α-干扰素对血管瘤血管内皮细胞周期、凋亡的影响

目的 观察α-干扰素对体外培养血管瘤内皮细胞周期、凋亡的影响,探讨干扰素治疗血管瘤的机制.方法 用组织块法培养增生期血管瘤内皮细胞,分别用1×104U,1×105U,1×106Uα-干扰素干预,对照组不加任何药物,继续培养24h后,用流式细胞仪检测细胞周期、凋亡变化.结果 α-干扰素作用24 h后血管瘤内皮细胞G1期前出现二倍体凋亡峰;1×104U、1×105U、1×106Uα-干扰素组G1期百分率分别为(63.68±0.66)%、(72.97±1.56)%、(63.27±5.64)%,对照组为(58.75±0.32)%,与对照组比较,P＜0.05;1×104U、1×105U、1×106Uα-干扰素组S期百分率分别为(32.99±2.01)%、(25.02±1.31)%、(37.93±5.31)%,对照组为(26.46±1.94)%,与对照组比较,P＞0.05;1×104U、1×105U、1×106Uα-干扰素组G2/M期百分率分别为(0.01±0.05)%、(2.43±0.27)%、(3.99±1.27)%,其百分率随α-干扰素浓度升高而增高.细胞凋亡百分率随α-干扰素浓度增加而增高,1×104U、1×105U、1×106Uα-干扰素组凋亡百分率分别为(11.89±0.56)%、(18.88±3.04)%、(31.92±1.92)%,对照组凋亡率为(3.25±0.23)%,与对照组比较,P＜0.01.结论 α-干扰素能导致血管瘤血管内皮细胞G1、G2期阻滞和凋亡,细胞凋亡率与药物浓度存在剂量依赖关系.干扰素可能通过血管内皮细胞G1、G2期阻滞,抑制血管瘤血管内皮细胞的增殖、诱导血管内皮细胞凋亡而达到治疗血管瘤的作用.

Interferon-a induces apoptosis in vascular endothelial cells in vitro

Objective To study the mechanism of interferon-α in hemangioma treatment. Methods The hemangioma vascular endothelial cells isolated from hemangioma were cultured. The cells were treated with 1×104 U, 1×105 U, 1×106U interferon-α fior 24 hours. The changes of cell cycles and apoptosis were assessed by flow cytometry. Results The percentage of G1 phase cells increased with the increasing concentration of interferon-α, and the hypodiploid apoptosis peak appeared before G1 phase. In the interferon-α treated groups (1×104 U,1×105 U, 1×106 U), the percentage of G1 phase were (63. 68 ± 0.66) %, (72. 97 ± 1.56) %, (63.27 ± 5.64) %respectively whereas in the control group, it was (58. 75 ± 0. 32) %. The percentages of S phase cells in the treated groups were (32. 99 ±2. 01 ) %, (25.02 ± 1.31 ) %, (37.93 ± 5.31 ) %, respectively whereas in the control group, it was (26.46±1.94) %. The percentage of G2/M phase were (0.01 ± 0.05) %, (2. 43 ± 0. 27) %, (3. 99 ±1.27) %. The percentage of S phase cells in the treated and the control groups showed no statistically significant change (P＞0.05). The G1, G2/M phase percentage of each group revealed significant differences (P＜0.01). The apoptosis rates in the treated groups were (11.89 ± 0. 56)%, (18.88 ±3.04) %, (31.92 ± 1.92) % respectively. Compared to the control group of 3.25 ± 0.2) %, the apoptosis rates were increased (P＜0.01 ). Conclusions The mechanisms of the interferon-α in hemangioma treatment might be related with G1, G2 arrest and apoptosis. The rate of apoptosis increase was dose-dependent.