清肠栓对大鼠溃疡性结肠炎淋巴细胞凋亡调控蛋白Bcl-2及Bax表达的影响

Effect of Qingchang Suppository on the Expression of Its Regulatory Proteins Bcl-2 and Bax in an Experimental Models of Ulcerative Colitis

目的:探讨清肠栓治疗溃疡性结肠炎的作用机制。方法:SD大鼠48只随机分为正常组、模型组(空白组)、西药组(SASP组)、中药组(清肠栓组)共4组,正常组6只,其余每组14只。用5%2,4,6三硝基苯璜酸100mg.kg-1灌肠建立大鼠溃疡性结肠炎模型,第3天开始,除正常组外,各组分别给予生理盐水、柳氮磺胺吡啶、清肠栓处理,至7天后处死动物。运用电镜、TUNEL染色法、Bcl-2及Bax蛋白免疫组化染色,分别检测溃疡性结肠炎大鼠结肠黏膜固有层淋巴细胞凋亡及固有层淋巴细胞Bcl-2及Bax蛋白的表达。结果:与各对照组相比,模型组结肠黏膜固有层淋巴细胞凋亡减慢;其结肠黏膜固有层淋巴细胞上Bcl-2的表达率增加,而Bax的表达率下降(P<0.01)。结论:清肠栓可能通过调节Bcl-2及Bax二者之间的比例变化,诱导淋巴细胞凋亡,发挥治疗溃疡性结肠炎的作用。

Objective： To survey the effect of Qingchang Soppority on intestine mucosa in ulcerative colitis. Methods： 48SD rats were randomly divided into 4 equal groups, six animals normal control in group , with 14 animals in other three groups： blank group; SASP ,solution group; Qingchang Soppority group. The rat model of ulcerative colitis was brought about by an enema of 100 mg·kg^-1 of TNBS. Beginning from the third day, except for the normal group, each group was treated with an enema of 0.9 % NACL, SASP, Qingchang Soppority respectively. The rats were ,sacrificed 1 week later. Apoptosis of lymphocyte was detected with the technique of transmission electron microscope （H600）, terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling （TUNEL） while Bcl- 2 and Bax proteins expressions were assayed with immunohistochemieal staining. Resuits： Colonic lamina propria （LP） from rats with UC showed lower rates of apoptosis than normal controls. Rats of Bcl -2 - expressing cells in LP were higher in UC than in controls. Rats of Bax-expressing cells in LP were lower in UC than in controls （P 〈 0.01 ）. Conclusions： Increased expression of bcl- 2 on UC colonic LPL and decreased the expression of Bax on colonic LPL may indicate a reduced susceptibility to the Bcl - 2/Bax - mediated apoptosis of lymphoid cells, which may tend to reduce the apoptosis of LPL. Qingchang Soppority was shown to exert a treatment effect on the rat model of ulcerative colitis possibly by promoting the expression of Bax on UC colonic LP and declining the expression of bcl - 2 on colonioc LP as well as increasing the apoptosis of LPL.