目的 构建放射性肠损伤大鼠模型，观察丁酸钠对肠损伤的保护作用。方法 SPF级成年SD大鼠90只，分为对照组、模型组和丁酸钠组，每组各30只。除对照组外，造模大鼠暴露腹部上至胸骨剑突下至耻骨联合，VarianClinic600直线加速器6MV高能X射线定位照射，其余部位用5 cm厚铅砖屏蔽，单次照射，总吸收剂量10 Gy。造模前3 d，丁酸钠组SD大鼠ig 40 mg/kg丁酸钠，1次/d，照射后继续给药3 d，对照组和模型组ig生理盐水。多普勒血流仪检测肠黏膜血流量；FITC荧光标记的葡聚糖检测肠黏膜血管通透性；ELISA法检测外周血浆二胺氧化酶（DAO）活性和肠组织一氧化氮（NO）水平；肠黏膜组织切片HE染色，显微镜下测量肠黏膜绒毛高度、黏膜厚度。结果 丁酸钠组造模成功率为83.3%，显著低于模型组的100%（P<0.05）。模型组和丁酸钠组肠黏膜血流量、黏膜绒毛高度和黏膜厚度显著低于对照组（P<0.05、0.01），丁酸钠组肠黏膜血流量、黏膜绒毛高度和黏膜厚度显著高于模型组（P<0.05）。模型组和丁酸钠组肠黏膜葡聚糖、DAO和NO显著高于对照组（P<0.05），丁酸钠组肠黏膜葡聚糖、DAO和NO显著低于模型组（P<0.05）。结论 丁酸钠可以增加放射性肠损伤大鼠肠黏膜血流量，降低NO表达，发挥肠黏膜保护作用。

Objective To establish radiation-induced intestinal injury rat model and study the protective effect of sodium butyrate on intestinal injury. Methods Totally 90 adult SPF SD rats were divided into control group, model group, and sodium butyrate group, with 30 rats in each group. Except for the control group, the model rats were exposed to 6MV high energy X-ray localization irradiation from abdomen to sternal xiphoid process and pubic symphysis. The rest parts were shielded with 5 cm thick lead brick, single irradiation, and the total absorbed dose was 10 Gy. SD rats in the sodium butyrate group were ig administrated with sodium butyrate (40 mg/kg, once daily) for 3 d. The control group and model group were given normal saline. The intestinal mucosal blood flow was detected by Doppler blood flow meter. The intestinal mucosal vascular permeability was detected by FITC labeled dextran. DAO and NO in peripheral blood were detected by ELISA analysis. Intestinal mucosal tissue sections were treated with HE staining, and the villus height and mucosal thickness of intestinal mucosa were measured under microscope. Results The success rate of modeling in sodium butyrate group was 83.3%, which was significantly lower than that of 100% in model group (P<0.05). In the model and intervention group, the intestinal mucosal blood flow, villous height and thickness of mucous membrane were significantly lower than that in control group (P<0.05 or 0.01), but the intestinal mucosal blood flow, villus height and the thickness of the mucosa in intervention group were significantly higher than that in model group (P<0.05). In the model and intervention group, the dextran, DAO, and NO were significantly higher than that in control group (P<0.05), but the dextran, DAO, and NO in intervention group were significantly lower than that in model group (P<0.05). Conclusion Sodium butyrate can increase the intestinal mucosal blood flow, reduce the expression of NO, and protect intestinal mucosa in rats with intestinal injury induced by radiation.