2019 年 68 巻 3 号 p. 301-306
Inflammation-related animal model is necessary to better understanding the association of inflammation with tumorigenesis. Although mouse models of inflammation-related lung tumorigenesis on A/J mice strain have been set up in previous study, there is no report on the model on C57BL/6J mice. In this study, C57BL/6J mice were randomly divided into two groups and instilled with benzo(a)pyrene [B(a)p] plus lipopolysaccharide (LPS) with different treatments. Mice in Group I were instilled intratracheally with B(a)p (1 mg/mouse) and LPS (5 µg/mouse), once a week for 4 times, on Tuesday and Friday, respectively [the week of the last time of B(a)p treatment named Week 0]. At Week 4, mice continued to be treated with LPS, once every four weeks for 5 times. Mice in Group II were exposed to B(a)p (1 mg/mouse, once a week for 4 times) and 3 weeks later instilled intratracheally with LPS (2.5 µg/mouse) once every three weeks for 5 times. At Week 30, the incidence, number, size and histopathology of lung tumor in two models were compared. The tumor incidence (96.97%) and mean tumor count (13.0 ± 12.4) of mice in Group II were significantly increased compared with those in Group I (69.23%, 4.9 ± 5.1), respectively. In addition, smaller tumors (≤1 mm) were more abundant in Group II than Group I. Histopathological examination found the tumors induced by B(a)p plus LPS in Group II were more advanced tumors. In conclusion, a better mouse model of inflammation-related lung tumorigenesis induced by B(a)p plus LPS in C57BL/6J mice was set up successfully.