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烟雾吸入性损伤修复模型IL-1β和PGE2的动态变化分析

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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.
Analysis of dynamic changes of interleukin 1β and prostaglandin E2 in smoke inhalation injury repair model
AIM: To investigate the dynamic changes of interleukin 1 β ( 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 upregulated in 1 d group[(196.2±67.8) ng/L] 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-1 β concentration was the lowest at day 21 [ (9.3±3.7) ng/L] and no significant differ-ence was observed compared with that in normal group (P >0.05). PGE2 concentrations were upregulated 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 play some important role in the smoke inhalation injury repair.

interleukin 1βdinoprostonesmoke inhalation injuryrepair

淦鑫、郭光华、王年云

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南昌大学第一附属医院呼吸科,江西,南昌,330006

南昌大学第一附属医院烧伤科,江西,南昌,330006

白细胞介素-1β 地诺前列酮 烟雾吸入损伤 修复

2009

第四军医大学学报
第四军医大学

第四军医大学学报

CSTPCDCSCD北大核心
影响因子:0.599
ISSN:1000-2790
年,卷(期):2009.30(15)
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