医学IL1β对成纤细胞合成Ⅰ型胶原蛋白作用及机制.docVIP

IL1β对成纤维细胞合成Ⅰ型胶原蛋白作用及机制 作者：李学森 褚言琛 邹云雯 王志杰 【摘要】 目的 研究白细胞介素1β (IL1β)对成纤维细胞合成Ⅰ型胶原蛋白的作用及机制，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IL1β组、IL1β+SB202190(p38 MAPK特异性阻断剂)组和对照组,各组经无血清培养20 h后，IL1β组加入10 μg/L的IL1β，IL1β+SB202190组用10 μmol/L的SB202190预作用1 h后加入10 μg/L的IL1β，对照组直接加体积分数0.02的血清。各组培养24 h后收集细胞，采用RTPCR法检测Ⅰ型胶原α2基因(COL1A2)mRNA的表达，Western blotting法检测COL1A2蛋白的表达。结果 IL1β组COL1A2 mRNA和COL1A2蛋白表达均明显低于IL1β+SB202190组和对照组，差异有显著性(F=55.67、251.01,q=11.88～28.79,Plt;0.01);IL1β+SB202190组低于对照组，但差异无显著性(q=1.88、2.93,Pgt;0.05)。结论 IL1β可能通过抑制NIH3T3细胞COL1A2的合成而抑制硬膜外瘢痕的形成，p38信号通路在IL1β抑制瘢痕形成过程中起到重要的作用。 【关键词】 白细胞介素1;p38信号通路;硬膜外隙;瘢痕;成纤维细胞;胶原蛋白 [ABSTRACT] Objective To investigate the role and mechanism of interleukin1β in the synthesis of typeⅠ collagen by fibroblast so as to explore the impact of interleukin1β on the formation of epidural scar. Methods The NIH3T3 cells were divided into three groups: IL1β group, IL1β + SB202190 (specific p38 MAPK blocker) group and control group. After serumfree culturing for 20 hours, 10 μg/L of IL1β was added to IL1β group. The IL1β + SB202190 group was treated with SB202190 (10 μmol/L) for 1 hour before adding IL1β (10 μg/L), and the control group received same volume of 2% serum. After culturing for another 24 hours, cells were collected, and both mRNA and protein expressions of typeⅠ collagen A2 (COL1A2) detected with RTPCR and Western blotting, respectively. Results The mRNA and protein expressions of COL1A2 in IL1β group were significantly lower than that of the IL1β + SB202190 group and the control group (F=55.67, 251.01;q=11.88-28.79;Plt;0.01). The expressions of COL1A2 mRNA and protein in IL1β + SB202190 group were lower than that of the control group, but the difference was not significant (q=1.88,2.93;Pgt;0.05). Conclusion IL1β might inhibit the formation of epidural scar by inhibiting the expression of COL1A2 in NIH3T3 cells, and p38 signaling pathway may play an important role in the process of scar formation. 　　[KEY WORD