清肠栓对溃疡性结肠炎大鼠结肠黏膜纤丝状肌动蛋白的影响

Effect of Qingchang Suppository on filamentous actin in an experimental rat model of ulcerative colitis

[目的]探讨复方中药清肠栓对溃疡性结肠炎(UC)大鼠结肠黏膜纤丝状肌动(F-actin)蛋白的修复作用。[方法]清洁级雄性SD大鼠36只,随机分为正常组,模型组,柳氮磺胺吡啶(SASP)组,清肠栓高、中、低剂量组,每组6只。选用三硝基苯磺酸(TNBS)诱导的UC大鼠模型,采用免疫荧光的方法观察各组大鼠结肠黏膜F-actin蛋白的表达,并运用图像分析软件进行平均光密度测定,观察清肠栓对UC大鼠结肠屏障的修复作用。[结果]UC发病对结肠黏膜细胞骨架系统严重损害,模型组大鼠结肠黏膜F-actin蛋白几乎完全被破坏,荧光染色暗淡。图像分析测其平均光密度较正常组明显降低(P<0.01)。清肠栓能不同程度减轻UC黏膜的破坏,改善F-actin蛋白的分布,并使其表达升高(P<0.01)。[结论]清肠栓能有效地调节肠黏膜屏障功能,有效抑制UC大鼠结肠通透性的升高,改善肠黏膜屏障功能,促进溃疡愈合。

To observe the effect of Qingchang Suppository（QS）on filamentous actin（F-actin） of colon in an experimental rat model of ulcerative colitis（UC）. [Methods]Thirty-six SD rats were randomly divided into 6 equal groups： normal control group,model group, SASP solution group,QS groups of high, medium and low doses. The rat model of ulcerative colitis was induced by trinitro-benzene-sulfonic acid （TNBS）. The modulatory effect of QS on UC was examined by immunofluorescent labeling of F-actin in rat colonic mueosa. [Results]UC caused severe damage of the cytoskeleton system in colonic mucosa, which was showed by disruption of Factin. Compared to normal control group, the expression of F-actin was significantly lower in model group （P〈0. 01） Treatment with QS attenuated the disruption of F actin（P〈0.01）. [Conclusion]This study demonstrated that QS can effectively modulate intestinal mucosal barrier function and inhibit colonic permeability, thus improve ulcer healing.