Animal Model of Lung Adenoma in C57BL/6J Mice Induced by Urethane / 中国药学杂志

OBJECTIVE: To compare and optimize the animal model of lung cancer on C57BL /6J mice by three different experimental methods. METHODS: Female C57BL /6J mice were divided into four groups: control group, model group , Ⅱ and III. The mice in model groupreceived 800 mg•kg-1 urethane by intraperitoneal injection twice a week, followed by 5 weeks. The mice in model group Ⅱ were injected intraperitoneally with 1 000 mg•kg-1 urethane in the same way with model group . The mice in model group III received urethane at the dose of 1 000 mg•kg-1 intraperitoneally, every 5 day continuing for 8 weeks. The control group was given equal volume of sodium chloride solutions in the same way as the model group Ⅱ. The main organs of all the groups were taken such as heart, liver, spleen, lung, kidney, brain and thymus at the 28th week, and their organs index was calculated. At the same time the lung tissues were examined to get the amount of adenomas and the diameters, and developed the lung and thymus histopathological examination. The bronchial alveolar lavage fluids were collected to classify the cells of the control and experimental groups. RESULTS: Compared with the control group, all the three experimental groups could induce lung adenomas absolutely, the number of tumors in model groupand III was 6, while tumors in model Ⅱ group was about 2. In the three experimental groups the index of lung increased and the brain, spleen and thymus decreased compared with the control group. The bronchial alveolar lavage fluids analysis showed that the number of lymphocytes and polymorphonuclear leukocytes in the model group are more than that in control group. CONCLUSION: All the three experimental groups could induce lung adenomas absolutely. Compared with model group Ⅱ, the model III and are more stable and homogeneous with the similar results of experiment.

Lung adenoma development and NK activity in mice treated with multiple carcinogens

A wide-spectrum initiation model was investigated in mice. Sequential treatments with diethylnitrosamine, urethane and N-methylnitrosourea, with or without a promoter, phenobarbital, resulted in tumor formation in the lungs in 85-90% of animals, but did not produce any tumorous lesions in other organs. The lung tumors were adenomas and the mean number of adenomas was 2.2-2.6 per mouse. Phenobarbital combination had no additive effect on lung tumor incidence and multiplicity. Splenic NK cell activity showed inconsistent increment in the carcinogen plus phenobarbital-treated group during the experiment (P less than 0.05).