摘要
目的:探讨IL-1β和PGE2在新西兰白兔烟雾吸入性损伤修复中动态水平变化.方法:新西兰白兔36只,随机分为正常对照组、烟雾吸入性损伤后第1,4,7,14,21日,共6组,应用ELISA方法检测各组IL-1β和PGE2的水平.建立烟雾吸入性损伤修复模型,光镜下观察烟雾吸入对新西兰白兔气管、肺组织的病理变化.结果:①病理变化表明烟雾吸入性损伤第1,4,7日组以损伤后炎症反应为主(损伤期),第14,21日组以损伤后修复为主(修复期);②ELISA结果表明:IL-1β含量在烟雾吸入性损伤后第1日[(196.2±67.8)ng/L]立即升高,与正常对照组[(7.1±0.2)ng/L]比较有统计学差异(P<0.05),至第7日[(398.5±161.4)ng/L]达到顶峰后逐渐下降,至第21日[(9.3±3.7)ng/L]最低,与正常对照组比较无统计学差异;PGE2含量在烟雾吸入性损伤后第1日[(4.4±1.0)μg/L]至14日[(120.9±61.1)μg/L]逐渐升高,在第14日达到顶峰后下降,第14日组与正常对照组[(4.4±1.0)μg/L]比较有显著差异(P<0.05),至第21日[(6.4±2.8)ng/L]最低,与正常对照组比较无统计学差异.结论:通过建立烟雾吸入性损伤修复模型,观察IL-1β与PGE2的动态水平变化,可为临床上判断烟雾吸入性损伤修复过程不同阶段(损伤期、修复期)提供帮助,也表明IL-1β与PGE2在烟雾吸入性损伤修复过程中可能具有重要作用.
AIM:To investigate the dynamic changes of interleukin 1β ( IL-1β ) and prostaglandin E2 ( PGE2 ) levels in smoke inhalation injury repair in New Zealand white rabbits. METHODS : New Zealand white rabbits ( n = 36 ) were randomly divided into normal control group, and 1,4, 7, 14 and 21 d after smoke inhalation injury groups, with 6 animals in each group. ELISA was used to measure the levels of IL-1β and PGE2. The smoke inhalation injury repair model was established and the pathologic changes of smoke inhalation on trachea and lung tissues were observed by light microscope. RESULTS: The pathologic changes showed that mainly inflammatory reaction (injury stage) was seen in 1, 4 and 7 d after injury groups and mainly repair (repair stage) was observed in 14 and 21 d after injury groups. The results of ELISA showed that IL-1β concentration was upregn- lated in 1 d group[ ( 196.2 -±67.8) ng/L1 after smoke inhalation injury, higher than that in normal group[ (7.1±0.2) ng/L, P 〈 0.05 ]. IL-1β concentration peaked at day 7 [ ( 398.5 ± 161.4 ) ng/L] and then began to decrease. IL-1β concentration was the lowest at day 21 [ (9.3 ± 3.7) ng/L] and no significant difference was observed compared with that in normal group (P 〉 0.05 ). PGE2 concentrations were upregnlated gradually from 1 d [ (4.4 ± 1.0)μg/L] to 14 d[ ( 120.9 ± 61.1 ) μg/L] following smoke inhalation injury. PGE2 concentrations peaked at day 14 and then began to decrease, with significant difference from those in normal control group [ (4350 ± 1021 ) ng/L,P 〈 0.05 ]. PGE2 concentration was the lowest at day 21 [ (6423± 2812 ) ng/L], with no significant difference from that in normal group (P 〉 0.05). CONCLUSION: The dynamic changes of IL-1β and PGE2 levels in smoke inhalation injury repair may indicate the different stages (injury stage or repair stage) of smoke inhalation injury repair process. IL-1β and PGE2 levels may important role in the smoke inhalation injury repair.
出处
《第四军医大学学报》
CAS
北大核心
2009年第15期1371-1374,共4页
Journal of the Fourth Military Medical University