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目的探讨治疗和预防直肠癌患者围手术期放射性小肠损伤的有效方法及其机制。方法应用复制缺陷型单纯疱疹病毒(HSV)作为锰超氧化物歧化酶(MnSOD)和(或)绿色荧光蛋白(GFP)基因载体转染小鼠小肠上皮;应用逆转录聚合酶链反应(RT-PCR)测定MnSOD在小鼠小肠上皮细胞内的表达,酶活性检测法测定MnSOD活性;全腹腔照射(0,7.5,10.0,12.5,15 Gy)24 h和72 h后取标本,应用SZ-PT光学系统测量小肠绒毛的长度。结果MnSOD在小鼠小肠上皮细胞过度表达,酶活性检测表明,MnSOD活性显著增高,转染组MnSOD对超氧阴离子的抑制率达39.33%±0.67%。全腹腔照射24 h和72h后,对照组小鼠小肠绒毛长度分别降低了40.1%~59.3%和44.2%~65.1%;而MnSOD组小鼠小肠绒毛长度分别降低了3.1%~12.4%和6.3%~29.1%,两者差异具有统计学意义(P<0.01)。结论复制缺陷型HSV作为载体可有效转染MnSOD。小肠上皮内MnSOD的过度表达具有显著的放射性保护作用。
Objective To investigate the effective methods and mechanisms of radiation therapy for the treatment and prevention of perioperative radiation-induced intestinal damage in patients with rectal cancer. Methods Mouse intestinal epithelium was transfected with replication-defective herpes simplex virus (HSV) as a vector of manganese superoxide dismutase (MnSOD) and / or green fluorescent protein (GFP). Reverse transcriptase-polymerase chain reaction PCR) was used to detect the expression of MnSOD in mouse intestinal epithelial cells. MnSOD activity was measured by enzymatic activity assay. The samples were taken 24 h and 72 h after intraperitoneal irradiation (0, 7.5, 10.0, 12.5, 15 Gy) The optical system measures the length of the intestinal villus. Results MnSOD was overexpressed in mouse intestinal epithelial cells and the activity of MnSOD was significantly increased. The inhibitory rate of MnSOD to superoxide anion in the transfected group was 39.33% ± 0.67%. After 24 h and 72 h of whole abdominal irradiation, the small intestine villus length of control mice decreased by 40.1% -59.3% and 44.2% -65.1%, respectively, while that of MnSOD mice decreased by 3.1% -12.4% and 6.3%, respectively ~ 29.1%, the difference between the two groups was statistically significant (P <0.01). Conclusion Replication-defective HSV as a vector can effectively transfect MnSOD. Overexpression of MnSOD in the small intestinal epithelium has significant radioprotective effect.