摘要
[目的]研究白介素1β(IL-1β)对成纤维细胞合成基质金属蛋白酶3的作用及机制,以探讨IL-1β对硬膜外瘢痕形成的影响。[方法]将NIH3T3细胞随机分为3组,分别为IL-1β组、IL-1β+SB202190(p38MAPK特异性阻断剂)组和对照组,各组经无血清培养20h后,IL-1β组加入10ng/ml的IL-1β、IL-1β+SB202190组用10μmol/L的SB202190预作用1h后加入10ng/ml的IL-1β,对照组直接加2%血清。各组细胞培养24h后收集细胞,采用RT-PCR和Western blotting检测MMP-3的表达。[结果]IL-1β组MMP-3表达较对照组明显增加(P<0.01);IL-1β+SB202190组MMP-3的表达较IL-1β组明显减少(P<0.01),但与对照组无明显差异(P>0.05)。[结论]IL-1β可促进NIH3T3细胞MMP-3的合成,可能对硬膜外瘢痕的形成有一定的抑制作用,而p38通路在IL-1β抑制瘢痕形成过程中起到重要的作用。
[Objective]To investigate the role and mechanism of interleukin-1β on fibroblast synthesis of matrix metalloproteinase-3,and explore the impact of interleukin-1β on the formation of epidural scar.[Method]The NIH3T3 cells were divided into three groups：IL-1β group,IL-1β ＋ SB202190 group and control group. After serum-free culture for 20 hours,IL-1β group was treated by IL-1β （10ng/ml） and IL-1β ＋ SB202190 group was treated by the SB202190 （10μmol/L） for 1 hour before treatment with IL-1β（10ng/ml） and the control group was treated with 2% serum. Then those 3 groups were cultured for 24 hours under standard conditions （37℃ in a humidified atmosphere flushed with 5% CO2 in air）. The expression of MMP-3 gene was examined by RT-PCR and Western blotting.[Result]The expression of MMP-3 significantly increased in the IL-1β group than that in the control group（P0.01）. The expression of MMP-3 in the IL-1β ＋ SB202190 group significantly reduced compared with IL-1β group（P0.01）,but no significant difference was noted between the IL-1β ＋ SB202190 group and the control group（P0.05）. [Conclusion]IL-1β could stimulate the expression of MMP-3 in NIH3T3 cells which might inhibit the formation of epidural scar. Besides,the author found that the p38 pathway played an major role in this process.
出处
《中国矫形外科杂志》
CAS
CSCD
北大核心
2010年第10期849-852,共4页
Orthopedic Journal of China
基金
青岛市科技局科研项目(编号:KZJ-30)
