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In this work, we assessed the anti-inflammatory effects of paeonol (PAE) in LPS-activated N9 microglia cells, as well as its underlying molecular mechanisms. PAE had no adverse effect on the viability of murine microglia N9 cell line within a broad range (0.12∼75 μM). When N9 cell line was activated by LPS, PAE (0.6, 3, 15 μM) significantly suppressed the release of proinflammatory products, such as nitric oxide (NO), interleukin-1β (IL-1β), and prostaglandin E2 (PGE2), demonstrated by the ELISA assay. Moreover, the levels of cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) were significantly reduced in PAE-treated N9 microglia cells. We also examined some proteins involved in immune signaling pathways and found that PAE treatment significantly decreased the expression of TLR4, MyD88, IRAK4, TNFR-associated factor 6 (TRAF6), p-IkB-α, and NF-kB p65, as well as the mitogen-activated protein kinase (MAPK) pathway molecules p-P38, p-JNK, and p-ERK, indicating that PAE might act on these signaling pathways to inhibit inflammatory responses. Overall, we found that PAE had anti-inflammatory effect on LPS-activated N9 microglia cells, possibly via inhibiting the TLR4 signaling pathway, and it could be a potential drug therapy for inflammation-associated neurodegenerative diseases.

Titanium-based composite coatings reinforced by in situ synthesized TiB and TiC particles between titanium and B 4 C were successfully fabricated on Ti6Al4V by laser cladding. Phase constituents of the coatings were predicted by thermodynamic calculations in the Ti-B 4 C-Al and Ti-B-C-Al systems, respectively, and were validated well by X-ray diffraction (XRD) analysis results. Microstructural and metallographic analyses were made by scanning electron microscopy (SEM) and electron probe micro-analysis (EPMA). The results show that the coatings are mainly composed of α-Ti cellular dendrites and the eutecticum in which a large number of needle-shaped TiB and a few equiaxial TiC particles are embedded. C is enriched in α-Ti cellular dendrites and far exceeds the theoretical maximum dissolubility, owing to the extension of saturation during laser cladding. The coatings have a good metallurgical bond with the substrate due to the existence of the dilution zone, in which a great amount of lamella β-Ti grains consisting of a thin needle-shaped martensitic microstructure are present and grow parallel to the heat flux direction; a few TiB and TiC reinforcements are observed at the boundaries of initial β-Ti grains.

Protective effect of catalpol on myocardium was studied in relation to endothelial progenitor cells, Notch1 signaling pathway and angiogenesis in rats with isoprenaline (INN)-induced acute myocardial infarcts. To analyze the pathological status and impact of catalpol on the rats, 3 weeks after intragastric gavage, the animals were verified for myocardial infarcts with electrocardiogram and measured for enzyme activity of lactate dehydrogenase (LDH), malondialdehyde (MDA), creatine kinase (CK) and superoxide dismutase (SOD) in myocardium, and further analyzed using HE and TTC staining, as well as visual examination of infarct area. Flow cytometry study of endothelial progenitor cells (EPCs) indicated that the EPCs were mobilized during infarction. The roles of Notch1 signaling pathway in angiogenesis of the infracted animals were studied using immunohistochemistry analysis of RBPjκ and Western blot analysis of Notch1 and Jagged1. Our results obtained from the rats treated with catalpol, positive drug and control showed that catalpol could protect rats from infarction probably by mobilization of EPCs and activation of Notch1 signaling pathway.