本文選題：丁苯酞膠囊 + 一氧化碳中毒　； 參考：《中國臨床藥理學雜志》2017年08期

【摘要】：目的研究丁苯酞對大鼠急性重度CO中毒后腦組織中半胱氨酸蛋白-3(Caspase-3)和半胱氨酸蛋白酶-9(Caspase-9)表達的影響。方法通過數(shù)字表法將大鼠隨機分為3組:正常組、模型組和實驗組(均n=10)。用CO染毒法制作大鼠急性重度CO中毒模型。實驗組大鼠給予丁苯酞80 mg·kg~(-1),灌胃1次/天,連續(xù)7 d,正常組和模型組給予等量的0.9%NaCl。在7 d后,用免疫組化染色法觀測Caspase-3和Caspase-9陽性細胞數(shù),用反轉錄酶-聚合酶鏈鎖反應(RT-PCR)法及蛋白質印跡法檢測Caspase-3和Caspase-9mRNA和蛋白的表達水平。結果正常組大鼠腦組織中Caspase-3和Caspase-9的陽性細胞數(shù)分別為4.98±1.34,8.65±1.89,mRNA表達水平分別為0.19±0.02,0.18±0.03,蛋白表達水平分別為0.09±0.01,0.08±0.01;模型組大鼠腦組織中Caspase-3和Caspase-9陽性細胞數(shù)分別為29.43±4.53,40.45±5.23,mRNA表達水平分別為0.47±0.05,0.75±0.05,蛋白表達水平分別為0.78±0.05,0.86±0.07。與正常組對比,模型組的Caspase-3和Caspase-9mRNA和蛋白表達水平顯著增高,差異均有統(tǒng)計學意義(均P0.05)。實驗組大鼠腦組織中的Caspase-3和Caspase-9陽性細胞數(shù)分別為22.26±3.12,25.09±4.25,mRNA表達水平分別為0.35±0.05,0.41±0.05,蛋白表達水平分別為0.37±0.02,0.45±0.02,與模型組對比,Caspase-3和Caspase-9 mRNA和蛋白表達水平較明顯下調,差異均有統(tǒng)計學意義(均P0.05)。結論丁苯酞可通過下調Caspase-3和Caspase-9的表達水平來抑制神經細胞凋亡進程,從而減輕CO對大鼠腦神經的損害。
[Abstract]:Objective to study the effects of butyphthalide on the expression of cysteine protein-3 (caspase-3) and cysteine protease-9 (Caspase-9) in brain tissue of rats with acute severe CO poisoning. Methods the rats were randomly divided into 3 groups: normal group, model group and experimental group (n = 10). The acute severe CO poisoning model of rats was made by means of CO poisoning. Rats in the experimental group were given butylphthalide (80 mg 路kg ~ (-1) by gavage once a day for 7 days. The normal group and the model group were given the same amount of 0.9 NaCl. After 7 days, the number of Caspase-3 and Caspase-9 positive cells were detected by immunohistochemical staining, and the expression levels of Caspase-3 and Caspase-9 mRNA and protein were detected by reverse transcriptase polymerase chain reaction (RT-PCR) and Western blotting. Results the number of Caspase-3 and Caspase-9 positive cells in the brain tissue of normal rats was 4.98 鹵1.34, 8.65 鹵1.89, respectively, 0.19 鹵0.02 鹵0.18 鹵0.03, and 0.09 鹵0.01 鹵0.08 鹵0.01, respectively, and the number of Caspase-3 and Caspase-9 positive cells in brain tissue of model group was 29.43 鹵4.53, 40.45 鹵5.23, respectively. The expression level of protein was 0.78 鹵0.05 and 0.86 鹵0.07, respectively. Compared with the normal group, the expression of Caspase-3 and Caspase-9 mRNA and protein in the model group was significantly higher than that in the normal group (all P 0.05). The number of Caspase-3 and Caspase-9 positive cells in brain tissue of experimental group was 22.26 鹵3.12n25.09 鹵4.25, respectively. The expression levels of Caspase-3 and Caspase-9 mRNA and protein were 0.35 鹵0.05, 0.41 鹵0.05, 0.37 鹵0.02, 0.45 鹵0.02, respectively. Compared with the model group, the expression levels of Caspase-3 and Caspase-9 mRNA and protein were significantly down-regulated (P 0.05). Conclusion butyphthalide can inhibit the process of neuronal apoptosis by down-regulating the expression levels of Caspase-3 and Caspase-9, thereby reducing the damage of CO to the brain nerve of rats.
【作者單位】： 福建醫(yī)科大學附屬泉州第一醫(yī)院神經內科;
【基金】：泉州市衛(wèi)生科研基金資助項目
【分類號】：R595.1;R747.9

【相似文獻】

相關期刊論文 前6條

1 嚴金海;嚴亞琪;李曉輝;;丁苯酞治療糖尿病新發(fā)腦梗死效果觀察[J];中國鄉(xiāng)村醫(yī)藥;2014年17期

2 徐昕;;丁苯酞治療急性腦梗死合并糖尿病臨床分析[J];吉林醫(yī)學;2014年21期

3 楊會欣;趙靈敏;;丁苯酞聯(lián)合依達拉奉預防一氧化碳中毒遲發(fā)性腦病的臨床研究[J];河北醫(yī)藥;2014年19期

4 閆春雷;張林紅;張軍峰;;丁苯酞聯(lián)合馬來酸桂哌齊特治療一氧化碳中毒遲發(fā)性腦病療效觀察[J];臨床合理用藥雜志;2012年08期

5 葛建新;文U喦，

本文編號：2036009