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目的探讨大鼠烧伤后早期切痂对肺组织核因子-κB(NF-κB)活化和促炎细胞因子表达的影响,进一步阐明烧伤早期切痂有利于控制全身炎症反应的机制。方法采用Wistar大鼠Ⅲ°35%TBSA烧伤模型,实验分正常对照组(A组)、烧伤后非切痂组(B组)和烧伤后早期切痂组(C组)。大鼠烧伤后12、24h凝胶电泳迁移率分析法(EMSA)检测肺组织NF-κB活性;逆转录-聚合酶链式反应(RT-PCR)检测肺组织TNF-αmRNA表达;酶联免疫吸附分析(ELISA)检测肺组织TNF-α含量。数据采用Excel统计分析软件行t检验。结果B组大鼠伤后12、24h肺组织NF-κB活性分别为(19.56±1.36)×10~4积分灰度值(A)和(15.23±1.94)×10~4A,均明显高于A组[(4.36±0.38)×10~4A,P<0.01]。B组伤后12h肺组织TNF-αmRNA表达(1.37±0.47)较A组(0.28±0.04)升高(P<0.01),TNF-α含量(1.88±0.75)ng/ml也明显高于A组[(0.62±0.05) ng/ml,P<0.01]。C组肺组织NF-κB活性伤后12h为(7.12±1.15)×10~4A,24h为(6.33±0.90)×10~4 A,分别较B组显著降低(P<0.01);C组大鼠肺组织伤后12、24h时TNF-αmRNA表达和含量均显著低于B组(P<0.01)。结论严重烧伤可激活大鼠肺组织NF-κB,烧伤后早期切痂可有效抑制肺组织NF-κB活化,从而下调肺组织对致炎细胞因子的合成和释放,减轻机体全身炎症反应。
Objective To investigate the effect of early escharectomy on nuclear factor-κB (NF-κB) activation and proinflammatory cytokine expression in lungs of rats after burn, and to further elucidate the mechanism by which escharectomy is beneficial to control the systemic inflammatory response. Methods The Wistar rats were divided into 3 groups (35% TBSA burn). The rats were divided into normal control group (group A), non-bums after burn group (group B) and early escharectomy group (group C). The expression of TNF-αmRNA in lung tissue was detected by reverse transcription-polymerase chain reaction (RT-PCR) at 12,24 h after EMSA and the expression of TNF-α mRNA in lung tissue was detected by enzyme linked immunosorbent assay The levels of TNF-α in lung tissue were detected by ELISA. Data using Excel statistical analysis software t test. Results The NF-κB activities of lung tissue in group B were (19.56 ± 1.36) × 10-4 integral gray value (A) and (15.23 ± 1.94) × 10-4A, respectively, which were significantly higher than those of A Group [(4.36 ± 0.38) × 10 ~ 4A, P <0.01]. The level of TNF-α mRNA (1.37 ± 0.47) in group B was significantly higher than that in group A (0.28 ± 0.04) (P <0.01) and TNF-α (1.88 ± 0.75) ng / ml in group B [(0.62 ± 0.05) ng / ml, P <0.01]. The activity of NF-κB in lung tissue of group C was (7.12 ± 1.15) × 10-4A at 12h after injury, and (6.33 ± 0.90) × 10-4A at 24h respectively, which was significantly lower than that in group B (P <0.01) The expression of TNF-αmRNA and the content of TNF-αin lung tissue of rats were significantly lower than those in group B at 12 and 24 hours after injury (P <0.01). Conclusion Severe burns can activate NF-κB in rat lung tissue and early post-burn excision can effectively inhibit the activation of NF-κB in lung tissue, thereby reducing the synthesis and release of inflammatory cytokines in lung tissue and alleviating the systemic inflammatory response.