ObjectiveTo reveal the pharmacological mechanisms of astragaloside Ⅳ（AS-Ⅳ）in treating diabetic retinopathy based on network pharmacology and molecular docking and to provide reference for new drug development and mechanism research. MethodPotential targets of AS-Ⅳ were obtained from SwissTargetPrediction and Targetnet. The targets of diabetic retinopathy were screened using GeneCards，Online Mendelian Inheritance in Man（OMIM） and Therapeutic Target Database. The targets of AS-Ⅳ and diabetic retinopathy were intersected by Venny 2.1.0. STRING platform and Cytoscape 3.7.2 were used to construct protein-protein interaction（PPI） network and screen core targets， respectively. Then，Gene ontology （GO） and Kyoto Encyclopedia of Genes and Genomes （KEGG） pathway enrichment analyses were performed. Furthermore，the binding affinity of AS-Ⅳ to key target receptors was assessed by molecular docking with Autodock Vina， and the key target signaling transduction pathway was ResultA total of 56 intersected targets of AS-Ⅳ and diabetic retinopathy were found，and the top five key targets were obtained through PPI network analysis：protein kinase B（Akt）1，vascular endothelial growth factor A（VEGFA），epidermal growth factor receptor（EGFR），Src and signal transducer and activator of transcription 3（STAT3）. Molecular docking verified the strong binding affinity of AS-Ⅳ to the five key target receptors. In addition，in vitro tests have been confirmed that AS-Ⅳ attenuated high glucose-induced injury in human retinal pigment epithelial cell line ARPE-19 by regulating Akt/Nrf2/HO-1 and Akt/glycogen synthase kinase-3β（GSK-3β）signaling pathways. ConclusionThere was a significant overlap in the targets of AS-Ⅳ and diabetic retinopathy. The key targets and pathways may reveal the main pharmacological mechanism of AS-Ⅳ in the treatment of diabetic retinopathy.

Objective The ileum of porcine intestines with radiofrequency (RF) energy was fused through a novel linkage-type pressure controlled electrode, so as to verify feasibility and security of intestinal reconstruction in the RF energy tissue fusion technology. Methods Fresh porcine intestines were fixed on negative electrode in the order of ‘mucosa-serosa’, and then different compressive pressures （497，796，995，1 194，1 492 kPa）and RF energy were applied to the tissues through positive electrode of pressure cone to complete intestinal anastomosis. Biomechanical properties of the fused area were studied by tensile strength and bursting pressure test, and the thermal diffusion and tissue microstructure also studied. ResultsThe anastomotic tensile strength and bursting pressure could reach （8.73±1.11） N and （8.29±0.41） kPa, respectively, when the energy output power, pressure and welding time were 160 W, 995 kPa and 13 s, respectively, and an intact microstructure with little free collagen in the fused area could be observed. Conclusions The technology of RF energy-based tissue fusion could accomplish fast and stable intestinal tract reconstruction, showing great potential in clinical application. It is of great significance to shorten the operation time, simplify the operation process and improve the operation quality.

ObjectiveTo observe the effects of Wendantang on the expression of inflammatory cytokines， autophagy markers， and key molecules of phosphatidylinositol-3-kinase/protein kinase B/mammalian target of rapamycin （PI3K/Akt/mTOR） signaling pathway in the adipocytes of the rat model of obesity （syndrome of phlegm-dampness） and to explore the material basis of inflammation in obesity （syndrome of phlegm-dampness） and the underlying mechanism of Wendantang intervention. MethodA total of 126 SD rats were randomized into 2 groups： 16 rats in the blank group and 110 rats in the modeling group. The blank group was fed with a basic diet while the modeling group with a high-fat diet to establish the animal model of obesity （syndrome of phlegm-dampness） for 8 weeks. After successful modeling， 48 obese rats were selected according to their body mass and randomized into a model control group， an orlistat （ORLI， 32.40 mg·kg^-1） group， a rapamycin （RAPA， 2 mg·kg^-1） group， and low-， medium-， and high-dose （4.45， 8.90， 17.80 g·kg^-1， respectively） Wendantang groups， with 8 rats in each group. In addition， 8 rats were randomly selected from the blank group to be set as the normal control group. The corresponding agents in each group were administrated by gavage and the model and control groups were administrated with equal amounts of distilled water once daily for 6 weeks. The body mass， Lee's index， body fat ratio， and obesity rate were measured or calculated. The expression of UNC51-like kinase-1 （ULK1）， Beclin1， human autophagy-related protein 5 （Atg5）， p62， and microtubule-associated protein 1 light chain 3 （LC3） Ⅰ/Ⅱ （markers of autophagy in adipocytes） was detected by the immunohistochemical two-step method. Enzyme-linked immunosorbent assay （ELISA） was employed to determine the expression of tumor necrosis factor （TNF）-α， interleukin-6 （IL-6）， IL-1β， monocyte chemotactic protein-1 （MCP-1）， IL-4， IL-10， IL-13， and transforming growth factor （TGF）-β in adipocytes. Western blot was employed to measure the protein levels of classⅠ-PI3K， phosphatidylinositol triphosphate （PIP3）， Akt， mTORC1， ULK1， TSC1， and TSC2 in adipocytes. ResultCompared with the blank group， the modeling group showed increased body mass and Lee's index （P<0.01）， the obesity rate >20%， and phlegm-dampness syndrome manifestations such as physical obesity， decreased mobility， decreased appetite， lusterless and tight fur， loose stools， decreased responsiveness to the outside world， and decreased water intake. Compared with the normal control group， the model control group showed increased body mass， Lee's index， body fat ratio， adipocyte autophagy marker expression， pro- and anti-inflammatory cytokine levels （P<0.05， P<0.01）， down-regulated protein levels of classⅠ-PI3K， PIP3， Akt， mTORC1， TSC1， and TSC2 （P<0.01）， and up-regulated protein level of ULK1 （P<0.01）. The intervention groups showed lower body mass， body fat ratio， adipocyte autophagy marker protein expression， and protein levels of TNF-α， IL-6， IL-1β， MCP-1， IL-4， and IL-13 than the model control group （P<0.05， P<0.01）. Moreover， the RAPA and Wendantang （medium and high dose） groups showed lowered levels of IL-10 and TGF-β （P<0.01）， and the ORLI group showed down-regulated expression of TGF-β （P<0.01）. The expression of key molecules of the signaling pathway was up-regulated （P<0.05， P<0.01） while that of ULK1 was down-regulated （P<0.01） in all the intervention groups. Compared with the RAPA group， the Wendantang groups showed up-regulated expression of all autophagy marker proteins in adipocytes （P<0.01）. In addition， the low-dose Wendantang group showed elevated levels of inflammatory cytokines （except TNF-α） （P<0.05， P<0.01） and down-regulated expression of all key molecules of the signaling pathway （P<0.05， P<0.01）. The levels of inflammatory cytokines （except IL-16， MCP-1， and IL-10） were elevated in the medium-dose Wendantang group （P<0.05， P<0.01）. The expression of key molecules except PI3K of the signaling pathway was down-regulated in the medium- and high-dose Wendantang groups （P<0.05， P<0.01）. Compared with the ORLI group， low- and medium-dose Wendantang groups showed up-regulated expression of autophagy markers in adipocytes （P<0.01）， and the low-dose group showed elevated levels of inflammatory cytokines （IL-6， IL-4， and TGF-β） （P<0.01） and down-regulated expression of all key molecules of the signaling pathway （P<0.01）. The medium-dose Wendantang group showed up-regulated expression of IL-4 （P<0.01） and down-regulated expression of key molecules except PI3K of the signaling pathway （P<0.05， P<0.01）. The high-dose Wendantang group showed increased body mass， up-regulated expression levels of autophagy markers （ULK1， LC3 Ⅰ/Ⅱ） （P<0.05， P<0.01）， down-regulated expression of PIP3， mTORC1， and TSC1 （P<0.05， P<0.01）， and lowered levels of Beclin1， Atg5， TNF-α， and IL-13 （P<0.05， P<0.01）. ConclusionThe inflammation in obesity （syndrome of phlegm-dampness） is closely associated with the PI3K/Akt/mTOR pathway-mediated adipocyte autophagy. Wendantang can treat the chronic inflammation in obese rats with the syndrome of phlegm-dampness by regulating this signaling pathway and thus improve adipocyte autophagy.