汉黄芩苷抑制NOD2过度激活缓解人支气管上皮细胞炎症及脓毒症小鼠肺损伤OA

[Objective]To investigate the effects of baicalein on inflammation model of human bronchial epithelial cells and acute lung injury in mice with sepsis.[Methods]An inflammation model of human bronchial epithelial cells induced by lipopolysaccharide(LPS)was established,and the cells were divided into control group,model group(LPS 10 ng·mL-1),baicalin 25 μmol·L-1 group,baicalin 50 μmol·L-1 group and baicalin 100 μmol·L-1 group,and the cells were treated with baicalin for 24 h.A sepsis model was established in C57BL/6 mice through cecum puncture,and the mice were randomly divided into sham operation group,operation group and baicalin 50 mg·kg-1 group,with 10 mice in each group.The drug was administered at 0,6,12,18 and 24 h after surgery by intraperitoneal injection.One hour after the last administration,bronchoalveolar lavage fluid(BALF)and lungs were taken from mice.Expression levels of IL-1β,IL-6 and TNF-α in model cells and mice BALF were detected by ELISA,reactive oxygen species(ROS)kit was used to detect the levels of ROS in cells,nuclear factor-κB(NF-κB)p65 nuclear translocation in cells was detected with immunofluorescence,HE staining was used to observe the inflammation in lungs,and nucleotide-binding oligomerization domain-containing protein 2(NOD2)expression in model cells and lung tissues,NF-κB p65 and phosphorylated-NF-κB p65(p-NF-κB p65)protein expression levels in lung tissues detected by Western blot.[Results]Compared with model group,baicalin significantly reduced the levels of IL-1β,IL-6 and TNF-α(P<0.05,P<0.01),decreased ROS levels(P<0.01),and inhibited NF-κB p65 nuclear translocation in cells.Compared with operation group,baicalin significantly lowered the levels of IL-1β,IL-6 and TNF-α in BALF(P<0.01)and alleviated inflammatory infiltration in lung tissues(P<0.05).Mechanistic studies showed that baicalin significantly inhibited the protein expression of NOD2 and p-NF-κB p65/NF-κB p65(P<0.01).[Conclusion]Baicalin significantly inhibits LPS-induced inflammation in human bronchial epithelial cells and lung inflammation in mouse sepsis model caused by cecum puncture,which may be related to the inhibition of NOD2 expression.