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Effects of Different Calcium Silicate Cements on the Inflammatory Response and Odontogenic Differentiation of Lipopolysaccharide-Stimulated Human Dental Pulp Stem Cells.

This study aimed to analyze the effects of different calcium silicate cements (CSCs) on the inflammatory response and odontogenic differentiation of lipopolysaccharide-stimulated human dental pulp stem cells. Human dental pulp stem cells (hDPSCs) were stimulated with lipopolysaccharide (LPS) to induce inflammation. These LPS-induced dental pulp stem cells (LDPSCs) were cultured with ProRoot MTA, Biodentine, Retro MTA, and Dycal. Cell viability was evaluated using the Cell Counting Kit-8 assay. Interleukin (IL)-6, IL-8, and transforming growth factor (TGF)-β1 cytokine levels were assessed using the enzyme-linked immunosorbent assay. The expressions of alkaline phosphatase (ALP), osteocalcin, and runt-related transcription factor 2 (RUNX2) were analyzed through real-time polymerase chain reaction. ProRoot MTA, Biodentine, and Retro MTA did not significantly decrease the cell viability of LDPSCs for up to 48 h ( < 0.05). Retro MTA significantly decreased the expression of IL-6 and IL-8 by LDPSCs. ProRoot MTA and Biodentine significantly reduced TGF-β expression by LDPSCs ( < 0.05). Regarding odontogenic differentiation, all CSCs had no effect on ALP expression but increased the production of RUNX2 at 12 h.

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microRNA-146a downregulates IL-17 and IL-35 and inhibits proliferation of human periodontal ligament stem cells.

Periodontitis is characterized by increased levels of proinflammatory factors, such as interleukin-17 (IL-17) and IL-35. In this study, the expression of microRNA-146a (miRNA-146a), IL-17, and IL-35 in the plasma of patients with periodontitis and healthy controls were detected by quantitative reverse transcription polymerase chain reaction and enzyme-linked immunosorbent assay, respectively. miRNA-146a mimic was transfected into periodontal ligament stem cells (PDLSCs) isolated from periodontitis-affected teeth and healthy teeth. Cell proliferation and expression of IL-17 and IL-35 were detected by cell counting kit-8 assay and Western blot analysis, respectively. It was observed that miRNA-146a was downregulated but IL-17 and IL-35 were upregulated in the plasma of patients with periodontitis than in healthy controls. miRNA-146a was inversely correlated with IL-17 and IL-35 in patients with periodontitis. miRNA-146a overexpression inhibited proliferation of PDLSCs derived from both periodontitis-affected teeth and healthy teeth. miRNA-146a overexpression led to downregulated IL-17 and IL-35 expression in PDLSCs isolated from periodontitis-affected teeth. We, therefore, conclude that miRNA-146a may improve periodontitis by downregulating IL-17 and IL-35 expression and inhibiting proliferation of human PDLSCs.

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Ginsenoside Rg1 Regulates SIRT1 to Ameliorate Sepsis-Induced Lung Inflammation and Injury via Inhibiting Endoplasmic Reticulum Stress and Inflammation.

To investigate the protective effect of ginsenoside Rg1 on relieving sepsis-induced lung inflammation and injury and .

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Extracellular acidification-induced CXCL8 production through a proton-sensing receptor OGR1 in human airway smooth muscle cells: a response inhibited by dexamethasone.

Human airway smooth muscle cells (ASMCs) contribute to bronchial contraction and airway hyperresponsiveness in patients with bronchial asthma. They also generate cytokines, chemokines, and matricellular proteins. Ovarian cancer G protein-coupled receptor 1 (OGR1) senses extracellular protons and mediates the production of interleukin-6 (IL-6) and connective tissue growth factor (CTGF) in ASMCs.

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SERUM CYTOKINE OF IL-2, IL-10 AND IL-12 LEVELS IN PATIENTS WITH STOMACH ADENOCARCINOMA.

Gastric adenocarcinoma is the fourth most common cause of cancer-associated death worldwide.

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Emodin Attenuates Lipopolysaccharide-Induced Injury via Down-Regulation of miR-223 in H9c2 Cells.

Emodin is a natural product extracted from Rheum palmatum. There are few recent studies on emodin in the treatment of myocarditis. This study aimed to investigate the effect of emodin on lipopolysaccharide (LPS)-induced inflammatory injury in cardiomyocytes. H9c2 cells were treated with 10 μM of LPS and different concentrations (0, 1, 5, 10, 15, and 20 μM) of emodin. The expression of miR-223 was changed by transient transfection. Thereafter, cell viability, apoptosis, the expression of CyclinD1 and Jnk-associated proteins, and the release of pro-inflammatory factors were assessed by cell Counting Kit-8, flow cytometry analysis, quantitative real-time polymerase chain reaction Western blot, and enzyme-linked immunosorbent assay respectively. The results showed that 20 μM of emodin significantly decreased H9c2 cells viability. LPS significantly damaged H9c2 cells, as cell viability was reduced, CyclinD1 was down-regulated, apoptosis was induced, the release of interleukin-1β (IL-1β), IL-6, and tumor necrosis factor-alpha were increased, and the phosphorylation of Jnk and c-Jun were promoted. Emodin protected H9c2 cells against LPS-induced inflammatory injury. miR-223 expression was significantly up-regulated by LPS exposure, while emodin lessened this up-regulation. LPS-injured H9c2 cells were attenuated by the overexpression of miR-223; emodin has protective actions on LPS-injured H9c2 cells and targets. Besides, SP600125 (an inhibitor of Jnk) eliminated miR-223-modulated inflammatory injury in H9c2 cells. These data demonstrated that emodin could attenuate LPS-induced inflammatory injury and deactivate Jnk signaling pathway through down-regulation of miR-223.

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Adiponectin Relieves Human Adult Cardiac Myocytes Injury Induced by Intermittent Hypoxia.

BACKGROUND Obstructive sleep apnea (OSA) is associated with many cardiovascular disorders. Intermittent hypoxia (IH) is a key pathological hallmark of OSA. This study was conducted to evaluate the potential therapeutic effects and the associated mechanisms of adiponectin (APN) on IH induced human adult cardiac myocytes (HACMs) injury. MATERIAL AND METHODS HACMs were exposed to normoxia or IH (1% to 21% O₂) using a novel cell culture bio-reactor with gas-permeable membranes. Cell viability was detected by Cell Counting Kit-8 assay. Cell membrane integrity was assessed by the detection of lactate dehydrogenase (LDH) release. Cell apoptosis was analyzed by flow cytometry. Malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione peroxidase (GSH-Px) levels were determined using specific assay kits. P-AMPK (AMP-activated protein kinase), p-LKB1, and p-p65 protein levels were measured by western blotting. Pro-inflammatory factors including interleukin (IL)-1β, IL-6, IL-8 expressions were detected by enzyme-linked immunosorbent assay and quantitative real-time polymerase chain reaction. RESULTS The results showed that APN had no cytotoxic to HACMs. Compared with the control group, HACMs cell viability significantly decreased, LDH release increased and cell apoptosis increased in the IH group. The levels of IL-1β, IL-6, IL-8, MDA, and p-p65 were higher, while the levels of SOD, GSH-Px, p-AMPK, and p-LKB1 were lower in HACMs cells in the IH group than that in the control group. However, APN treatment significantly rescued these effects compared with the IH group in a dose-dependent manner. CONCLUSIONS In conclusion, these results indicated that APN protected against IH induced HACMs injury possibly mediated by AMPK and NF-κB pathway.

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Anti-inflammatory and antioxidative effects of the buds from different species of Populus in human gingival fibroblast cells: Role of bioflavanones.

Poplar leaf-buds (Populi gemmae) are used traditionally as anti-inflammatory agents to the treatment of skin injuries or cough. They differ in their diverse chemical composition and different types of activities, whose mechanisms are not fully recognized.

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Effect of miR-30e regulating NK cell activities on immune tolerance of maternal-fetal interface by targeting PRF1.

Natural killer (NK) cells, as key regulatory cells, accumulate at the maternal-fetal interface in large numbers. This study explored the effect of miR-30e on regulating the activity and function of peripheral blood NK cells (PB-NK cells) and decidua NK cells (D-NK cells) by targeting PRF1 in immune tolerance of maternal-fetal interface.

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Evaluation of serum sST2 and sCD40L values in patients with microvascular angina.

Coronary microvascular dysfunction plays a major role in the pathogenesis of microvascular angina (MVA). Along with endothelial dysfunction, microvascular atherosclerosis and inflammation seem to contribute to the development of coronary microvascular dysfunction. Serum soluble ST2 (sST2) and serum soluble CD40 ligand (sCD40L) are two biomarkers associated with inflammation and atherosclerosis. The aim of this study was to investigate the role of these biomarkers in the pathogenesis of MVA and determine their possible association with coronary microvascular dysfunction.

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