661 research outputs found

    Anti-inflammatory effects of bitongling granules are mediated through the suppression of miR-21/p38 MAPK/TLR4/NF-κB signaling in H9C2 rat cardiac cells exposed to lipopolysaccharides

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    Purpose: To assess the protective effects of bitongling granules on H9C2 cells exposed to lipopolysaccharides (LPS) in the management of rheumatoid arthritis (RA)-induced myocardial inflammation.Methods: The effects of bitongling granule (BTLG) drug-containing serum were assessed in myocarditis models established in rat cardiac cells. MicroRNA-21 (miR-21) levels were evaluated by qRT-PCR while MTT assays were performed to assess cell viability. ELISA assay was used to evaluate tumor necrosis factor α (TNF-α), interleukin 17 (IL-17) and interleukin 6 (IL-6) levels in cell culture supernatants. Apoptosis was determined by flow cytometry (FCM). Quantitative mitogen-activated protein kinase (MAPK)/p38, toll-like receptor 4 (TLR4) and nuclear factor kappa B (NF-kB)/p65 levels were evaluated by western blot and immunofluorescenceResults: BTLG increased cardiac cell activity and exhibited anti-inflammatory effect. It also inhibited LPS-induced H9C2 apoptosis and suppressed p65 NF-κB phosphorylation (p-p65 NF-κB), TLR4, and p38 MAPK phosphorylation (p-p38 MAPK). BTLG also reduced miR-21 expression, and the overexpression of the miR-21 inhibitor in H9C2 suppressed apoptosis. Moreover, p-p38 MAPK, TLR4 and p-p65 NF-κB expression were down-regulated in miR-21 inhibitor transfected H9C2s. The inhibition of p38/TLR4/ NF-κB signaling might have occurred via the suppression of miR-21 by BTLG.Conclusion: The results show that BTLG inhibits the inflammatory reaction involved in p38MAPK/TLR4/ NF-κB signaling pathway and can prevent RA-induced cardiac disease, suggesting that BTLP treatment may be beneficial for the management of arthritic cardiomyopathy

    Expression and Localization of Stanniocalcin-1 in Bovine Osteoblasts

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    As a novel glycoprotein hormone, Stanniocalcin-1 (STC-1) was first identified in teleost species, and it is involved in the regulation of mineral homeostasis in bony fish and mammals. STC-1 can not only affect the mammals bone development, but also protect neurons from the damage of ischemia, and stimulate the angiogenic response. Although it is widely expressed in rodent skeletons, whether this hormone is expressed in the skeleton of ruminant animals, like bovines, is still unknown. Here, we investigated the expression of STC-1 in bovine osteoblasts by using immunocytochemical staining and RT-PCR. Our results show that the mRNA and protein of STC-1 are expressed in the bovine osteoblasts during later differentiation periods 10th day in vitro. The present data support the notion that STC-1 may play a role in the process of bovine bone development

    Anti-Angiogenic and Anti-Inflammatory Effects of SERPINA3K on Corneal Injury

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    SERPINA3K is a member of the serine proteinase inhibitor (SERPIN) family. Here we evaluated the therapeutic effects of SERPINA3K on neovascularization and inflammation in a rat cornea alkali burn model that is commonly employed to study corneal wounding. Topical treatment of the injured rat cornea with SERPINA3K (20 µg/eye/day) for 7 days significantly decreased the neovascular area, compared with the groups treated with BSA or PBS. The SERPINA3K treatment also ameliorated the corneal inflammation as evaluated by the inflammatory index. Furthermore, SERPINA3K enhanced the recovery of corneal epithelium after the alkali injury. Toward the mechanism of action, SERPINA3K down-regulated the expression of the pro-angiogenic and pro-inflammatory factors, vascular endothelial growth factor and tumor necrosis factor-α and up-regulated the expression of the anti-angiogenic factor, pigment epithelium-derived factor. SERPINA3K specifically inhibited growth of vascular endothelial cells. Meanwhile, SERPINA3K significantly up-regulated the expression of EGFR in the corneal epithelium. These findings suggest that SERPINA3K has therapeutic potential for corneal inflammation and NV

    Storage of multiple single-photon pulses emitted from a quantum dot in a solid-state quantum memory

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    Quantum repeaters are critical components for distributing entanglement over long distances in presence of unavoidable optical losses during transmission. Stimulated by Duan-Lukin-Cirac-Zoller protocol, many improved quantum-repeater protocols based on quantum memories have been proposed, which commonly focus on the entanglement-distribution rate. Among these protocols, the elimination of multi-photons (multi-photon-pairs) and the use of multimode quantum memory are demonstrated to have the ability to greatly improve the entanglement-distribution rate. Here, we demonstrate the storage of deterministic single photons emitted from a quantum dot in a polarization-maintaining solid-state quantum memory; in addition, multi-temporal-mode memory with 11, 2020 and 100100 narrow single-photon pulses is also demonstrated. Multi-photons are eliminated, and only one photon at most is contained in each pulse. Moreover, the solid-state properties of both sub-systems make this configuration more stable and easier to be scalable. Our work will be helpful in the construction of efficient quantum repeaters based on all-solid-state devicesComment: Published version, including supplementary materia
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