Objectives. In an attempt to develop new method of treating the end ormid stage pancreatic cancer, we examined the effect of ischemic re perfusion injury plus particle embolism on the pathology and cell apoptosis of p...Objectives. In an attempt to develop new method of treating the end ormid stage pancreatic cancer, we examined the effect of ischemic re perfusion injury plus particle embolism on the pathology and cell apoptosis of pancreatic cancer in Sprague Dawely rats. Methods. 9 mg dimethylbeneanthracine (DMBA) were implanted directly into the parenchyma of pancreatic tail of Sprague Dawely rats. After establishment of tumor, the inferior splenic artery, a main supplying vessel to pancreatic tail was subjected to blockade and re opening for 30 min separately, then embolism particles were infused via the artery. Afterwards, artery was ligated. Pathological changes and cell apoptosis indicators (AI) of pancreatic cancer were observed by light microscopy and ISEL respectively 14 days after the operation. Results. The prevalence of pancreatic cancer among DMBA implanted rats evaluated 3 months to 4 months after implantation was 59%. The volumes of the tumor in positive control group (B), pancreatic ischemic group (C), pancreatic ischemic re perfusion injury group (D) were significantly larger than pancreatic ischemic re perfusion injury plus particle thrombus group (E) (P< 0.01). Thevolumes of the tumor in groups D, E were significantly smaller than that in group C (P< 0.01). There was a significant difference in tumor size between group Band group C (P< 0.01), but the difference was not significant between group D and group E (P >0.05). There was a significant infiltration of tumor tissue in group B rats, but strong inflammatory reaction was not noted. In groups C, D, E, alocalized tumor growth was observed; infiltration of inflammatory cells and proliferation of fibroblasts and connective fiber were obvious, and some of these fibers grew into cancer nests and separate the tumor. The above findings were most conspicuous in group E. There was a significant difference in AI between group E (13.7±1.5)and other groups (P< 0.01), with the difference being also significant between group C(4.3±2.4), D (8.5±1.1)and group B (1.2±0.8)(P< 0.01), and between group C and group D (P< 0.01) or between group D and group E (P< 0.01). In the samples of group A, the apoptotic cells were not found. Conclusions. Pancreatic ischemic re perfusion injury plus particle thrombus can cause significant infiltration of inflammatory cells in tumor tissues thereby limiting its growth, and inducing cell apoptosis of pancreatic cancer. This effect is superior to either pancreatic ischemia alone or pancreatic ischemia plus re perfusion injury.展开更多
基金This study was supportedbytheChinaHealthSciencesFoundation(No.981134).
文摘Objectives. In an attempt to develop new method of treating the end ormid stage pancreatic cancer, we examined the effect of ischemic re perfusion injury plus particle embolism on the pathology and cell apoptosis of pancreatic cancer in Sprague Dawely rats. Methods. 9 mg dimethylbeneanthracine (DMBA) were implanted directly into the parenchyma of pancreatic tail of Sprague Dawely rats. After establishment of tumor, the inferior splenic artery, a main supplying vessel to pancreatic tail was subjected to blockade and re opening for 30 min separately, then embolism particles were infused via the artery. Afterwards, artery was ligated. Pathological changes and cell apoptosis indicators (AI) of pancreatic cancer were observed by light microscopy and ISEL respectively 14 days after the operation. Results. The prevalence of pancreatic cancer among DMBA implanted rats evaluated 3 months to 4 months after implantation was 59%. The volumes of the tumor in positive control group (B), pancreatic ischemic group (C), pancreatic ischemic re perfusion injury group (D) were significantly larger than pancreatic ischemic re perfusion injury plus particle thrombus group (E) (P< 0.01). Thevolumes of the tumor in groups D, E were significantly smaller than that in group C (P< 0.01). There was a significant difference in tumor size between group Band group C (P< 0.01), but the difference was not significant between group D and group E (P >0.05). There was a significant infiltration of tumor tissue in group B rats, but strong inflammatory reaction was not noted. In groups C, D, E, alocalized tumor growth was observed; infiltration of inflammatory cells and proliferation of fibroblasts and connective fiber were obvious, and some of these fibers grew into cancer nests and separate the tumor. The above findings were most conspicuous in group E. There was a significant difference in AI between group E (13.7±1.5)and other groups (P< 0.01), with the difference being also significant between group C(4.3±2.4), D (8.5±1.1)and group B (1.2±0.8)(P< 0.01), and between group C and group D (P< 0.01) or between group D and group E (P< 0.01). In the samples of group A, the apoptotic cells were not found. Conclusions. Pancreatic ischemic re perfusion injury plus particle thrombus can cause significant infiltration of inflammatory cells in tumor tissues thereby limiting its growth, and inducing cell apoptosis of pancreatic cancer. This effect is superior to either pancreatic ischemia alone or pancreatic ischemia plus re perfusion injury.
