单次大剂量X线照射对大鼠胰腺的损伤作用

目的观察单次大剂量X线照射后,胰腺放射性损伤随照射时间的改变情况,为大分割放疗正常组织的保护提供实验依据。方法以6 MV-X线12 Gy照射大鼠腹部,在不同时间观察胰腺形态学改变,免疫组织化学方法测定Bcl-2、Bax蛋白的表达。结果照射后7 d腺细胞萎缩,个别坏死,14 d腺细胞间纤维增生,42 d腺细胞增生。照射后21 d胰岛细胞间出现纤维增生。随照射时间延长,腺细胞中Bcl-2蛋白表达阳性率升高,各实验组与对照组比较差异有显著性（t=7.44~148.40,P〈0.001）,随照射时间延长Bax蛋白表达由可疑阳性变为阴性,仅照射后2 d时与对照组相比差异有显著性（t=4.43,P〈0.001）。随照射时间延长,胰岛细胞中Bcl-2蛋白表达阳性率升高,Bax表达阳性率降低,与对照组相比差异有显著性（t=7.11~85.80,P〈0.001）。结论单次大剂量照射后,胰岛细胞间仅发生纤维增生;腺细胞初始有一过性急性损伤,然后出现代偿性修复,机制可能与随照射时间延长抗凋亡基因bcl-2表达渐增高,凋亡基因bax表达降低有关。

DAMAGE OF RAT PANCREAS AFTER A SINGLE LARGE-DOSE RADIATION

Objective To observe the damage of pancreas after a single high-dose X-ray radiation,and provide experimental evidence for clinical application of hyper-fractionated radiotherapy. Methods The abdominal areas of rats were radiated by 12 Gy 6 MV X-ray.At different time points after radiation,the morphologic changes of pancreatic tissue were observed and the expressions of Bcl-2 and Bax proteins were measured with immunohistochemistry technique. Results Seven days after radiation exposure,acinar cells showed atrophy with individual necrotic cells;14 days after,interstitial fibroplasias could be seen,and gland cell hyperplasia was observed after 42 days.With prolongation of exposure time,the positive expression of Bcl-2 protein in the experiment groups increased,which were significantly different from that of the control group（t=7.44-148.40,P〈0.001）.Along with the extension of the exposure time,the expressions of Bax protein in the experiment groups changed from probable positive to negative,with only those mice at second post-irradiation day showed statistical difference from the control group（t=4.43,P〈0.001）.In islet cells,the expression of Bcl-2 protein increased,while the expression of Bax protein decreased,which were statistically different from those of the control groups（t=7.11-85.80,P0.001）. Conclusion After a single high-dose radiation,only fibroplasia was seen in islet cells.Initially,there was a transient acute injury followed by compensatory repairing.The possible mechanism may be related to the increased expression of bcl-2 and reduced expression of Bax.