.71), indicating that the expression of mRNA and protein was low. The number of Bcl-2 and Bax positive cells in the brain tissue of the model group was (22.62 卤4.39), () 38.65 卤7.54), mRNA and the protein expression level was significantly higher than that in the normal group. The number of Bcl-2 and Bax positive cells in brain tissue of experimental group was (35.13 卤6.69), () 27.36 卤5.57, which indicated that the expression of mRNA and protein in Bcl-2 was up-regulated than that in model group, but the expression of mRNA and protein in Bax was significantly lower than that in model group (P0.05). Conclusion butyphthalide has neuroprotective effect on acute severe CO poisoning rats, and its mechanism may be related to promoting the expression of Bcl-2 and inhibiting the expression of Bax.
【作者单位】：福建医科大学附属泉州第一医院神经内科;
【基金】：2014年泉州市卫生科研基金资助项目
【分类号】：R595.1

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