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目的探讨核转录因子-κB(NF-κB)抑制剂吡咯烷二硫代氨基甲酸(PDTC)对脂多糖(LPS)所致急性肺损伤(ALI)大鼠NF-κB P65蛋白表达的影响。方法雄性大鼠54只,随机分三组。对照组(N组)6只,腹腔注射生理盐水3 ml/kg。ALI组(L组)24只,腹腔注射LPS 3 mg/kg。PDTC干预组(P+L组)24只,先腹腔注射PDTC 120 mg/kg,0.5 h后再腹腔注射LPS 3 mg/kg。后两组分别于腹腔注射LPS后1、2、4、8 h作为观测时间点。观察肺组织胞质及胞核中NF-κB P65蛋白表达强度的变化。结果 ALI组各时相肺组织胞质中P65蛋白的表达强度较对照组显著降低(P<0.01),而胞核中P65蛋白表达强度较对照组显著升高(P<0.01),但PDTC干预组P65蛋白与ALT组比较,肺组织胞质中P65蛋白的表达强度较ALT组升高(P<0.05),而胞核中P65蛋白表达强度较ALT组降低(P<0.05)。结论 LPS引起肺组织NF-κB P65蛋白由胞质向胞核转移而活化,NF-κB参与炎症的调控,在ALI中发挥重要作用。而PDTC可抑制炎性介质的表达和释放,可有效地减轻LPS所致大鼠ALI。
Objective To investigate the effects of pyrrolidine dithiocarbamate (PDTC), an inhibitor of NF-κB, on the expression of NF-κB P65 protein in acute lung injury (ALI) induced by lipopolysaccharide (LPS). Methods 54 male rats were randomly divided into three groups. Control group (N group) 6, intraperitoneal injection of saline 3 ml / kg. ALI group (L group) 24, intraperitoneal injection of LPS 3 mg / kg. Twenty-four PDTC intervention groups (P + L group) were injected intraperitoneally with PDTC 120 mg / kg and intraperitoneal injection of LPS 3 mg / kg 0.5 h later. The latter two groups were injected intraperitoneally LPS 1,2,4,8 h as the observation time point. The changes of NF-κB P65 protein expression in the cytoplasm and nucleus of lung tissue were observed. Results The expression of P65 protein in the cytoplasm of lung tissue in ALI group was significantly lower than that in control group (P <0.01), while the expression of P65 protein in nucleus was significantly higher than that in control group (P <0.01) Compared with ALT group, the expression of P65 protein in cytoplasm of lung tissue in P65 group was higher than that in ALT group (P <0.05), while the expression of P65 protein in nucleus was lower than that in ALT group (P <0.05). Conclusion LPS causes NF-κB P65 protein activation in the lung from the cytoplasm to the nucleus. NF-κB is involved in the regulation of inflammation and plays an important role in ALI. PDTC can inhibit the expression and release of inflammatory mediators, which can effectively reduce ALI induced by LPS in rats.