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Circulating miR-146a/b correlates with inflammatory cytokines in COPD and could predict the risk of acute exacerbation COPD.

The aim of this study was to investigate the predicting value of miR-146a/b for acute exacerbation chronic obstructive pulmonary disease (AECOPD) and COPD, and to explore their associations with inflammatory cytokines in AECOPD and stable COPD patients.One hundred six AECOPD, 122 stable COPD patients, and 110 health volunteers with age and sex matched to total COPD patients (AECOPD and stable COPD) were enrolled. Blood samples were collected from all participants. Relative expression of miR-146a/b was determined by real-time polymerase chain reaction. Tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6), interleukin-8 (IL-8), leukotriene B4 (LTB-4) expression in serum from AECOPD and stable COPD patients were assessed using commercial ELISA kit.Serum levels of miR-146a and miR-146b were down regulated in AECOPD patients compared with stable COPD patients and HCs. miR-146a and miR-146b are of good values for predicting the risk of AECOPD in HCs with AUC of 0.702 and 0.715. Additionally, miR-146a and miR-146b could distinguish AECOPD from stable COPD patients with AUC of 0.670 and 0.643. In AECOPD patients, levels of miR-146a in AECOPD patients were negatively associated with TNF-α, IL-6, IL-8, and LTE-4 expression. In stable COPD patients, miR-146a expressions were negatively correlated with TNF-α, IL-1β, IL-6, IL-8, and LTE-4 levels. And, the expressions of miR-146b in AECOPD patients were negatively associated with IL-1β and LTB-4 expression. While in stable COPD patients, miR-146b expressions were only negatively correlated with TNF-α level.In conclusion, miR-146a and miR-146b were negatively correlated with inflammatory cytokines, and could be promising biomarkers for predicting the risk of AECOPD in stable COPD patients and healthy individuals.

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Tormentic acid inhibits IL-1β-induced chondrocyte apoptosis by activating the PI3K/Akt signaling pathway.

Interleukin-1β (IL-1β) accelerates degradation of the cartilage matrix and induces apoptosis of chondrocytes. Tormentic acid (TA) is a triterpene isolated from the stem bark of the Vochysia divergens plant, which has been demonstrated to exert in vitro inhibitory activity against hepatocyte apoptosis. However, the effects of TA on IL‑1β‑induced apoptosis of human chondrocytes remain unclear. Therefore, the present study investigated the in vitro effects of TA on human osteoarthritic chondrocyte apoptosis cultivated in the presence of IL‑1β. Human chondrocytes were pretreated with or without various concentrations of TA and then co‑incubated in the absence or presence of IL‑1β for 24 h. Cell viability was determined using the MTT assay, and cell apoptosis was detected using a Nucleosome ELISA kit. Caspase‑3 activity was detected using a caspase‑3 colorimetric assay kit. The levels of B‑cell lymphoma 2 (Bcl‑2)‑associated X protein (Bax), Bcl‑2, phosphorylated (p)‑phosphoinositide 3‑kinase (PI3K), PI3K, p‑protein kinase B (Akt) and Akt were measured by western blotting. The results revealed that pretreatment with TA inhibited IL‑1β‑induced cytotoxicity and apoptosis in chondrocytes. In addition, TA pretreatment increased B‑cell lymphoma (Bcl)‑2 expression, and decreased caspase‑3 activity and Bax expressionin human chondrocytes. In addition, pretreatment with TA markedly increased the expression of p‑PI3K and p‑Akt in IL‑1β‑induced chondrocytes. Collectively, these results indicate that TA inhibits IL‑1β‑induced chondrocyte apoptosis by activating the PI3K/Akt signaling pathway. Therefore, TA may be considered a potential therapeutic target for the treatment of osteoarthritis.

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AKT PKB Signaling Phospho Human Epstein-Barr Virus Hh Signaling Pathway Anta Mouse Epstein-Barr Virus AP-1 Reporter – HEK293 Wnt Signaling Pathway TCF BYL-719 Mechanisms: PI3K- Apoptosis antibody array AKT Phospho-Specific Arra AMPK Signaling Phospho-Sp Cancer Apoptosis Phospho- ErbB Her Signaling Phosph

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Interleukin-17 promotes the production of underglycosylated IgA1 in DAKIKI cells.

Interleukin 17 (IL-17) plays an important role in the pathogenesis of autoimmune diseases and might be associated with IgA nephropathy (IgAN). This study aimed to investigate the effect of IL-17 on autoimmune pathogenesis in IgA nephropathy.

1619 related Products with: Interleukin-17 promotes the production of underglycosylated IgA1 in DAKIKI cells.

Human Interleukin-17E (IL Human Interleukin-17F IL- Human Interleukin-17AF He Human Interleukin-17A IL- Mouse Interleukin-17A IL- Mouse Interleukin-17E (IL Mouse Interleukin-17AF He Mouse Interleukin-17F IL- interleukin 17 receptor C Recombinant Human Interle Recombinant Human Interle Recombinant Human Interle

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A dual-functional microfluidic chip for on-line detection of interleukin-8 based on rolling circle amplification.

Interleukin 8 (IL-8), also known as C-X-C motif ligand 8(CXCL8), is a proinflammatory chemokine functioned in neutrophil chemotaxis and activation. And it plays an important role in the process of glioma stem-like cell vascularization in the latest research. Herein, a dual-function microfluidic biosensor based on rolling circle amplification (RCA) was fabricated for cell culture and online IL-8 detection. A microfluidic chip was designed with two high passages connected by the vertical channels. One of the channels with immobilized capture antibody was prepared for IL-8 detection and another channel for cell culture. Immunoassays were achieved by a sandwich structure consisting of antibodies, IL-8, and aptamers. Signal amplification was mainly due to RCA and biotin-streptavidin linkage. The linear range for IL-8 was 7.5 -120pgmLin this assay. Moreover, the developed method was successfully applied to detect the IL-8 in tumor-derived endothelial cells (TDEC) and Human Umbilical Vein Endothelial cells (HUVEC) under chemical hypoxia condition. Semi-quantitative detection of IL-8 consumption in HUVEC cells in low oxygen condition was also achieved. These results were in statistical agreement with those obtained by commercial assay of enzyme-linked immunoassay kit (ELISA). The microfluidic chip based biosensor reported hereby has a large prospect in the basic research and clinical diagnosis of cancer stem cell.

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MarkerGeneTM Fluorescent 5-Acetylamino-6-formylami 6-Amino-1-benzyl-5-(N-for 4 Formylphenylboronic aci 4 Formylphenylboronic aci Interleukin-34 IL34 (N-t Interleukin-34 IL34 anti CRF Anti-Polyvalent HRP HAV VP1 P2A recombinant a Recombinant Viral antige MOUSE ANTI BOVINE ROTAVIR Detection Buffer A&B Anti

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Radiosensitization by CpG ODN7909 in an epidermoid laryngeal carcinoma Hep-2 cell line.

Objective To evaluate the radiosensitivity effect of CpG oligodeoxyribonucleotide (ODN) 7909 on human epidermoid cancer strain-2 (Hep-2) cells in vitro and discuss the potential for improved radiotherapy treatment in patients with laryngeal squamous cell carcinoma. Methods Toll-like receptor ( TLR) 9 expression was assessed in Hep-2 cells using Western blots and reverse transcription polymerase chain reaction. Cell Counting Kit-8 was used to detect Hep-2 cell viability at 24 and 48 h following treatment with different CpG ODN7909 concentrations. Cellular colonization was evaluated using microscopy. Cell cycle distribution and apoptosis rate was determined with flow cytometry. Interleukin (IL)-12 and tumour necrosis factor (TNF)-α concentrations were detected by enzyme-linked immunosorbent assay. Results Hep-2 cells were found to express TLR9, and CpG ODN7909 treatment suppressed Hep-2 cell viability in a dose- and time-dependent manner. Cell survival curve analyses revealed a sensitivity enhancement ratio of the mean death dose of 1.225 for CpG ODN7909 plus irradiation versus irradiation alone. Furthermore, the population of Gap 2/mitotic-phase cells, apoptosis rate and secreted IL-12 and TNF-α levels were significantly increased in Hep-2 cells treated with CpG ODN7909 plus irradiation versus IR alone. Conclusion CpG ODN7909 enhanced the radiosensitivity of Hep-2 cells in vitro.

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Esophageal squamous cell Kidney clear cell carcino Non small cell lung carci Lung small cell carcinoma Cell Cycle Control Phosph Kidney clear cell carcino Breast invasive ductal ca Rabbit Anti-Cell death in Rabbit Anti-Cell death in Colon carcinoma antibody Colon carcinoma tissue ar Colon carcinoma tissue ar

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Advanced glycation end-products increase IL-6 and ICAM-1 expression via RAGE, MAPK and NF-κB pathways in human gingival fibroblasts.

Diabetes mellitus (DM) is a risk factor for periodontal diseases and may exacerbate the progression of the pathogenesis of periodontitis. Advanced glycation end-products (AGEs) cause DM complications relative to levels of glycemic control and larger amounts accumulate in the periodontal tissues of patients with periodontitis and DM. In the present study, we investigated the effects of AGEs on the expression of inflammation-related factors in human gingival fibroblasts (HGFs) to elucidate the impact of AGEs on DM-associated periodontitis.

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Anti-inflammatory effects of Artemisia scoparia and its active constituent, 3,5-dicaffeoyl-epi-quinic acid against activated mast cells.

Artemisia scoparia Waldst. et Kit. (AS) has been used to treat inflammation, urticaria and hepatitis. However, the scientific studies of AS and its active compound for inflammatory reactions in activated human mast cell line, HMC-1 cells have not yet been elucidated.

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anti CD38 Hematopoietic p anti Transferrin receptor Anti C Reactive Protein A anti HSV (II) gB IgG1 (mo anti HCMV IE pp65 IgG1 (m anti HCMV gB IgG1 (monocl Epidermal Growth Factor ( Epidermal Growth Factor ( Fibroblast Growth Factor Fibroblast Growth Factor anti SLAM anti CDw150 IgG Mouse Anti-Human Matrix M

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MicroRNA-106b overexpression alleviates inflammation injury of cardiac endothelial cells by targeting BLNK via the NF-κB signaling pathway.

We aim to investigate whether microRNA-106b (miR-106b) affects the inflammation injury of cardiac endothelial cells (ECs) by targeting B-cell linker (BLNK) via the NF-κB signaling pathway. Human cardiac microvascular endothelial cells (HCMECs) were assigned into the control, hypoxia/reoxygenation (H/R), negative control (NC), pyrrolidine dithiocarbamate (PDTC), miR-106b mimic, miR-106b inhibitor, and si-BLNK, and miR-106b inhibitor+si-BLNK groups. Quantitative real-time polymerase chain reaction (qRT-PCR) and Western blotting were conducted for miR-106b expression and expressions of BLNK, interleukin (IL)-6, IL-1β, tumor necrosis factor (TNF)-α, NF-κB, pIκBα, BTK, and PLC-γ2. Enzyme-linked immunosorbent assay was applied for levels of IL-6, IL-10, and TNF-α; cell counting Kit-8 assay for cell proliferation; and flow cytometry for cell cycle and ensuing apoptosis. In-vitro tube formation assay was performed for tube formation ability. Dual-luciferase reporter assay revealed that BLNK was verified as the target gene of miR-106b. Compared with the H/R and NC groups, the PDTC, miR-106b mimic, and si-BLNK groups had declined expressions of IL-6, IL-1β, TNF-α, BTK, PLC-γ2, NF-κB p105/p50, and pIκBα as well as levels of L-6 and TNF-α, but contrarily elevated levels of NF-κB p105/p50 and IL-10. The PDTC, miR-106b mimic, and si-BLNK groups had less cell number in G/Gphase but higher cell count in both S and Gphases, decreased cell apoptosis but increased proliferation and tube formation ability, while opposite trends were observed in the miR-106b inhibitor group. Our findings indicated that the overexpression of miR-106b alleviated the inflammation injury of cardiac ECs by targeting BLNK via the NF-κB signaling pathway.

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AP-1 Reporter – HEK293 Wnt Signaling Pathway TCF NF-kB II Phospho-Specific Human Cardiac Microvascul Hh Signaling Pathway Anta Rat Mesenchymal Cells anti CD7 All T cells Reco anti Transferrin receptor SRE Reporter - HEK293 Cel JAK pathway ISRE reporter Nrf antioxidant pathway A NF kB reporter (Luc) HEK2

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Human umbilical cord-derived mesenchymal stem cells ameliorate insulin resistance by suppressing NLRP3 inflammasome-mediated inflammation in type 2 diabetes rats.

Insulin resistance is one of the most common and important pathological features of type 2 diabetes (T2D). Recently, insulin resistance is increasingly considered to be associated with systemic chronic inflammation. Elevated levels of tumor necrosis factor (TNF)-α and interleukin (IL)-1β in blood are predictive indicators of the development of T2D. Mesenchymal stem cell (MSC)-based therapies have been proven to have potential immunomodulation and anti-inflammatory properties through their paracrine effects; however, the mechanism for the anti-inflammatory effect of MSCs in enhancing insulin sensitivity is still uncertain.

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IL-17 Activates the IL-6/STAT3 Signal Pathway in the Proliferation of Hepatitis B Virus-Related Hepatocellular Carcinoma.

We performed this study to determine the role of IL-17 in the immune microenvironment of hepatitis B virus- (HBV-) related hepatocellular carcinoma (HCC).

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Human Epstein-Barr Virus Mouse Epstein-Barr Virus AMPK Signaling Phospho-Sp GPCR Signaling to MAPK ER TGF-Beta Signaling Phosph Interleukins Recombinant CELLKINES Natural Human I Human Interleukin-17E (IL Human Interleukin-17F IL- Human Interleukin-17AF He Human Interleukin-1-beta Human Interleukin-17A IL-

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