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作 者:张永锋[1] 吴正治[1] 熊鹰[1] 杨敏[1] 丁民[2]
机构地区:[1]深圳市第二人民医院中西医结合临床研究所,深圳518035 [2]湖北中医学院硕士研究生,武汉430061
出 处:《中国中医药科技》2008年第1期16-17,共2页Chinese Journal of Traditional Medical Science and Technology
基 金:深圳市科信局立项资助No.200204078
摘 要:目的:探讨结肠康泰对结肠炎大鼠结肠黏膜细胞凋亡及调控基因Bcl-2、c-Myc、P^(53)表达的影响。方法:雌性SD大鼠60只,随机分为4组,分别为正常对照、模型、柳氮磺胺吡啶(SASP)及结肠康泰组,以5%2,4,6-三硝基苯磺酸(TNBs)诱导大鼠形成结肠炎症,TUNEL法检测细胞凋亡及免疫组化法观察Bcl-2、c-Myc、P^(53)的表达。结果:SASP及结肠康泰组大鼠细胞凋亡指数(AI)明显降低,c-Myc、p^(53)蛋白低表达,Bcl-2高表达,与模型组比较有显著性意义(均为P<0.05)。结论:结肠康泰通过调控基因bcl -2、c-myc、p53对结肠炎大鼠结肠黏膜细胞凋亡有抑制作用。Objective:To discuss the effects of jiechang kangtai(JCKT) on apoptosis and expression of Bcl-2,c-Myc and P^(53) gene protein in colonic mucous cells of colitis rats. Methods:60 female SD rats were randomly divided into four groups:normal,model,solfasalazine(SASP) and JCKT groups.Experimental colitis models were induced by trinitrobenzene sulphonic acid(TNBs).The apoptosis of cells were tested by TUNEL and the expression of Bcl -2,c-Myc and p^(53) gene protein were observed by immunohistochemistry. Results:The AI,expression of c-Myc and P^(53) in the two treated groups(JCKT,SASP) were obviously lower than those in the model group, the expression of Bcl-2 in the two treated groups were higher than that in the model group(P<0.05). Conclusion:JCKT can inhibit the apoptosis of colonic mucous cells in colitis rats which maybe by means of regulating the expression of Bcl -2,c-Myc and P^(53) genes protein.
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