Objective: To explore the effect of glycyrrhizin (GA) on the proliferation, invasion and migration of non-small cell lung cancer HCC827 andA549 cells via regulating miR-142/ZEB1 (Zinc finger E-box-binding homeobox 1) axis. Methods:After being cultured and transfected, HCC827 andA549 cells were divided into 4 groups: NC group (untransfected+3 mmol/L GA), miR-142 inhibitor group (miR-142 knockdown+3 mmol/L GA), pcDNA3.1-ZEB1 group (ZEB1 over-expression+3 mmol/L GA) and pcDNA3.1-ZEB1+ miR-142 mimic group (ZEB1 over-expression+miR-142+3 mmol/L GA). qPCR was used to detect the expression level of miR-142 in HCC827 andA549 cells treated with different concentrations of GA. MTT and Transwell assays were used to examine the proliferation, invasion and migration of HCC827 and A549 cells. WB was used to detect the expression level of ZEB1 protein in HCC827 and A549 cells. Dual-luciferase reporter gene assay was used to explore the relationship between miR-142 and ZEB1. Results: GA significantly inhibited the proliferation, invasion and migration of HCC827 and A549 cells, and up-regulated the expression level of miR-142 ( P < 0.05 or P <0.01). Dual-luciferase reporter gene assay showed that miR-142 could targetedly combine with 3'-UTR of ZEB1 and downregulate the expression of ZEB1 ( P <0.05 or P <0.01). Further experiment validated that GAinhibited ZEB1 expression via up-regulating miR-142, thus suppressed proliferation, invasion and migration of HCC827 and A549 cells ( P <0.05 or P <0.01). Conclusion: GA inhibits the proliferation, invasion and migration of NSCLC HCC827 and A549 cells, the mechanism of which is that GA inhibits the malignant biological behavior of NSCLC HCC827 andA549 cells via up-regulating the inhibition effect of miR-142 on ZEB1.

ObjectiveTo investigate the molecular mechanism of action of artemisinin in attenuating asthmatic airway inflammation and airway remodeling through the phosphoinositide 3-kinase（PI3K）/protein kinase B（Akt） signaling pathway. MethodFifty male SD rats were randomly divided into blank group， model group， and low-dose， medium-dose， and high-dose groups of artemisinin， with 10 rats in each group. The ovalbumin （OVA）-induced asthma model of the rats was established， and after successful modeling， the blank group and model group received tail vein injection of 1.0 mL·kg^-1 normal saline， while the low-dose， medium-dose， and high-dose groups of artemisinin received tail vein injection of 12.5， 25， and 50 mg·kg^-1 artemisinin daily for seven days. Airway resistance was measured by the acetylcholine chloride method. Cell number and species changes in the alveolar lavage fluid of each group were determined by flow cytometry. Morphological changes in airway endothelial tissue were determined by the hematoxylin-eosin （HE） staining method. Apoptosis was determined by CytoTox 96 method， and enzyme-linked immunosorbent assay （ELISA） method was used to determine the NOD-like receptor thermal protein domain associated protein 3 （NLRP3） inflammasome， interleukin-1β （IL-1β）， and interleukin-10 （IL-10） expression. Western blot method was used to detect the （p）-PI3K/p-Akt level in the alveolar bronchial tissue of each group. ResultCompared with the blank group， the total number of cells， total number of macrophages， total number of eosinophils， total number of lymphocytes， and total number of neutrophils were significantly higher in the model group （P<0.05）. HE staining showed that the airway mucosa of the rats had obvious edema， and a large number of inflammatory cells were infiltrated （P<0.05）. The rate of apoptosis was significantly higher （P<0.05）， and the levels of the inflammasome NLRP3， IL-1β， and IL-10 increased significantly （P<0.05）. p-PI3K/p-Akt level increased significantly （P<0.05）. Compared with the model group， the total number of cells， total number of macrophages， total number of eosinophils， total number of lymphocytes， and total number of neutrophils were significantly decreased after the intervention of artemisinin at low， medium， and high concentrations （P<0.05）. HE staining showed that the degree of edema of the airway mucosa of the rats was reduced， and the area of the inflammatory cell infiltration was drastically reduced （P<0.05）. The apoptosis rate was significantly reduced （P<0.05）， and the levels of the inflammasome NLRP3， IL-1β， and IL-10 decreased significantly （P<0.05）. p-PI3K/p-Akt level decreased significantly （P<0.05）. ConclusionArtemisinin significantly inhibits NLRP3 inflammasome activation， reduces cellular pyroptosis and inflammatory cell expression， and attenuates airway inflammatory manifestations and airway remodeling in asthmatic rats， which may be related to the regulation of p-PI3K/p-Akt， and the results may provide laboratory insights and basis for the treatment of bronchial asthma with artemisinin.