中文摘要：

目的研究苯肾上腺素对大鼠颌下腺放射损伤后水通道蛋白5（Aquaporin 5，AQP5）表达的影响。方法取Wistar大鼠27只，随机分为空白对照组、单纯照射组及照射给药组（照射后1h通过腹腔注射给予大鼠苯肾上腺素5mg／kg。两次／天），以直线加速器对大鼠颌下腺区域行20Gyx射线照射。照射后7天取大鼠颌下腺组织，采用免疫组织化学法检测大鼠颌下腺AQP5蛋白质分子的定位与表达；免疫印迹法（Western blot）半定量检测大鼠颌下腺AQP5蛋白质表达的丰度变化。结果免疫组织化学结果显示：在空白对照组AQP5分子主要表达在颌下腺腺泡细胞及导管细胞的顸膜和侧膜，呈针孔样表现；单纯照射组AQP5分子在腺泡及导管细胞顶膜和侧膜的表达较空白对照组明显减少；而苯肾上腺素连续给药组AQP5分子在腺泡及导管细胞顶膜及侧膜的表达较单纯照射组显著增加。Western blot结果显示：单纯照射组AQP5蛋白质的表达较空白对照组减少了71．6％（P〈0．05），照射给药组AQP5的表达较单纯照射组增加了42．6％（P〈0．05）。结论大鼠颌下腺AQP5在放射损伤早期表达下调，而给予苯肾上腺素能够上调AQpS的表达，提示苯肾上腺素促放射损伤后涎腺腺体修复的机制可能与活化1-肾上腺素受体刺激AQP5的表达增加有关。

英文摘要：

Objective To investigate the effect of phenylephrine on the expression of AQP5 in irradiated submandibular gland in rat during the early stage. Methods 27 Wistar rats were randomly divided into three groups： the control group, the simple irradiated group, and the irradiated group with phenylephrine treatment[phenylephrine （Smg/kg） was intraperitoneally injected after irradiation, twice per day], 20 Gy X-ray irradiation was delivered to the submandibular region by applying a medical linear accelerator. After seven days, submandibular glands were removed. The distribution and expression of AQP5 was then detected by immunohistochemical assay, and the protein expression of AQP5 was determined by Western Blot. Results The distribution of AQP5 was mainly located in the apical membrane and lateral membrane of both acinar cells and ductal cells in the control group, was decreased in the apical membrane and lateral membrane of acinar cells and ductal cells in the simple irradiated group, and was markedly increased in the irradiated group with phenylephrine treatment. Also, results from Western Blot demonstrated that the expression of AQP5 protein was down-regulated 71.6% （P〈0.05） in the simple irradiated group compared with the control group, but was up-regulated 42.6% （P〈0.05） in the irradiated group with phenylephrine treatment compared with the simple irradiated group. Conclusion The expression of AQP5 in the rat submandibular gland could be decreased after irradiation during the early stage and could be increased by phenylephrine treatment. The results indicated that the mechanism of treatment phenylephrine improving salivary gland recovery after irradiation damage might be involving in the increased expression of AQP5 by activation of ctl-adrenergic receptor, which might provide a new strategy in preventing and treating salivary gland irradiated damage.