Acute radiation enteritis (ARE) is a common complication with radiotherapy for pelvic and abdominal malignancy. This research is designed to investigate the efficacy of Tong-Xie-Yao-Fang (TXYF) on ARE and to explore the underlying mechanisms by microarray analysis. The ARE rat model was established by a single abdominal irradiation with a gamma-ray dose of 10 Gy. Next, the ARE rats were treated with distilled water, TXYF, and glutamine by gavage for 7 consecutive days according to the scheduled groups. For each group, the jejunal tissue was taken at 6 h after gastric lavage. The morphology of intestinal tissue was observed by hematoxylin and eosin (H&E) stain under a light microscope. The height of the villus and the thickness of the whole layer of the TXYF-treated groups were significantly ameliorative than that of the model control group. The transcriptome analysis was produced using the Agilent SurePrint G3 Rat GE V2.0 microarray. A total of 90 differentially expressed genes (DEGs), including 48 upregulated genes and 42 downregulated genes, were identified by microarray and bioinformatics analysis. Protein–protein interaction (PPI), Gene Ontology (GO), and Kyoto Encyclopedia of Genes and Genomes (KEGG) were conducted to explore the possible mechanisms of DEGs taking part in the TXYF-mediated therapeutic process for ARE. In conclusion, we reveal that TXYF has a protective effect on the intestinal tissue of rats with ARE and summarize several DEGs, suggesting the possible mechanisms of TXYF-mediated efficacy for ARE.

中文翻译：

---

复方中药药方对急性放射性肠炎的疗效及其潜在机制：转录组分析的证据

急性放射性肠炎（ARE）是盆腔和腹部恶性肿瘤放疗的常见并发症。这项研究旨在调查通邪药方（TXYF）对ARE的疗效，并通过微阵列分析探索其潜在机制。通过用10 Gy的伽马射线单次腹部照射建立ARE大鼠模型。接下来，根据预定的组，用蒸馏水，TXYF和谷氨酰胺通过连续管饲法对ARE大鼠进行连续7天的治疗。对于每组，在洗胃后6小时取空肠组织。通过苏木精和曙红（H＆E）染色在光学显微镜下观察肠组织的形态。TXYF处理组的绒毛高度和整个层的厚度均明显优于模型对照组。转录组分析是使用Agilent SurePrint G3 Rat GE V2.0微阵列进行的。通过微阵列和生物信息学分析鉴定出总共90个差异表达基因（DEG），包括48个上调基因和42个下调基因。进行了蛋白质间相互作用（PPI），基因本体论（GO）和《京都基因与基因组百科全书》（KEGG），以探索DEG参与TXYF介导的ARE治疗过程的可能机制。总之，我们揭示了TXYF对ARE大鼠的肠组织具有保护作用，并总结了几种DEG，表明TXYF介导的ARE功效的可能机制。通过微阵列和生物信息学分析鉴定了包括48个上调基因和42个下调基因的基因。进行了蛋白质间相互作用（PPI），基因本体论（GO）和《京都基因与基因组百科全书》（KEGG），以探索DEG参与TXYF介导的ARE治疗过程的可能机制。总之，我们揭示了TXYF对ARE大鼠的肠组织具有保护作用，并总结了几种DEG，表明TXYF介导的ARE功效的可能机制。通过微阵列和生物信息学分析鉴定了包括48个上调基因和42个下调基因的基因。进行了蛋白质间相互作用（PPI），基因本体论（GO）和《京都基因与基因组百科全书》（KEGG），以探索DEG参与TXYF介导的ARE治疗过程的可能机制。总之，我们揭示了TXYF对ARE大鼠的肠组织具有保护作用，并总结了几种DEG，表明TXYF介导的ARE功效的可能机制。和京都基因与基因组百科全书（KEGG）进行了探讨DEGs参与TXYF介导的ARE治疗过程的可能机制。总之，我们揭示了TXYF对ARE大鼠的肠组织具有保护作用，并总结了几种DEG，表明TXYF介导的ARE功效的可能机制。和京都基因与基因组百科全书（KEGG）进行了探讨DEGs参与TXYF介导的ARE治疗过程的可能机制。总之，我们揭示了TXYF对ARE大鼠的肠组织具有保护作用，并总结了几种DEG，表明TXYF介导的ARE功效的可能机制。