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Objective:To explore important signaling pathways and effects on neurovascular unit of Buyang-Huanwu Decoction in the treatment of ischemic stroke. Methods:Used TCMSP database, Chinese Medicine and Chemical Composition Database of Shanghai institute of Organic Chemistry and searched related literature to obtain and screen the active compounds and their targets of Buyang-Huanwu Decoction. DrugBank database, OMIM database, TTD database and GeneCards database were used to obtain targets of ischemic stroke. Metascape database was used to carry out KEGG pathway enrichment analysis on therapeutic targets. AlzData database was used to analyze the gene expression of therapeutic targets in different cells. Results:Through network analysis, the key targets of Buyang-Huanwu Decoction in the treatment of ischemic stroke were obtained, including PTGS2, PTGS1, CHRM1, ADRB2, CHRM2, F10, F7, HIF1A, PDE3A, ADRA1B and CHRM3, etc. Through enrichment analysis, multiple key signaling pathways of Buyang-Huanwu Decoction in the treatment of ischemic stroke were obtained, including PI3K-Akt signaling pathway, calcium signaling pathway, IL-17 signaling pathway, platelet activation, Apelin signaling pathway, NF-κB signaling pathway, AMPK signaling pathway and arachidonic acid metabolism, etc. Through gene expression analysis, the effect of Buyang-Huanwu Decoction on different cells was analyzed, and it was found that the targets regulate a variety of biological processes, cellular components and molecular functions in endothelial, astrocytes, microglia, oligodendrocytes, oligodendrocyte precursor cells (OPCs) and neurons. Conclusion:Buyang-Huanwu Decoction is characterized by multiple components, multiple targets, multiple pathways and complex connections in the treatment of ischemic stroke, and its effect is closely related to neurovascular units (NVU) at the cellular expression level of genes, and the mechanism of therapeutic effect included neuroprotection, neurogenesis, antithrombotic, vascular regeneration, glial cell regulation, etc.

Objective To study and evaluate the therapeutic efficacy of CT-guided radioactive 125Iseeds implantation combined with percutaneous vertebroplasty for spinal vertebra metastases.Methods Fifteen patients and 21 lesions were enrolled in this study.Based on the CT images,a computer-based treatment planning system (TPS) was used to determine the optimal seeds distribution.Under CT-guided,radioactive 125I seeds were implanted into the lesions.Based on the X-ray and CT image after the implantation,quality check was carried out with TPS.The ostalgia-relieving degree and the image alterations of the spinal vertebra metastases lesions were observed.Two months later,15 patients underwent percutaneous vertebroplasty with DSA guidance,bone cement was made according to the ratio methyl acrylic resin polymer/liquid methyl acrylic resin monomer/contrast as 3 ∶ 2 ∶ 1 in injecting paste form.The puncturation through pedicle of vertebral arch and lateral posterior body of vertebra was both adopted in thoracic and lumbosacral vertebrae site.After making sure that the puncturation was completed and there was no leakage in vertebral body,the bone cement was injected into vertebral body quickly.Results Accepted radioactive 125I seeds plantation,relief of pain was obtained.Among 15 patients,8 patients were powerful,6 patients were effective and 1 patient was inefficiency.After treatment,the pain grading significantly decreased.After treatment for 2 months,CT was used to recheck,7 lesions were local controlled,12 lesions had no changes,2 lesions were progress.The responsive rate was 90.5％ (19/21).No serious side-effect happened.Conclusions Radioactive 125I seeds implantation can be a safe and effective method in treating spinal vertebra metastases and obtaining good clinical effects with minimal damage and few complications.Percutaneous vertebroplasty can strengthen the target and relief pain quickly.CT-guided radioactive 125I seeds implantation combined with percutaneous vertebroplasty for the treatment of spinal vertebra metastases has complementary advantages.

BACKGROUND:The principle of lyophilization is to sublimate the solvent of frozen materials in vacuum and retain the solute, thus making a pore structure. OBJECTIVE: To produce a chitosan tubular scaffold by lyophilization, and to test its physicochemical properties. METHODS: The chitosan tubular material was prepared by lyophilization method, folowed by gross observation and electron microscopic observation. The chitosan tubular material samples were placed into PBS solution and pure water for 50 days, respectively, and then immersed in trypsin liquid for 1 day folowed by embedded into the muscle and dorsal skin of neonatal Sprague-Dawley rats for 30 days. The degradation rate and porosity of the material were observed and calculated. The breaking strength and compressive strength of the material were determined both under drying and soaking conditions using tensile instrument and pressure meter, respectively. RESULTS AND CONCLUSION:The external form of the chitosan tubular material was normaly tubular. Under the electron microscope, it was composited by different size pores, and the pore size was 50-200μm. The degradation rates of the material were (5.33±0.12)% in PBS, (11.26±0.15) in water, 0.012% in the trypsin liquid and (35.2±3.7)in vivo. The porosity rate was (97.5±1.5)%. The breaking strength and compressive strength of the material was higher under the drying state than under the soaking state (P < 0.05). These findings indicate that the lyophilization method can produce the chitosan tubular material with good porosity rate and degradation rate as wel as good tensile ability and compressive capability.

Objective Using middle cerebral artery occlusion (MCAO) model to observe protective effect of effective components of bezoar on brain damage.To discuss the anti-cerebral ischemia mechanism and compare the efficacy of effective components of bezoar from the endoplasmic reticulum stress intervention angle.Methods Rats were stratified randomly divided into sham group,model group,Qingkailing group (positive drug,3 mL/kg),taurine group,ursodeoxycholic acid (UDCA,78 mg/kg) group,taurine-conjugated ursodeoxycholic acid (TUDCA,100 mg/kg) group.Through establish MCAO model in rats,observed the scores of the neurologic impairment,measured infarct volume by TTC.Immunohistochemistry and Western blotting were Used to detect the content of P-PERK,P-EIF2α,and ATF4.Results Compared with sham group,neurologic impairment scores of model group significantly reduced (P ＜ 0.01).Compared with model group,Qingkailing group,UDCA group,and TUDCA group significantly improved neurological function in rats (P ＜ 0.05,0.01).Compared model group,all the treatment groups could significantly reduce the volume of cerebral infarction (P ＜ 0.01).Compared with sham group,expression of P-PERK,P-EIF2α,and ATF4 was significantly increased (P ＜ 0.01).Compared with model group,all the treatment groups reduced the expression of P-PERK,P-EIF2α,and ATF4 in varying degrees,effect of Qingkailing and TUDCA were more obvious.Conclusion The effective components ofbezoar alleviate cerebral ischemia reperfusion injury in rats by inhibiting endoplasmic reticulum stress,the effect of TUDCA is better than that of taurine and UDCA.

The theory of preventive treatment of disease in Jinguiyaolue (Synopsis of Prescriptions of the Golden Chamber) includes following 4 aspects:preventing disease at the first,stopping disease transmission,treating disease overall and deciding diagnosis and treatment plan before disease onset.There are 3 theoretical principles for this theory:disease preventive principle,overall therapeutic principle,and principle for selecting diagnosis and treatment steps.The therapeutic principles for damp disease,phlegm-fluid retention,water-qi disease in Jinguiyaolue is analyzed based on the theory for getting ZHANG Zhong-jing's therapeutic thinking,expand understanding to original texts,and enrich the content of modern system of pattern differentiation and treatment.

Objective: To investigate the regulatory effect of Jieduan Niwan Formula (JDNWF) drug-containing serum on AMPK-mediated mitochondrial quality control in D-GalN-induced HepG2 cells. Methods: Twenty male Wistar rats were randomly divided into blank control and JDNWF-containing serum groups, 10 rats per group. The JDNWF-containing serum group was gavaged with JDNWF (21.7 g/kg), whereas the blank control group was gavaged with saline. Blood was collected to prepare JDNWF-containing and blank control serum. Cell viability, mitochondrial damage indicators, and MQC pathway protein expression levels were evaluated to determine the optimal volume fraction of JDNWF. HepG2 cells were divided into control, D-GalN, DMSO, AMPK inhibitor, JDNWF drug-containing serum, and JDNWF drug-containing serum plus AMPK inhibitor groups, and corresponding drug interventions were administered to each group. Cells were collected after the interventions, and the CCK-8 assay was used to measure cell viability, the 2′-7′-dichlorodihydrofluorescein diacetate fluorescent probe was used to detect reactive oxygen species (ROS) levels, JC-1 was used to detect mitochondrial membrane potential, thiobarbituric acid was used to measure malondialdehyde (MDA) levels, WST-8 was used to measure superoxide dismutase (SOD) activity, and western blotting was used to detect the expression levels of mitochondrial quality control-related proteins, including p-AMPK, AMPK, PGC-1α, NRF1, TFAM, MFN2, and DRP1. Results: 5% JDNWF drug-containing serum most significantly restored cell viability, mitochondrial damage markers, and MQC pathway protein expression in the model group. Therefore, it was chosen for intervention in subsequent experiments. Compared to the control group, the cell viability of the D-GalN, DMSO, and AMPK inhibitor groups was significantly reduced (P<0.01). In contrast, the heterogeneity of mitochondrial membrane potential, ROS, and MDA levels was significantly increased (P<0.01), and SOD activity was significantly decreased (P<0.01). The p-AMPK, PGC-1α, NRF1, TFAM, MFN2, and DRP1 protein expression levels were significantly decreased (P<0.01). After JDNWF drug-containing serum intervention, compared to the DMSO group, cell viability significantly increased (P<0.01), mitochondrial membrane potential heterogeneity, ROS, and MDA levels significantly decreased (P<0.01), SOD activity significantly increased (P<0.01), and p-AMPK, PGC-1α, NRF1, TFAM, and MFN2 protein expression levels significantly increased (P<0.01), whereas DRP1 protein expression significantly decreased (P<0.01). Compared to the JDNWF drug-containing serum group, the cell viability in the JDNWF plus AMPK inhibitor group significantly decreased (P<0.01), mitochondrial membrane potential heterogeneity and ROS levels significantly increased (P<0.01), MDA levels significantly increased (P<0.05), SOD activity significantly decreased (P<0.05), p-AMPK, PGC-1α, NRF1, and TFAM protein expression levels significantly decreased (P<0.01), MFN2 protein expression significantly decreased (P<0.05), and DRP1 protein expression significantly increased (P<0.01). Conclusion JDNWF drug-containing serum may restore mitochondrial function and improve D-GalN-induced HepG2 cell injury by regulating AMPK-mediated mitochondrial quality control.

Objective:To discuss the molecular association pattern of Shenling Baizhu Powder for type 2 diabetes (T2DM) and ulcerative colitis through network pharmacology method based on the theory of "treating different diseases with same method" in TCM.Methods:The TCMSP and ETCM Chinese medicine chemical composition databases were used to obtain the chemical composition and predict the targets of Shenling Baizhu Powder. The OMIM, GeneCards, DrugBank and TTD disease databases were used to obtain the disease targets of T2DM and ulcerative colitis. The intersection targets of chemical composition of Shenling Baizhu Powder, T2DM and ulcerative colitis were obtained by Bioinformatics platform. Cytoscape 3.8.2 software was used to map the "Chinese materia medica-component-target" network and "effective component- intersection target" network. The GO enrichment analysis and KEGG pathway analysis of the intersection targets were performed with the STRING platform. The intersection target protein-protein interaction network was constructed by STRING database, and core targets were obtained using the CytoNCA plugin of Cytoscape 3.8.2 software. AutodockTools software was applied to validate the molecular docking between the core chemical components and the core targets of Shenling Baizhu Powder.Results:Totally 176 chemical components of Shenling Baizhu Powder, 226 corresponding targets, 11 478 T2DM targets, 4 857 Ulcerative targets of ulcerative colitis, and 162 intersection targets of medicinal chemistry components and diseases were obtained. 1 789 related biological processes, 163 molecular functions, 92 cell constituents, and 192 signaling pathways were obtained by GO enrichment analysis and KEGG pathway analysis. The signaling pathways were mainly about AGE-RAGE, TNF, IL-17,MAPK, PI3K-Akt signaling pathways, etc. The core components of Shenling Baizhu Powder were mainly sitosterol, luteolin, kaempferol, naringenin, beta-carotene, etc. The core targets were EGFR, ALB, IL1B, CASP3, ESR1, VEGFA, PTGS2, TNF, IL6, MYC, AKT 1, JUN, TP53, etc. The core chemical components had tight correlation with the core targets by the molecular docking.Conclusions:By acting on core targets such as TNF, IL1B, IL6, AKT1, VRGFA, PTGS2, MYC, JUN, TP53, and regulating IL-17 signaling pathway, TNF signaling pathway, MAPK signaling pathway, AGE-RAGE signaling pathway, etc., Shenling Baizhu Powder improves tissue inflammation damage, mucosal barrier damage, immune regulation imbalance, intestinal flora dysbiosis, insulin resistance, apoptosis, oxidative stress and other biological processes. Therefore Shenling Baizhu Powder can treat T2DM and ulcerative colitis with the same method.

Objective:The Qinzhi Zhudan formula(QZZD)exhibits a prominent therapeutic effect in the treatment of vascular dementia(VaD).This study combined a network pharmacology approach and experimental validation to identify the underlying biological mechanism of QZZD against VaD.Methods:Male Wistar rats received bilateral common carotid artery occlusion(BCCAO)surgery,and after 4 weeks of intragastric administration of QZZD,the therapeutic effect was assessed using the Morris water maze test and cerebral blood flow(CBF)assessment.Hematoxylin and eosin staining,Nissl staining,and electron microscopy were used to measure the histopathological changes in the neurons of rats.The effect of QZZD treatment on hippocampal neurotransmitters was assessed by high-performance liquid chromatography with electrochemical detection and liquid chromatography mass spectrometry.Immunofluorescence was used to observe VaD-induced microglia activation.The inflammatory cytokine levels were assessed by enzyme linked immunosorbent assay.Western blot was used to examine the TNFR1-mediated TNF pathway,which was screened out by network pharmacology analysis.Results:QZZD treatment alleviated pathological changes and neuronal damage in VaD rats and atten-uated their cognitive impairment.In addition,QZZD increased CBF and the expression of acetylcholine and 5-hydroxytryptamine in the hippocampal region.Notably,QZZD inhibited microglial activation and the expression of IL-6 and TNF-a.Network pharmacology and western blot indicated that QZZD inhibited the levels of TNFR1,NF-KBp65,p-ERK,TNF-α,and IL-6,which are related to the TNFR1-mediated TNF signaling pathway.Conclusion:QZZD clearly improved learning and memory function,reduced brain pathological damage,elevated CBF and hippocampal neurotransmitter levels,and alleviated neuroinflammation of VaD rats partly by inhibiting the TNFR1-mediated TNF pathway,indicating its potential value in the clinical therapy of VaD.