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目的:比较持续静压力与白介素-1β(IL-1β)诱导藻酸盐凝胶培养的兔纤维环细胞损伤模型的效果。方法:构建体外兔纤维环细胞凝胶培养模型,并将其分入5组:A组(空白对照组),B组(IL-1β10ng/ml,干预24h),C组(IL-1β10ng/ml,干预48h),D组(1Mpa静压力,持续24h),E组(1Mpa静压力,持续48h)。CCK-8法及流式细胞仪分别检测细胞增殖和凋亡情况;RT-PCR检测I、II型胶原、基质金属蛋白酶-3(MMP-3)及组织金属蛋白酶抑制因子-1(TIMP-1)的表达情况。结果:①两种方法均使纤维环细胞增殖减缓、凋亡增加。在D、E两组中这种作用更加明显。②RT-PCR结果显示,两种方法均使I、II型胶原表达减弱,其中E组II型胶原表达较A组下降约75%(P<0.01),最为明显;随着干预时间延长,两种方法均使MMP-3表达增强;两种损伤模型中,TIMP-1的表达在24h干预后均出现降低,而干预48h后又有所回升。结论:体外持续静态压力能够诱发与IL-1β干预相似的兔纤维环细胞损伤,可作逐步发展为构建体外纤维环细胞损伤模型的常规方法。
Objective: To compare the effects of continuous static pressure and rabbit alveolar epithelial cell injury model induced by interleukin-1β (IL-1β). Methods: Rabbit fibroblasts cultured in vitro were divided into 5 groups: group A (blank control group), group B (IL-1β10ng / ml, intervention 24h), group C (IL-1β10ng / ml , Intervention 48h), group D (1Mpa static pressure for 24h), group E (1Mpa static pressure for 48h). The proliferation and apoptosis of cells were detected by CCK-8 and flow cytometry respectively. The expressions of collagen type I, II, MMP-3 and TIMP-1 ) Of the expression. Results: ① Both methods slowed the proliferation of fibrocystic ring cells and increased the apoptosis. This effect was more pronounced in D and E groups. ② The results of RT-PCR showed that the expressions of type I and type II collagen decreased in both of the two methods. The expression of type II collagen in group E was decreased by about 75% (P <0.01) compared with that in group A, which was the most obvious. With the prolongation of intervention time, The expression of MMP-3 increased in both of the two models. The expression of TIMP-1 in both of the two models decreased after 24h intervention, but recovered after 48 hours intervention. CONCLUSION: Continuous static pressure in vitro can induce the injury of rabbit fibrocystic ring cells similar to the intervention of IL-1β, and can be gradually developed into a routine method for constructing a fibrocystic cell damage model in vitro.