摘要
目的探讨白细胞分化抗原14(CD14)-Toll样受体4(TLR4)-核因子激活的B细胞的κ-轻链增强(NF-κB)信号传导通路在脂多糖(LPS)诱导急性肺损伤/急性呼吸窘迫综合征(ALI/ARDS)中作用及机制。方法于2020年1—12月,选取购自北京宝元兴业科技有限公司的清洁级健康雄性SD大鼠90只,分为A、B、C三组,每组各30只,C组为正常大鼠模型组,B组为ALI/ARDS模型组大鼠,A组为ALI/ARDS+CD14、TLR4以及NF-κB模拟物模型组大鼠,比较三组大鼠相关指标的差异。结果造模12 h后,A、B、C三组大鼠的呼吸频率(RR)分别是(127.92±17.04)次/分、(87.51±8.42)次/分、(55.28±3.73)次/分,A组>B组>C组,动脉血氧分压(PaO2)分别是(7.63±1.16)mmHg、(10.58±1.65)mmHg、(13.46±2.05)mmHg,A组<B组<C组,均差异有统计学意义(P<0.05)。A、B、C三组大鼠的CD14蛋白表达水平分别是(0.94±0.23)、(0.69±0.18)、(0.48±0.13),TLR4蛋白表达水平分别是(0.97±0.26)、(0.65±0.13)、(0.43±0.11),NF-κB P65蛋白表达水平分别是(1.03±0.28)、(0.67±0.17)、(0.47±0.12),脂多糖蛋白表达水平分别是(0.98±0.27)、(0.66±0.16)、(0.45±0.12),均A组>B组>C组,均差异有统计学意义(P<0.05)。Pearson相关性分析显示,A组大鼠的脂多糖蛋白分别与CD14蛋白、TLR4蛋白以及NF-κB P65蛋白均呈正相关(P<0.05)。结论CD14-TLR4-NF-κB信号传导通路能够增强脂多糖表达并促进机体炎性活动,参与ALI/ARDS的发生发展。
Objective To investigate the role and mechanism of leukocyte differentiation antigen 14(CD14)-Toll like receptor 4(TLR4)-nuclear factor-activatedκ-light chain enhancement(NF-κB)signaling pathway in lipopolysaccharide(LPS)induced acute lung injury/acute respiratory distress syndrome(ALI/ARDS).Methods From January 2020 to December 2020,90 SPF SD rats purchased from Beijing Baoyuan Xingye Technology Co.,LTD were assigned into three groups:A,B and C group,30 rats in each group.Group C was the normal rat model group,group B was the ALI/ARDS model group,group A was the ALI/ARDS+CD14,TLR4 and NF-κB mimic model group.The differences of related indexes among the three groups were compared.Results 12 hours after the establishment of the model,the respiratory rate(RR)of rats in groups A,B and C was(127.92±17.04)times/min,(87.51±8.42)times/min,and(55.28±3.73)times/min,respectively,group A>group>group C;the arterial partial blood oxygen pressure(PaO2)was(7.63±1.16)mmHg,(10.58±1.65)mmHg,and(13.46±2.05)mmHg,group A<group B<group C;and the difference was statistically significant(P<0.05).The expres⁃sion level of CD14 protein in group A,B and C was(0.94±0.23),(0.69±0.18)and(0.48±0.13),respectively,TLR4 protein was(0.97±0.26),(0.65±0.13)and(0.43±0.11),respectively,NF-κB P65 protein was(1.03±0.28),(0.67±0.17)and(0.47±0.12),respectively,lipid polyglycol protein was(0.98±0.27),(0.66±0.16)and(0.45±0.12),respectively,group A>group B>group C,and the differences were sta⁃tistically significant(P<0.05).Pearson correlation analysis showed that LPS protein in group A was positively correlated with CD14 pro⁃tein,TLR4 Protein and NF-κB p65 protein,respectively(P<0.05).Conclusion CD14-TLR4-NF-κB signaling pathway can enhance the expression of LPS and promote inflammatory activity of the body,and participate in the development of ALI/ARDS.
作者
金肇权
张文彬
陈欣
朱滨
JIN Zhaoquan;ZHANG Wenbin;CHEN Xin;ZHU Bin(Department of Emergency,Changzhou First People's Hospital,Changzhou Jiangsu 213000,China)
出处
《安徽医药》
CAS
2022年第4期643-647,共5页
Anhui Medical and Pharmaceutical Journal
基金
江苏省第五期“333工程”培养项目(KY201711)。
