Objective:To investigate the mechanism of overexpression of miR-320e in inhibiting inflammatory response of re-spiratory syncytial virus(RSV)infected bronchial epithelial cells.Methods:Human bronchial epithelial cells 16HBE were cultured in vitro and infected with RSV,and cells were divided into Con group,RSV group,RSV+miR-NC group,RSV+miR-320e group,RSV+miR-320e+vector group,RSV+miR-320e+TLR4 group.RT-qPCR was used to detect expression levels of miR-320e and TLR4 mRNA;MTT to detect cell proliferation changes;flow cytometry to detect cell apoptosis;Western blot was used to detect Bcl-2,Bax,TLR4,IκBα,p-IκBα,NF-κB and p-NF-κB protein expressions;ELISA to detect TNF-α,IL-6,IL-1β and IFN-α,IFN-β expres-sions;dual luciferase experiment to verify the tageting relationship between miR-320e and TLR4.Results:Compared with Con group,miR-320e expression level,survival rate,Bcl-2 and IκBα protein expressions were significantly reduced,apoptosis rate,Bax protein expression,TNF-α,IL-6,IL-1β and IFN-α,IFN-β expressions,TLR4 mRNA and protein expression,and p-IκBα protein expres-sion and p-NF-κB/NF-κB were increased significantly in RSV group.Compared with RSV+miR-NC group,miR-320e expression level,survival rate,IFN-α,IFN-β expressions,Bcl-2 and IκBα protein expressions were significantly increased,apoptosis rate,Bax pro-tein expression,TNF-α,IL-6,IL-1β expressions,TLR4 mRNA and protein expression,and p-IκBα protein expression and p-NF-κB/NF-κB in RSV+miR-320e group were significantly reduced.miR-320e targets and negatively regulates the expression of TLR4.Up-regulation of TLR4 can partially restore the effect of overexpression of miR-320e on apoptosis and inflammatory response of RSV-infected bronchial epithelial cells 16HBE.Conclusion:miR-320e inhibits 16HBE apoptosis and inflammation in RSV-infected bronchial epi-thelial cells by targeting and negatively regulating TLR4 expression.

ObjectiveTo explore the effect of Polygonati Odorati Rhizoma polysaccharides on hyperlipidemia in mice by modulating the gut microbiota. MethodsNinety male C57BL/6J mice were randomized into the following groups （n=15）： control， model， simvastatin， low- （100 mg·kg^-1）， medium- （200 mg·kg^-1）， and high-dose （400 mg·kg^-1） Polygonati Odorati Rhizoma polysaccharides groups. Other groups except the control group were fed with a high-fat diet for the modeling of hyperlipidemia， and drug interventions lasted for 12 weeks. Serum levels of total cholesterol （TC）， triglycerides （TG）， low-density lipoprotein cholesterol （LDL-C）， and high-density lipoprotein cholesterol （HDL-C） were measured by an automatic biochemical analyzer. The pathological changes in the liver and epididymal fat were observed by hematoxylin-eosin staining， and lipid accumulation in the liver was assessed by oil red O staining. The gut microbiota was analyzed by 16S rRNA gene sequencing. ResultsCompared with the control group， the model group exhibited an increase in body weight （P<0.01）， along with marked elevations in serum levels of TC， TG， and LDL-C （P<0.05，P<0.01）. Furthermore， the model group showcased increase in the liver index and epididymal fat coefficient （P<0.05）， increased liver fat accumulation， enlargement of adipocytes in the epididymal fat， decreases in both alpha and beta diversity of the gut microbiota， and an increase in the relative abundance of Allobaculum （P<0.01）. Compared with the model group， Polygonati Odorati Rhizoma polysaccharides suppressed the increase in body weight （P<0.01）， lowered the serum levels of TC， TG， and LDL-C （P<0.05，P<0.01）， reduced the liver index and epididymal fat coefficient （P<0.05）， alleviated liver fat accumulation， and decreased the size of adipocytes in the epididymal fat. Furthermore， it enhanced the alpha and beta diversity of the gut microbiota in mice， reduced the relative abundance of Allobaculum， Erysipelotrichaceae， and Clostridium （P<0.01）， and increased the relative abundance of Akkermansia and Blautia （P<0.01）. ConclusionPolygonati Odorati Rhizoma polysaccharides can ameliorate hyperlipidemia induced by a high-fat diet in mice by regulating the diversity and composition of the gut microbiota.

The theory of "liver opens at the eyes" was first seen in Yellow Emperor's Internal Canon of Medicine， which is the ancient people's summary of the connection between the liver and the eyes. The theory of "liver opens at the eyes" suggests the characteristic of "co-damage and co-recover of liver and eyes". It has been found in clinical practice that liver diseases and eye diseases often occur together， and "liver and eyes co-recover" is an ideal choice. The key to achieving "liver and eyes co-recover" is to analyze its pharmacological material basis and mechanism. With the development of modern medicine， more and more evidence indicates that the liver and eyes have complex and close relationships in physiological and pathological aspects. In a pathological state， there is a phenomenon of "liver and eyes co-damage"， and after the intervention of traditional Chinese medicine， "liver and eyes co-recover" occurs. "Liver and eyes co-damage and co-recover" can be explained through the "co-material basis and co-action mechanism". On this basis， the research group tentatively proposed that the liver and eyes had "four common characteristics" （4CCs）， namely "co-damage， co-recover， co-material basis， and co-action mechanism" from the theoretical connotation of traditional Chinese medicine， clinical practice， and molecular biology. Additionally， the group also took the intervention of Prunella vulgaris， traditional Chinese medicine， for removing liver fire and improving eyesight on immune liver injury （ILI） and allergic conjunctivitis （AC） as examples to analyze 4CCs. This project aims to deeply analyze the scientific connotation of the theory of "liver opens at the eyes"， reveal the common characteristics and biological essence of liver and eyes， explore a new research paradigm of "liver and eyes co-recover"， and provide a reference for the study of common problems of multi-organ associated diseases.