interleukin-8 and naringin

Systemic inflammation, circulating immune cell activation, and endothelial cell damage play a critical role in vascular pathogenesis. Flavonoids have shown anti-inflammatory effects. In this study, we investigated the effects of different flavonoids on the production of pro-inflammatory interleukin (IL) 1β, 6, and 8, and tumor necrosis factor α (TNF-α), in peripheral blood cells. Methods: We studied the whole blood from 36 healthy donors. Lipopolysaccharide (LPS)-stimulated (0.5 μg/mL) whole-blood aliquots were incubated in the presence or absence of different concentrations of quercetin, rutin, naringenin, naringin, diosmetin, and diosmin for 6 h. Cultures were centrifuged and the supernatant was collected in order to measure IL-1β, TNF-α, IL-6, and IL-8 production using specific immunoassay techniques. This production was significantly inhibited by quercetin, naringenin, naringin, and diosmetin, but in no case by rutin or diosmin. Flavonoids exert different effects, maybe due to the differences between aglycons and glucosides present in their chemical structures. However, these studies suggest that quercetin, naringenin, naringin, and diosmetin could have a potential therapeutic effect in the inflammatory process of cardiovascular disease.

Topics: Anti-Inflammatory Agents; Diosmin; Dose-Response Relationship, Immunologic; Female; Flavanones; Flavones; Flavonoids; Flavonols; Healthy Volunteers; Humans; Interleukin-1beta; Interleukin-6; Interleukin-8; Leukocytes, Mononuclear; Lipopolysaccharides; Male; Primary Cell Culture; Quercetin; Rutin; Tumor Necrosis Factor-alpha; Young Adult

Naringin is a bioflavonoid and has free radical scavenging and anti-inflammatory properties.. We examined the effects of naringin on skin after ultraviolet radiation B (UVB) irradiation and the signal pathways by in vitro and in vivo assay.. HaCaT cells pretreated with naringin significantly inhibited UVB induced-cell apoptosis and production of intracellular reactive oxygen species (ROS). The expressions of interleukin-1β (IL-1β), interleukin-6 (IL-6), interleukin-8 (IL-8) and cyclooxygenase-2 (COX-2) in HaCaT cells pretreated with naringin were decreased compared with the only UVB group. Also, the activation of p38 induced by UVB in HaCaT cells was reversed by naringin treatments. The inhibition function of naringin on p38 activity was more obvious than JNK. In vivo, topical treatments with naringin prevented the increase of epidermal thickness, IL-6 production, cell apoptosis and the overexpression of COX-2 in BALB/c mice skin irradiated with UVB. Naringin treatment also markedly blocked the activation of p38 in response to UVB stimulation in the mouse skin.. Naringin can effectively protect against UVB-induced keratinocyte apoptosis and skin damage by inhibiting ROS production, COX-2 overexpression and strong inflammation reactions. It seemed that naringin played its role against UVB-induced skin damage through inhibition of mitogen-activated protein kinase (MAPK)/p38 activation.

Topics: Animals; Apoptosis; Cell Line; Cyclooxygenase 2; Female; Flavanones; Humans; Inflammation; Interleukin-1beta; Interleukin-6; Interleukin-8; Keratinocytes; MAP Kinase Signaling System; Mice; Mice, Inbred BALB C; Mice, Nude; p38 Mitogen-Activated Protein Kinases; Reactive Oxygen Species; Skin; Ultraviolet Rays

Our previous study has demonstrated that naringin attenuates EGF-induced MUC5AC hypersecretion in A549 cells by suppressing the cooperative activities of MAPKs/AP-1 and IKKs/IκB/NF-κB signaling pathways. However, the volume of airway mucus is determined by two factors including the number of mucous cells and capacity of mucus secretion. The aim of the present study is to explore the mucoactive effects of naringin in lipopolysaccharide (LPS)-induced acute lung injury (ALI) mice and beagle dogs. The results demonstrated that naringin of 12.4 mg/kg treatment significantly decreased LPS-induced enhancement of sputum volume and pulmonary inflammation, remarkably increased the subglottic sputum volume and solids content in sputum of lower trachea, while partially, but not fully, significantly increased the elasticity and viscosity of sputum in lower trachea of beagle dogs. Moreover, the MUC5AC content in BALF and goblet-cells in large airways of LPS-induced ALI mice were significantly attenuated by dexamethasone (5 mg/kg), ambroxol (25 mg/kg), and naringin (15, 60 mg/kg). However, the goblet-cells hyperplasia in small airways induced by LPS was only significantly inhibited by dexamethasone and naringin (60 mg/kg). In conclusion, naringin exhibits mucoactive effects through multiple targets which including reduction of goblet cells hyperplasia and mucus hypersecretion, as well as promotion of sputum excretion.

Topics: Acute Lung Injury; Animals; Bronchoalveolar Lavage Fluid; Dogs; Elasticity; Female; Flavanones; Goblet Cells; Hyperplasia; Interleukin-8; Leukocyte Count; Lipopolysaccharides; Male; Mice; Mucin 5AC; Mucus; Pneumonia; Sputum; Tumor Necrosis Factor-alpha; Viscosity

Naringin has been reported to act as an effective anti-inflammatory compound. In a previous study, we demonstrated that the anti-inflammatory effect of naringin on lipopolysaccharide (LPS)-induced acute lung injury in mice correlated with the inhibition of the nuclear factor-κB (NF-κB) pathway. However, the effects and mechanism of action of naringin on LPS-induced chemokine expression are not yet fully understood. This study aimed to evaluate the effect of naringin on chemokine expression in LPS-induced RAW 264.7 macrophages and to provide insights into the possible underlying mechanisms. We found that the in vitro pre-treatment with naringin led to a significant attenuation in the LPS-induced secretion of interleukin-8 (IL-8), monocyte chemoattractant protein-1 (MCP-1) and macrophage inflammatory protein-1α (MIP-1α). RT-qPCR demonstrated that naringin significantly reduced the LPS-induced upregulation of IL-8, MCP-1 and MIP-1α mRNA expression in a dose-dependent manner. Additionally, western blot analysis revealed that naringin effectively suppressed NF-κB activation by inhibiting the degradation of IκB-α and the translocation of p65. Naringin also attenuated MAPK activation by inhibiting the phosphorylation of ERK1/2, JNK and p38 MAPK. Taken together, these demonstrate that naringin reduces IL-8, MCP-1 and MIP-1α secretion and mRNA expression, possibly by blocking the activation of the NF-κB and MAPK signaling pathways in LPS-induced RAW 264.7 macrophages.

Topics: Animals; Cell Line; Chemokine CCL3; Chemokines; Flavanones; Gene Expression; I-kappa B Proteins; Interleukin-8; JNK Mitogen-Activated Protein Kinases; Lipopolysaccharides; Macrophages; Mice; Mitogen-Activated Protein Kinase 1; Mitogen-Activated Protein Kinase 3; NF-kappa B; NF-KappaB Inhibitor alpha; p38 Mitogen-Activated Protein Kinases; Phosphorylation; Receptors, CCR2; RNA, Messenger; Signal Transduction; Transcription Factor RelA

Naringin, a well-known flavanone glycoside of grapefruit and citrus fruits, was found to be as an effective anti-inflammatory compound in our previous lipopolysaccharide-induced acute lung injury mouse model via blockading activity of nuclear factor κB. The current study sought to explore the anti-inflammatory effects of naringin on chronic pulmonary neutrophilic inflammation in cigarette smoke (CS)-induced rats. Seventy Sprague-Dawley rats were randomly divided into seven groups to study the effects of CS with or without various concentrations of naringin or saline for 8 weeks. The results revealed that naringin supplementation at 20, 40, and 80 mg/kg significantly increased body weight of CS-induced rats as compared to that in the CS group. Moreover, naringin of 20, 40, and 80 mg/kg prevented CS-induced infiltration of neutrophils and activation of myeloperoxidase and matrix metalloproteinase-9, in parallel with suppression of the release of cytokines, such as tumor necrosis factor-α and interleukin-8 (IL-8). IL-10 in bronchoalveolar lavage fluid was significantly suppressed after CS exposure, but dose dependently elevated by naringin. The results from hematoxylin and eosin staining revealed that naringin dose dependently reduced CS-induced infiltration of inflammatory cells, thickening of the bronchial wall, and expansion of average alveolar airspace. In conclusion, our data suggest that naringin is an effective anti-inflammatory compound for attenuating chronic pulmonary neutrophilic inflammation in CS-induced rats.

Topics: Animals; Anti-Inflammatory Agents; Bronchoalveolar Lavage Fluid; Female; Flavanones; Interleukin-10; Interleukin-8; Male; Matrix Metalloproteinase 9; Neutrophils; Peroxidase; Pneumonia; Pulmonary Disease, Chronic Obstructive; Rats; Rats, Sprague-Dawley; Smoking; Tumor Necrosis Factor-alpha