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Histamine Induced Production of Chemokine CXCL8 Through H1R/PLC and NF-κB Signaling Pathways in Nasal Fibroblasts |
Byungjin Kang, Joo-Hoo Park, Heung-Man Lee |
J Rhinol. 2020;27(2):95-101. Published online March 12, 2020 DOI: https://doi.org/10.18787/jr.2019.00302 |
Histamine Induced Production of Chemokine CXCL8 Through H1R/PLC and NF-κB Signaling Pathways in Nasal Fibroblasts Histamine Promotes the Release of Interleukin-6 via the H1R/p38 and NF-κB Pathways in Nasal Fibroblasts All‐
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retinoic acid regulates TGF‐β1‒induced extracellular matrix production via p38, JNK, and NF‐κB‒signaling pathways in nasal polyp‒derived fibroblasts Nrf2 and NF-κB Signaling Pathways Contribute to Porphyra-334-Mediated Inhibition of UVA-Induced Inflammation in Skin Fibroblasts Tumor Necrosis Factor α-Induced MicroRNA-18a Activates Rheumatoid Arthritis Synovial Fibroblasts Through a Feedback Loop in NF-κB Signaling Cigarette Smoke Extract Stimulates MMP-2 Production in Nasal Fibroblasts via ROS/PI3K, Akt, and NF-κB Signaling Pathways TNFR1-induced activation of the classical NF-κB pathway Acidic pH stimulates the production of the angiogenic CXC chemokine, CXCL8 (interleukin‐8), in human adult mesenchymal stem cells via the extracellular signal‐regulated kinase, p38 mitogen‐activated protein kinase, and NF‐κB pathways Sappanone A inhibits oxidative stress, inflammation and apoptosis in cigarette smoke-induced human bronchial epithelial cells through regulating Nrf2/HO-1 and TLR4/NF-κB signaling pathways Plantamajoside Inhibits Lipopolysaccharide-Induced MUC5AC Expression and Inflammation through Suppressing the PI3K/Akt and NF-κB Signaling Pathways in Human Airway Epithelial Cells |