Abstract
Basic fibroblast growth factor (bFGF) is the growth factor which accelerates cell proliferation differentiation, cell migration and angiogenesis. Previous studies have shown that administration of bFGF enhances epithelial cell proliferation and restitution as well as crypt stem cell survival after radiation injury to the intestine. In this study we examined the effect of bFGF on acute radiation induced injury in rat small intestine. Six-weeks male Wistar rats were administered 4 mg/kg bFGF intraperitoneally at 25 hours before irradiation. The jejunum and the colon tissue were removed at 3, 6, 16 hours, 1, 2, 3 and 5 days after 8 Gy whole-body irradiation. The sections were stained H&E. The length of villi and crypt in the jejunum were measured, and the number of apoptotic and mitotic cells per crypt were counted. We performed immunohistochemical staining against the Ki-67 antigen. The expression of PCNA, p53, p21 and Bax after irradiation were examined by Western blot analyses. The length of villi in the jejunum of control rats was decreased at 1, 2, 3 days after irradiation. In contrast, the length of villi of rat treated with bFGF was higher than that of control until 2 days after irradition. The length of crypt was also similar. bFGF treatment reduced the number of apoptotic cells per jejunum crypt at 3 and 6 h after irradiation to 29 % and to 11 % of the control values. bFGF treatment increased the number of mitotic cells at 2, 3 and 5 days after irradiation compared to control value. The Ki-67-positive cells in the jejunum of rat treated with bFGF were higher than in control rat. PCNA expression in rat treated with bFGF was significantly higher than in control at 2 days after irradiation. bFGF treatment resulted in decreases of p53 accumulation, p21 and Bax expression at 3 and 6 hours after irradiation. Our results suggested that bFGF has a protective effect against acute radiation-induced injury in rat jejunum by suppressing the apoptotic cells including the stem cells and accelerating the crypt cell proliferation.
