interleukin-8 and honokiol

Preterm birth is the most prominent complication attributing to poor pregnancy and neonatal outcome. Infection is most commonly implicated in preterm birth; it initiates a cascade of inflammatory events that leads to the rupture of fetal membranes and spontaneous uterine contractions. Anti-inflammatory agents may thus be a therapeutic approach to prevent the premature rupture of fetal membranes and block contractions. In non-gestational tissues, the polyphenol honokiol has been shown to possess potent anti-inflammatory properties.. The aim of this study was to investigate the effect of honokiol on pro-inflammatory mediators in human gestational tissues.. Fetal membranes, myometrium and freshly isolated amnion cells and primary myometrial cells were treated with honokiol in the absence or presence of the products lipopolysaccharide (LPS) and fibroblast-stimulating lipopeptide-1 (fsl-1), the viral dsRNA analogue polyinosinic:polycytidylic acid (poly(I:C)) or the pro-inflammatory cytokines TNF or IL1B. A luciferase assay was used to determine the effect of honokiol on nuclear factor kappa B (NF-κB) RelA transcriptional activity.. Honokiol significantly decreased pro-inflammatory cytokine (IL1A, IL6) and chemokine (CXCL8, CXCL1, CCL2) mRNA expression and secretion from fetal membranes (amnion and choriodecidua) and myometrium stimulated with LPS, fsl-1 or poly(I:C). In amnion cells, honokiol also significantly decreased the expression and secretion of the extracellular matrix degrading enzyme MMP9. Moreover, in myometrium, honokiol significantly suppressed the expression of the contraction associated protein PTGFR, the secretion of the uterotonic prostaglandins PGE. Honokiol reduced the expression of pro-inflammatory and pro-labour mediators in human amnion, choriodecidua and myometrium and that this may be facilitated through the suppression of NF-κB activation. These results indicate that the polyphenol honokiol may be a potent therapeutic for the prevention of preterm birth.

Topics: Anti-Inflammatory Agents; Biphenyl Compounds; Chemokine CCL2; Chemokine CXCL1; Dinoprost; Dinoprostone; Extraembryonic Membranes; Female; Humans; Interleukin-1beta; Interleukin-8; Lignans; Myometrium; Pregnancy; Premature Birth; Primary Cell Culture; Transcription Factor RelA; Tumor Necrosis Factor-alpha

Pollution, especially cigarette smoke, is a major cause of skin damage.. To assess the effects of the small molecule polyphenol, honokiol, on reversing cigarette smoke-induced damage in vitro to relevant skin cells.. Keratinocytes (HaCat) cultures were exposed to cigarette smoke and, after 48 hours, IL-1α and IL-8 were measured in cell supernatants. Moreover, TIMP-2 production, apoptosis rate, and senescence β-galactosidase expression were evaluated in primary human foreskin fibroblasts (HFF-1) cultures.. Honokiol at 10 μm reduced IL-1α production by 3.4 folds (P < 0.05) and at 10 and 20 μm reduced IL-8 by 23.9% and 53.1% (P < 0.001), respectively, in HaCat keratinocytes. In HFF-1, honokiol restored TIMP-2 production by 96.9% and 91.9% (P < 0.001), respectively, at 10 and 20 μm, as well as reduced apoptosis by 47.1% (P < 0.001) and 41.3% (P < 0.01), respectively. Finally, honokiol reduced senescence-associated β-galactosidase expression in HFF-1.. Honokiol protects both HFF-1 and HaCat against cigarette smoke-induced inflammation, collagenolysis, apoptosis, and senescence.

Topics: Antioxidants; Apoptosis; beta-Galactosidase; Biphenyl Compounds; Cells, Cultured; Cellular Senescence; Fibroblasts; Humans; Inflammation; Interleukin-1alpha; Interleukin-8; Lignans; Tissue Inhibitor of Metalloproteinase-2; Tobacco Smoke Pollution

To observe the anti-inflammatory effects of honokiol in primary cultures of peripheral blood mononuclear cells of rheumatoid arthritis patients, the pro-inflammatory cytokines and potential targets were investigated.. The levels of GM-CSF, IL-1β, TNF-α and IL-8 were determined by ELISA assay. The genes and proteins expression were analyzed by real-time PCR and Western blotting respectively.. The serum IL-1β, TNF-α and GM-CSF levels were 1.76-, 2.16- and 3.57-fold increased in patients with RA as compared to those of control group. Honokiol inhibited the expression levels of IL-1β, TNF-α, GM-CSF and IL-8 in PBMCs with a dose-dependent manner. Measurements obtained from supernatants were positively correlated between TNF-α and IL-1β, moreover, similar results found TNF-α levels positively correlated with GM-CSF and IL-8 activity in the supernatants of PBMCs isolated from RA patients. Furthermore, the mRNA and protein expression of IL-1β, GM-CSF and IL-8 were up-regulated when the PBMCs exposure to TNF-α, however, honokiol treatment significantly reversed the expression of IL-1β, TNF-α and GM-CSF in response to TNF-α with a dose-dependent manner.. This study demonstrates that honokiol could possess potential anti-inflammatory effects and inhibits TNF-α-induced IL-1β, GM-CSF and IL-8 production in PBMCs from rheumatoid arthritis patients.

Topics: Adult; Aged; Anti-Inflammatory Agents; Antirheumatic Agents; Arthritis, Rheumatoid; Biphenyl Compounds; Case-Control Studies; Cells, Cultured; Dose-Response Relationship, Drug; Female; Granulocyte-Macrophage Colony-Stimulating Factor; Humans; Inflammation Mediators; Interleukin-1beta; Interleukin-8; Leukocytes, Mononuclear; Lignans; Male; Middle Aged; Primary Cell Culture; Signal Transduction; Tumor Necrosis Factor-alpha

Interleukin-8 (IL-8) and tumour necrosis factor-alpha (TNF-α) from keratinocyte play important roles in initiating the inflammatory process of acne. They are used as major elements to evaluate the anti-inflammatory activity of drugs. In this study, various active constituents extracted from Chinese medicinal herbs were tested for their anti-inflammatory effects against P. acnes using ELISA. Among the constituents, matrine, baicalin, ursolic acid, sodium danshensu, magnolol, honokiol, hesperidin and andrographolide significantly reduced IL-8 and TNF-α by human HaCaT keratinocyte cells pretreated with heat-killed P. acnes. Excepting hesperidin, these active constituents presented dose-dependent inhibitory effects. Our studies showed that all of them exhibited low cytotoxicity at 5 µg mL⁻¹ in tested cell lines, and even at 50 µg mL⁻¹, in the cases of matrine, baicalin, ursolic acid and sodium danshensu. Based on the obtained results, it can be suggested that these active constituents are potential acne-mitigating candidates for cosmetic applications.

Topics: Anti-Inflammatory Agents; Biphenyl Compounds; Cell Line; Drugs, Chinese Herbal; Flavonoids; Humans; Interleukin-8; Keratinocytes; Lignans; Propionibacterium acnes; Triterpenes; Ursolic Acid

Propionibacterium acnes, an anaerobic pathogen, plays an important role in the pathogenesis of acne and seems to initiate the inflammatory process by producing proinflammatory cytokines. In order to demonstrate the anti-inflammatory effects and action mechanisms of magnolol and honokiol, several methods were employed. Through DPPH and SOD activity assays, we found that although both magnolol and honokiol have antioxidant activities, honokiol has relatively stronger antioxidant activities than magnolol {[for DPPH assay, % of DPPH bleaching of magnolol and honokiol (500 microM magnolol: 19.8%; 500 microM honokiol: 67.3%)]; [for SOD assay, SOD activity (200 microM magnolol: 53.4%; 200 microM honokiol: 64.3%)]}. Moreover, the production of interleukin-8 (IL-8) and tumor necrosis factor-alpha (TNF-alpha) induced by P. acnes in THP-1 cells, a human monocytic cell line, was reduced by magnolol and honokiol {[for IL-8 (10 microM magnolol: 42.7% inhibition; 10 microM honokiol: 51.4% inhibition)]; [for TNF-alpha (10 microM magnolol: 20.3% inhibition; 10 microM honokiol: 39.0% inhibition)]}. Cyclooxygenase-2 (Cox-2) activity was also suppressed by them [(15 microM magnolol: 45.8% inhibition), (15 microM honokiol: 66.3% inhibition)]. Using a nuclear factor-kappaB (NF-kappaB) luciferase reporter assay system and Western analysis, we identified that magnolol and honokiol exert their anti-inflammatory effects by inhibiting the NF-kappaB element, which exists in Cox-2, IL-8, and TNF-alpha promoters [(15 microM magnolol: 44.8% inhibition), (15 microM honokiol: 42.3% inhibition)]. Of particular note is that magnolol and honokiol operate downstream of the MEKK-1 molecule. Together with their previously known antibacterial activity against P. acnes and based on these results, we suggest that magnolol and honokiol may be introduced as possible acne-mitigating agents.

Topics: Anti-Bacterial Agents; Anti-Inflammatory Agents, Non-Steroidal; Antioxidants; Biphenyl Compounds; Cytokines; Humans; Interleukin-8; Lignans; Magnolia; MAP Kinase Kinase Kinase 1; Microbial Sensitivity Tests; Monocytes; NF-kappa B; Phytotherapy; Picrates; Plant Extracts; Propionibacterium acnes; Superoxide Dismutase; Tumor Necrosis Factor-alpha