Xu Xuan, Li Dengxiao, Gao Hong, Gao Yuejin, Zhang Long, Du Yuling, Wu Jian, Gao Pengfei
Department of TCM, Jinshan Hospital Affiliated to Fudan University Shanghai 201508, China.
Department of Rehabilitation, Jinshan Hospital Affiliated to Fudan University Shanghai 201508, China.
Int J Clin Exp Med. 2015 Feb 15;8(2):1768-79. eCollection 2015.
We investigated the effect of xuesaitong on intestinal barrier dysfunction and related mechanisms in a rat model for intestinal ischemia-reperfusion.
Rats were divided into sham-operated, disease-model and Xuesaitong-treated groups. In the disease-model and Xuesaitong-treated rats an intestinal ischemia-reperfusion injury (IRI) model was introduced, which was created by a temporary obstruction of the superior mesenteric artery (SMA). The xuesaitong group was pre-treated with injections into the abdominal cavity prior to the generation of the IRI model. Tissue changes were evaluated using H&E staining and electron microscopy. Samples were analyzed at 0, 3 and 24 h post IRI. Ascites volumes as well as small intestinal mucosa bleeding, injury scores, wet to dry weight ratios, and propulsions were evaluated. Apoptotic rates were determined with TUNNEL assays. Blood serum tumor necrosis factor-α (TNF-α) levels were measured using ELISA, and Bcl-2 and caspase-3 expression in small intestinal mucosa measured using immunohistochemistry.
We determined a significant increase of pathological damage to small intestinal tissues, intestinal wet to dry ratios, ascites volume, TNF-α levels, apoptosis rates of small intestinal mucosa, and expression of Bcl-2 and caspase-3 proteins in the disease-model group compared to the sham-operated group (P < 0.001), and intestinal motility was significantly decreased (P < 0.001). However, comparisons between disease-model and xuesaitong pre-treated animals revealed, that in the treatment group these changes occurred in significant less severities.
Xuesaitong can effectively alleviate intestinal barrier dysfunction caused by ischemia-reperfusion injury by reducing TNF-α, up-regulating Bcl-2 and down-regulating caspase-3 expression, in addition to increasing peristalsis.
我们在大鼠肠缺血再灌注模型中研究了血塞通对肠屏障功能障碍的影响及其相关机制。
将大鼠分为假手术组、疾病模型组和血塞通治疗组。在疾病模型组和血塞通治疗组大鼠中建立肠缺血再灌注损伤（IRI）模型，该模型通过暂时阻断肠系膜上动脉（SMA）来创建。血塞通组在IRI模型建立前经腹腔注射进行预处理。使用苏木精-伊红（H&E）染色和电子显微镜评估组织变化。在IRI后0、3和24小时对样本进行分析。评估腹水体积以及小肠黏膜出血、损伤评分、湿重与干重比和推进率。用TUNEL检测法测定凋亡率。使用酶联免疫吸附测定（ELISA）测量血清肿瘤坏死因子-α（TNF-α）水平，并用免疫组织化学法测量小肠黏膜中Bcl-2和半胱天冬酶-3的表达。
我们发现，与假手术组相比，疾病模型组小肠组织的病理损伤、肠湿重与干重比、腹水体积、TNF-α水平、小肠黏膜凋亡率以及Bcl-2和半胱天冬酶-3蛋白的表达均显著增加（P < 0.001），并且肠动力显著降低（P < 0.001）。然而，疾病模型组与血塞通预处理动物之间的比较显示，治疗组中这些变化的严重程度明显较低。
血塞通可通过降低TNF-α、上调Bcl-2和下调半胱天冬酶-3表达，以及增加肠蠕动，有效减轻缺血再灌注损伤引起的肠屏障功能障碍。
