【摘要】：目的研究丁苯酞(NBP)對急性重度一氧化碳(CO)中毒大鼠腦組織中凋亡相關(guān)因子B細(xì)胞淋巴瘤基因-2(Bcl-2)和Bcl-2相關(guān)X蛋白(Bax)表達(dá)的影響。方法按照體重將大鼠隨機(jī)分為正常組、模型組、實(shí)驗(yàn)組。用CO染毒法制作大鼠急性重度CO中毒模型。實(shí)驗(yàn)組于CO中毒后予以80 mg·kg~(-1)丁苯酞連續(xù)灌胃7 d,qd。各組大鼠在治療完畢后,取腦組織皮層區(qū),用免疫組織化學(xué)法、RT-PCR法和免疫印跡法檢測腦組織中Bcl-2和Bax的表達(dá)。結(jié)果正常組大鼠腦組織中Bcl-2和Bax的陽性細(xì)胞數(shù)分別為(4.23±0.71),(5.03±0.71),顯示mRNA和蛋白呈低水平表達(dá)。模型組大鼠腦組織中Bcl-2和Bax的陽性細(xì)胞數(shù)分別為(22.62±4.39),(38.65±7.54),mRNA和蛋白表達(dá)水平較正常組顯著增多;予以丁苯酞治療后,實(shí)驗(yàn)組大鼠腦組織中Bcl-2和的Bax陽性細(xì)胞數(shù)為(35.13±6.69),(27.36±5.57),表明Bcl-2的mRNA和蛋白表達(dá)水平較模型組顯蓍上調(diào)而Bax的mRNA和蛋白表達(dá)水平較模型組顯著下調(diào)(均P0.05)。結(jié)論丁苯酞對急性重度CO中毒大鼠有神經(jīng)保護(hù)作用,其機(jī)制可能與促進(jìn)Bcl-2的表達(dá)、抑制Bax的表達(dá)有關(guān)。
[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 鹵0.71), (5.03 鹵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 鹵4.39), () 38.65 鹵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 鹵6.69), () 27.36 鹵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.
【作者單位】： 福建醫(yī)科大學(xué)附屬泉州第一醫(yī)院神經(jīng)內(nèi)科;
【基金】：2014年泉州市衛(wèi)生科研基金資助項目
【分類號】：R595.1

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