Effect of Qingjin Huatan Decoction on transferrin and Iron regulatory protein in COPD rats

Objective:To explore the mechanism of Qingjin Huatan Decoction in regulating iron metabolism by regulating inflammatory factors in the inflammatory environment of chronic obstructive pulmonary disease.Methods:The COPD model was prepared by tracheal drops of lipopolysaccharide(LPS)combined with smoke.40 rats were randomly divided into normal group,COPD group,roxithromycin western medicine group and Qingjin Huatan Decoction traditional Chinese medicine group(n=10).Post-molding drug administration intervention,Qingjin Huatan Decoction Chinese medicine group was given 14.62 g/kg(Qingjin Huatan Decoction),roxithromycin western medicine group was given 0.01575 g/kg(roxithromycin),COPD group and normal group were given normal saline 10 mL/kg,twice a day.The expressions of Hepcidin,IL-1β,IL-10 and TGF-β1 in serum of rats in each group were detected by ELISA.WesternBlot and qRT-PCR were used to detect the expression of TF and IREB2 protein and mRNA in lung tissues of each group.Results:Compared with the normal group,the contents of serum Hepcidin and IL-10 in COPD group were significantly decreased(P<0.01),while the contents of serum IL-1βand TGF-β1 were significantly increased(P<0.01,P<0.05).Compared with COPD group,the contents of serum Hepcidin and IL-10 were significantly increased in the two drug groups(P<0.01),while the contents of serum IL-1βand TGF-β1 were significantly decreased in the two drug groups(P<0.05).Compared with normal group,TF mRNA and protein expression in COPD group were increased(P<0.01),while IREB2 mRNA and protein expression were decreased(P<0.01).Compared with COPD group,TF mRNA and protein expressions in lung tissues of the two-drug group were decreased(P<0.01,P<0.05),while IREB2 mRNA and protein expressions were increased(P<0.01).Conclusion:Iron metabolism is related to inflammation.Qingjin Huatan Decoction can regulate iron metabolism in inflammatory environment to treat COPD.

Qingjin Huatan decoction attenuates lipopolysaccharide-induced acute lung injury in mice by controlling platelet-associated formation of neutrophil extracellular traps

Background:Acute lung injury(ALI)is a severe and life-threatening lung inflammation with high morbidity and mortality,underscoring the importance to develop effective drugs.Qingjin Huatan decoction(QJHTD),as a classic ancient prescription,has been widely used for treating respiratory diseases.However,the role and mechanism of QJHTD against ALI remain unclear.Objective:This study aimed to explore the therapeutic effect of QJHTD on lipopolysaccharide(LPS)-induced ALI in mice and uncover its mechanism.Methods:The therapeutic effect of QJHTD on LPS-induced ALI in mice was evaluated by the histopathological changes in the lung tissue,the lung wet/dry weight ratio,and the levels of inflammatory cytokines and thrombin-antithrombin complexes.Transcriptomics was used to predict the mechanism of QJHTD in treating ALI.The expression levels of citrullinated histone 3 in the lung tissue,the content of cell-free DNA in the bronchoalveolar lavage fluid(BALF),and the platelet-associated formation of neutrophil extracellular traps(NETs)in vitro were determined.Results:Qingjin Huatan decoction exerted protective effect against LPS-induced ALI by suppressing interstitial edema,maintaining the alveolar-capillary barrier,inhibiting the infiltration of neutrophils and platelets in the lung tissue,and lowering the levels of tumor necrosis factorα,interleukin 1β,interleukin 6,and thrombin-antithrombin complexes in BALF.Kyoto Encyclopedia of Genes and Genomes pathway enrichment analysis indicated that the formation of NETs was the main regulatory pathway for QJHTD against ALI.Qingjin Huatan decoction could treat ALI by inhibiting the release of NETs via reducing the content of citrullinated histone 3 in lung tissue and cell-free DNA in BALF in vivo,and suppressing the NETs formation induced by LPS-stimulated platelets under flow and static conditions in vitro.The formation of NETs was considered to bridge the interactions between neutrophils and platelets.Conclusions:This research demonstrated the effects of QJHTD in treating ALI and provided new insights for clarifying the complex regulation of neutrophils,platelets,and NETs in ALI.