AIM: To explore the influence of prednisone on cell apoptosis of the peripheral blood mononuclear cell (PBMC) in children with primary nephrotic syndrome (PNS). METHODS: According to the results of prednison after tre...AIM: To explore the influence of prednisone on cell apoptosis of the peripheral blood mononuclear cell (PBMC) in children with primary nephrotic syndrome (PNS). METHODS: According to the results of prednison after treatment, we divided 50 cases into two groups. 37 cases were steroid responsive and 13 were not responsive. Taking blood from the two groups before and after prednison treatment (in the 2nd, 4th, 6th and 8th weeks), we calculated the apoptosis rate of PBMC. RESULTS: There was no significant differences in the apoptosis rate of PBMC between the two groups and the normal control before treatment. The apoptosis rate of PBMC increased obviously after the patients were treated in the 2nd, 4th, 6th weeks, and the highest was in the second week ( P <0.05, P < 0.01 ), in comparison with that before the treatment. During the eighth week, the apoptosis rate of PBMC was obviously higher in the steroid unresponsive than that of steroid response ( P <0.05). CONCLUSIONS: The cell apoptosis may be involved in the regulations during the process of treatment. Some disorders of cell apoptosis may be responsible for the steroid unresponsiveness in children with nephrotic syndrome.展开更多
文摘AIM: To explore the influence of prednisone on cell apoptosis of the peripheral blood mononuclear cell (PBMC) in children with primary nephrotic syndrome (PNS). METHODS: According to the results of prednison after treatment, we divided 50 cases into two groups. 37 cases were steroid responsive and 13 were not responsive. Taking blood from the two groups before and after prednison treatment (in the 2nd, 4th, 6th and 8th weeks), we calculated the apoptosis rate of PBMC. RESULTS: There was no significant differences in the apoptosis rate of PBMC between the two groups and the normal control before treatment. The apoptosis rate of PBMC increased obviously after the patients were treated in the 2nd, 4th, 6th weeks, and the highest was in the second week ( P <0.05, P < 0.01 ), in comparison with that before the treatment. During the eighth week, the apoptosis rate of PBMC was obviously higher in the steroid unresponsive than that of steroid response ( P <0.05). CONCLUSIONS: The cell apoptosis may be involved in the regulations during the process of treatment. Some disorders of cell apoptosis may be responsible for the steroid unresponsiveness in children with nephrotic syndrome.
