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In this paper, the solid solution and precipitation behavior of inclusions on the surface and 1/2 thickness of the tested steel plate under the condition of welding heat input of 400 kJ/cm is investigated by using laser confocal experiments with hot-rolled state DH36 ship plate steel as the research object, and the mechanism of the effect of inclusions on the phase transformation of an acicular ferrite is revealed. The results show that the inclusions of the tested steel are mainly composed of Oxide-MnS, MnS, Oxide, TiN, Spinel, etc. The amount of inclusions on the surface of the tested steel plate is significantly higher than that at the 1/2 thickness position. During the heating stage, the small inclusions on the surface immediately disappeared, and the large inclusions gradually solidified in the matrix; atomic diffusion occurred at the bond between the inclusions and the matrix; while the small inclusions at the 1/2 thickness position gradually disappeared at the beginning of the heating stage, and the inclusions began to precipitate and grow when the temperature was increased to 990 °C. The acicular ferrite preferentially nucleates and grows near the boundary of the inclusions during the post-weld cooling stage, and its growth ends when two acicular ferrites cross.
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In the present study, the welding thermal cycle of magnesium-treated EH36 steel was simulated by a thermal simulation experiment machine. The effects of welding heat input on the microstructure and low temperature toughness of the welded joint were studied, and the mechanism of acicular ferrite nucleation induced by MgAl 2 O 4 inclusion was revealed. The results showed that, when the welding heat input of 150 kJ/cm, 250 kJ/cm and 350 kJ/cm was utilized, the microstructure of heat affected zone in the experimental EH36 steel consisted of grain boundary ferrite, acicular ferrite, granular bainite, and a small amount of pearlite, but the volume fraction and grain size of each independent microstructure were different. With the increase of welding heat input, the content of acicular ferrite and granular bainite decreased, the content of grain boundary ferrite increased, and the average grain size increased, whereas the low temperature toughness of the experimental EH36 steel welded joint reduced from 174 to 67 J. Furthermore, MgAl 2 O 4 inclusions can induce acicular ferrite nucleation, whereas the nucleation mechanism is a combination of low lattice mismatch and low interfacial energy.
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Q690 steel is widely used as building steel due to its excellent performance. In this paper, the microstructure evolution of the heat-affected zone of Q690 steel under simulated high heat input welding conditions was investigated. The results show that under the heat input of 150-300 kJ/cm, the microstructures of the heat-affected zone are lath bainite and granular bainite. The content of lath bainite gradually decreased with the increase in heat input, while the content of granular bainite steadily increased. The proportion of large-angle grain boundaries decreased from 51.1% to 40.3%. Overall, the average size of original austenite increased, and the precipitates changed from Ti (C, N) to Cr carbides. During the cooling process, the nucleation position of bainitic ferrite was from high to low according to the nucleation temperature, and in order of inclusions at grain boundaries, triple junctions, intragranular inclusions, bainitic ferrite/austenite phase boundaries, twin boundaries, grain boundaries, and intragranular inclusions at the bainitic ferrite/austenite phase interface. The growth rate of bainitic ferrite nucleated at the phase interface, grain boundary, and other plane defects was faster, while it was slow at the inclusions. Moreover, it was noted that the Mg-Al-Ti-O composite inclusions promote the nucleation of lath bainitic ferrite, while the Al-Ca-O inclusions do not facilitate the nucleation of bainitic ferrite.
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Background: Alzheimer's disease (AD) is the most common neurodegenerative condition worldwide, with amyloid ß (Aß) fibrils presenting as its main pathological feature. This study investigated whether Ginsenoside Compound K (CK) has activity against Aß and its mechanism in reducing synaptic damage and cognitive impairment. Methods: The binding capacity of CK to Aß42 and Nrf2/Keap1 was determined using molecular docking. Transmission electron microscopy was used to monitor CK-mediated degradation of Aß fibrils. The effect of CK on the survival of Aß42-damaged HT22 cells was determined using a CCK-8 assay. The therapeutic efficacy of CK in a scopoletin hydrobromide (SCOP) induced cognitive dysfunction mouse model was measured using a step-down passive avoidance test. GO enrichment analysis of mouse brain tissue was peformed using Genechip. Hydroxyl radical scavenging and reactive oxygen species assays were performed to verify the antioxidant activity of CK. The effects of CK on the expression of Aß42, the Nrf2/Keap1 signaling pathway, and other proteins were determined by western blotting, immunofluorescence, and immunohistochemistry. Results: Molecular docking results showed that CK interacts with Lys16 and Glu3 of Aß42. CK reduced the aggregation of Aß42 as observed using transmission electron microscopy. CK increased the level of insulin-degrading enzyme and decreased the levels ß-secretase and γ-secretase; therefore, it can potentially inhibit the accumulation of Aß in neuronal extracellular space in vivo. CK improved cognitive impairment and increased postsynaptic density protein 95 and synaptophysin expression levels in mice with SCOP-induced cognitive dysfunction. Further, CK inhibited the expression of cytochrome C, Caspase-3, and cleaved Caspase-3. Based on Genechip data, CK was found to regulate molecular functions such as oxygen binding, peroxidase activity, hemoglobin binding, and oxidoreductase activity, thus affecting the production of oxidative free radicals in neurons. Further, CK regulated the expression of the Nrf2/Keap1 signaling pathway through its interaction with the Nrf2/Keap1 complex. Conclusion: Our findings show that CK regulates the balance between Aß monomers production and clearance, CK binds to Aß monomer to inhibits the accumulation of Aß, increases the level of Nrf2 in neuronal nuclei, reduces oxidative damage of neurons, improves synaptic function, thus ultimately protecting neurons.
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Background: The gut-cardiac axis theory provides new insights into the complex mechanisms of cardiac hypertrophy and provides new therapeutic targets. Cardiac hypertrophy is a risk factor for heart failure. Shengmaiyin (SMY) is a traditional Chinese medicine formula with clear effects in the treatment and prevention of cardiac hypertrophy, but the mechanism by which it improves cardiac hypertrophy is still unclear. Therefore, this study aimed to investigate the protective effect and mechanism of SMY on isoproterenol (ISO)-induced myocardial hypertrophy in rats. Methods: First, various pharmacodynamic methods were used to evaluate the therapeutic effect of SMY on ISO-induced myocardial hypertrophy in rats. Then, 16S rDNA amplicon sequencing technology was used to study the effect of SMY on the intestinal flora of rats with myocardial hypertrophy. Finally, the mechanism underlying the effect of SMY on cardiac hypertrophy was predicted by bioinformatics network analysis and verified by Western blotting. Results: SMY increased ejection fraction (EF%) and left ventricular fractional shortening (FS%), ameliorated myocardial cell injury and fibrosis, regulated blood lipids and energy metabolism, and decreased cardiac hypertrophy marker gene expression. The gut microbiota of ISO-induced myocardial hypertrophy rats were significantly changed, while SMY effectively ameliorated the dysbiosis of the intestinal flora in rats with myocardial hypertrophy, especially Prevotella 9, Lactobacillus, and Clostridium. Mechanistic studies have shown that the anticardiac hypertrophy effect of SMY is related to the inhibition of the expression of HIF1α/PPAR signalling pathway-related proteins. Conclusion: SMY significantly improves cardiac function, relieves myocardial cell fibrosis and necrosis, resists cardiac hypertrophy, improves blood lipid metabolism and energy metabolism, regulates intestinal microbial disturbance, and protects the heart.
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BACKGROUND AND OBJECTIVE: To explore the molecular mechanism by which Shengmaiyin (Codonopsis pilosula) (SMY) improves isoproterenol (ISO)-induced heart failure (HF) in rats via a traditional Chinese medicine (TCM) integrated pharmacology research platform, The Chinese Medicine Integrated Pharmacology Platform (TCMIP V2.0). METHOD: The chemical constituents and drug targets of SMY medicines were identified through TCMIP, and HF disease target information was collected. A prescription Chinese medicinecomponent- core target network was constructed through the TCM network mining module, and biological process and pathway enrichment analyses of core targets were conducted. In vivo experiments in rats were performed to verify the pathway targets. Hematoxylin and eosin staining was used to observe myocardial tissue morphology. ELISA kits were used to detect cAMP content, and Western blotting was used to detect the expression levels of signaling pathway-related proteins. RESULTS: The TCMIP analysis indicated that SMY treatment of HF activates the GS-ß-adrenergic receptor (ßAR)-cAMP-protein kinase A (PKA) signaling pathway. The in vivo experimental results confirmed this finding. High-dose SMY significantly improved the morphology of ISO-injured myocardium. The levels of G-protein-coupled receptor (GPCR), adenylate cyclase (AC), ßAR, and PKA proteins in myocardial tissue were significantly increased in the SMY group. In addition, the content of cAMP in myocardial tissue was increased, and the content of cAMP in serum was decreased. CONCLUSION: Based on the analysis of TCMIP, SMY treatment of HF may activate the GS-ßARcAMP- PKA signaling pathway. The findings provide a theoretical basis for further research on the anti-HF mechanism of SMY.
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Codonopsis , Medicamentos de Ervas Chinesas , Insuficiência Cardíaca , Adenilil Ciclases/metabolismo , Animais , Codonopsis/metabolismo , Proteínas Quinases Dependentes de AMP Cíclico , Medicamentos de Ervas Chinesas/farmacologia , Medicamentos de Ervas Chinesas/uso terapêutico , Amarelo de Eosina-(YS) , Insuficiência Cardíaca/tratamento farmacológico , Hematoxilina , Isoproterenol/farmacologia , Farmacologia em Rede , RatosRESUMO
We investigated the anti-aging effects of velvet antler polypeptide on D-galactose (D-gal)-induced aging mice. D-gal-induced aging mice were established and randomly divided into five groups, the control, model, vitamin E (VE), velvet antler polypeptide low-dose and velvet antler polypeptide high-dose groups. The Morris water maze test was used to evaluate the learning and memory abilities of aging mice. Hippocampal neurons were observed via hematoxylin-eosin staining and transmission electron microscopy. Biochemical methods were used to detect the activities of superoxide dismutase, malonaldehyde and other enzymes and evaluate the influence of velvet antler polypeptide on the antioxidant capacity of aging mice. Using 16S rRNA gene sequencing and meristem technology, we assessed the effect of velvet antler polypeptide on aging mice's intestinal flora and fatty acid metabolism. The experimental results showed that velvet antler polypeptide could significantly improve aging mice's learning and cognitive abilities, increase the activities of superoxide dismutase, glutathione peroxidase, and catalase in the serum decrease the malonaldehyde content. Intestinal microecological analysis showed that velvet antler polypeptide could significantly increase the beneficial bacterial genus Lactobacillus abundance. Western blot analysis further demonstrated that velvet antler polypeptide could promote fatty acid metabolism by activating peroxisome proliferator-activated receptor α (PPARα) and upregulating the expression of the downstream enzymes carnitine-palmitoyl transferase-1 A and acyl-CoA oxidase 1 while downregulating that of apolipoprotein E4 (APOE4), thereby reducing fatty acid accumulation and increasing adenosine-triphosphate (ATP) production. Therefore, velvet antler polypeptide improves the intestinal microecology and activates the PPARα/APOE4 pathway to regulate fatty acid metabolism.
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Envelhecimento/efeitos dos fármacos , Chifres de Veado , Apolipoproteína E4/efeitos dos fármacos , Disfunção Cognitiva/tratamento farmacológico , Microbioma Gastrointestinal/efeitos dos fármacos , Medicina Tradicional Chinesa , PPAR alfa/efeitos dos fármacos , Animais , Chifres de Veado/química , Comportamento Animal/efeitos dos fármacos , Feminino , Masculino , Aprendizagem em Labirinto/efeitos dos fármacos , Camundongos , Camundongos Endogâmicos ICR , Peptídeos/farmacologia , Transdução de Sinais/efeitos dos fármacosRESUMO
Amaranthus viridis is an important medicinal herb. In this study, the complete chloroplast genome (plastome) of A. viridis was repotred. It was a circular molecular of 150,452 bp in length and consists of a large single-copy region (LSC, 83,832 bp), a small single-copy region (SSC, 17,914 bp), and two inverted repeats (IRs, 24,353 bp for each) regions. The overall GC content was 36.6%. This plastome encodes 113 unique genes, including 79 protein-coding genes, 30 tRNAs, and four rRNAs. The phylogenetic tree of 18 Amaranthaceae chloroplast genomes supported that A. viridis was closely related to A. hybridus.