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目的观察核因子(NF)κB活化在大鼠烧伤后早期心肌组织表达肿瘤坏死因子(TNF)α及心肌功能损害中的作用,进一步阐明烧伤后早期心肌功能损害的发生机制。方法将170只Wistar大鼠随机分为对照组(20只)、烧伤组(90只)、吡咯烷二硫代氨基甲酸盐(PDTC)组(60只)。后两组大鼠均于背部造成35％TBSAⅢ度烧伤后,立即腹腔注射等渗盐水,且PDTC组同时皮下注射PDTC 250 mg／kg。对照组除不烧伤外,其余处理同烧伤组。伤后3、6、12、24 h采用八导生理记录仪记录左心室收缩压(LVSP),左心室舒张末期压(LVEDP),室内压最大上升、下降速率(+dp／dtmax、-dp／dtmax);逆转录聚合酶链反应和原位杂交法观察心肌组织TNF-αmRNA的表达。伤后1、3、6、12、24 h采用凝胶电泳迁移率变动分析法检测心肌组织NF-κB活性,以积分吸光度(A)值表示。对照组作相同检测。结果伤后3～24 h烧伤组大鼠LVSP、±dp／dtmax低于对照组(P<0．01),而LVEDP高于对照组(P<0．01)。伤后3 h烧伤组大鼠心肌组织TNF-αmRNA表达明显高于对照组, 6 h达峰值(P<0．01),它在心肌细胞中表达尤为明显。伤后1 h烧伤组大鼠心肌组织NF-κB活性迅速升高[积分A值为(20．3±3．4)×104],明显高于对照组积分A值(2．2±0．4)×104,3 h时达峰值,24 h时仍高于对照组(P<0．01)。与烧伤组比较,PDTC组上述指标有较明显的改善(P< 0．01)。结论大鼠严重烧伤后心肌组织NF-κB被活化,使其表达和释放促炎细胞因子,在心肌功能损害发生过程中起重要作用。
Objective To investigate the role of nuclear factor (NF) κB activation in the expression of tumor necrosis factor α (TNF α) and myocardial dysfunction in early postburn myocardium in rats, and to further elucidate the mechanism of early myocardial injury after burn injury. Methods 170 Wistar rats were randomly divided into control group (n = 20), burn group (n = 90) and pyrrolidine dithiocarbamate group (n = 60). Immediately after 35% TBSA third degree burns on the back, the rats in the latter two groups were injected intraperitoneally with isotonic saline immediately. PDTC group was given subcutaneous injection of PDTC 250 mg / kg. In addition to the control group does not burn, the rest deal with the burn group. The left ventricular systolic pressure (LVSP), left ventricular end-diastolic pressure (LVEDP), maximal increase of indoor pressure, and the rate of decrease (+ dp / dtmax, -dp / dtmax); Reverse transcription polymerase chain reaction and in situ hybridization were used to observe the expression of TNF-αmRNA in myocardium. At 1, 3, 6, 12 and 24 hours after injury, the activity of NF-κB in myocardium was detected by gel electrophoretic mobility shift assay and expressed as integral absorbance (A). Control group for the same test. Results The levels of LVSP and ± dp / dtmax in burn group were significantly lower than those in control group (P <0.01), while LVEDP was higher in control group (P <0.01). The expression of TNF-α mRNA in myocardium of burn rats 3 h after injury was significantly higher than that of the control group (P <0.01) at 6 h, especially in cardiomyocytes. The activity of NF-κB in myocardium rapidly increased in burn group 1 h after injury (the integral A was (20.3 ± 3.4) × 104), which was significantly higher than that of the control group (2.2 ± 0. 4) × 104, peaked at 3 and 3 h, still higher than that of the control group at 24 h (P <0.01). Compared with the burn group, the above indexes of PDTC group had obvious improvement (P <0.01). Conclusion The myocardial NF-κB is activated after severe burn in rats, which can induce the expression of proinflammatory cytokines and release of proinflammatory cytokines, which play an important role in the process of cardiac dysfunction.