目的 構(gòu)建放射性腸損傷大鼠模型，觀察丁酸鈉對(duì)腸損傷的保護(hù)作用。方法 SPF級(jí)成年SD大鼠90只，分為對(duì)照組、模型組和丁酸鈉組，每組各30只。除對(duì)照組外，造模大鼠暴露腹部上至胸骨劍突下至恥骨聯(lián)合，VarianClinic600直線加速器6MV高能X射線定位照射，其余部位用5 cm厚鉛磚屏蔽，單次照射，總吸收劑量10 Gy。造模前3 d，丁酸鈉組SD大鼠ig 40 mg/kg丁酸鈉，1次/d，照射后繼續(xù)給藥3 d，對(duì)照組和模型組ig生理鹽水。多普勒血流儀檢測(cè)腸黏膜血流量；FITC熒光標(biāo)記的葡聚糖檢測(cè)腸黏膜血管通透性；ELISA法檢測(cè)外周血漿二胺氧化酶（DAO）活性和腸組織一氧化氮（NO）水平；腸黏膜組織切片HE染色，顯微鏡下測(cè)量腸黏膜絨毛高度、黏膜厚度。結(jié)果 丁酸鈉組造模成功率為83.3%，顯著低于模型組的100%（P<0.05）。模型組和丁酸鈉組腸黏膜血流量、黏膜絨毛高度和黏膜厚度顯著低于對(duì)照組（P<0.05、0.01），丁酸鈉組腸黏膜血流量、黏膜絨毛高度和黏膜厚度顯著高于模型組（P<0.05）。模型組和丁酸鈉組腸黏膜葡聚糖、DAO和NO顯著高于對(duì)照組（P<0.05），丁酸鈉組腸黏膜葡聚糖、DAO和NO顯著低于模型組（P<0.05）。結(jié)論 丁酸鈉可以增加放射性腸損傷大鼠腸黏膜血流量，降低NO表達(dá)，發(fā)揮腸黏膜保護(hù)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.