Aim: To observe the effect of neutron radiation on intestinal epithelial cells 6 (IEC-6), to study the effect of IL-2 on the proliferation and recovery of neutron-injured IEC-6, and to investigate the regulatory mechanisms of IL-2 on the injured IEC-6.
Methods: 4Gy-neutron-injured IEC-6 were treated by IL-2, with or without the blocking agent JAK(1) (A77-1726). The change of proliferative activity and death manner of the treated IEC-6 were detected by MTT colorimetry and flow cytometry at 10, 15, 30 minutes and 1, 3, 6, 12, 24, 48, 72 hours respectively. The expression of IL-2Rbeta and the activation of JAK(1) of neutron-injured IEC-6 treated by IL-2 were detected by immunocytochemical stainning and Western blot.
Results: After IEC-6 were radiated by 4 Gy neutron for 24 hours, the proliferative activity of IEC-6 decreased markedly but increased strikingly after IL-2 treatment (P<0.05). The apoptosis of IEC-6 in IL-2-treated group decreased (P<0.05), but there was no obvious difference in necrotic cell number. After neutron-injured IEC-6 were treated by IL-2, JAK(1) was activated at 10 and 15 minutes, and the expression of IL-2Rbeta increased apparently at 24 hours. When treated by JAK(1) and IL-2, the proliferative activity of neutron-injured IEC-6 was much lower than that in IL-2-treated group.
Conclusion: IL-2 can accelerate the proliferation of neutron-radiated IEC-6 and protect them from neutron injury. IL-2Rbeta and JAK(1) participate in the regulation of neutron-injured IEC-6 by IL-2.
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