RESUMEN
Objective To investigate the protective effect and possible mechanism of amentoflavone (AF) on bone marrow cells of mice injured by irradiation. Methods Primary bone marrow cells of male C57BL/6 mice were cultured and randomly divided into 4 groups (normal control, radiation control,AF 2.5μmol/L and 5μmol/L), with 3 samples in each group. After treated with AF for 12 h, the cells were injured by 12 Gy 60Coγirradiation. 6 h and 12 h post-irradiation, apoptosis was evaluated by using Hoechst 33258 stain, cell cycle was determined by flow cytometry while the level of TNF-α was tested by ELISA. Results The cell cycle arrest and apoptosis were not significantly affected by Amentoflavone. Amentoflavone (5 μmol/L)could significantly inhibit the production of TNF-α on cell supernatant of mouse bone marrow cells at 6 h or 12 h after radiation and 2.5 μmol/L Amentoflavone could significantly inhibit the production of TNF-α at 6 h after radiation. Conclusion Taken together, the data suggest that AF may have radioprotection against damage in mice bone marrow by inhibiting the production of TNF-α.
RESUMEN
Objective To investigate the protective effect and possible mechanism of amentoflavone (AF) on bone marrow cells of mice injured by irradiation. Methods Primary bone marrow cells of male C57BL/6 mice were cultured and randomly divided into 4 groups (normal control, radiation control,AF 2.5 μmol/L and 5 μmol/L), with 3 samples in each group. After treated with AF for 12 h, the cells were injured by 12 Gy60Co γ irradiation. 6 h and 12 h post-irradiation, apoptosis was evaluated by using Hoechst 33258 stain, cell cycle was determined by flow cytometry while the level of TNF-α was tested by ELISA. Results The cell cycle arrest and apoptosis were not significantly affected by Amentoflavone. Amentoflavone 5 μmol L) could significantly inhibit the production of TNF- α on cell supernatant of mouse bone marrow cells at 6 h or 12 h after radiation and 2.5 μmol/L Amentoflavone could significantly inhibit the production of TNF- α at 6 h after radiation. Conclusion Taken together, the data suggest that AF may have radioprotection against damage in mice bone marrow by inhibiting the production of TNF-α.
RESUMEN
In order to evaluate the changes in T cell subsets after acute irradiation injury, and investigate the mechanism of deficiency of cellular immunity in acute irradiation syndrome, Balb/c mice were exposed to a single total body irradiation of 5Gy gamma rays from a 60 Co source. On days 10, 28 and 120, the amounts of CD4 + and CD8 + subsets in spleen cells were evaluated by flow cytometry (FCM), and expression of IL 4 gene in ConA stimulated spleen cells was evaluated by reverse transcription linked polymerase chain reaction, in which ?-actin gene was used as an internal control. It was found that after irradiation, the ratio of CD4 + /CD8 + became significantly higher than that of the controls, and then the ratio lowered gradually until day 120. However, it still did not return to the level of the controls. On day 10, expression of IL 4 gene at mRNA level increased significantly. The results indicated that CD8 + subset was more radiosensitive than CD4 + , and the pattern of cytokine seeretion shifted to that of Th2 soon after irradiation.