interleukin-8 and puerarin

To study the effect and acting mechanism of puerarin preconditioning (PP) on blood level of cytokines in patients undergoing cardiopulmonary bypass (CPB) in perioperative period.. Forty patients with heart diseases scheduled to take surgical operation were randomized into the control group and the PP group equally. They were treated with the same program, excepting that 0.6 g of puerarin was given to the PP group by adding in 5% glucose solution 250 mL for intravenous dripping every day for one week before operation, but to the control group, normal saline was given instead. The levels of tumor necrosis factor-alpha (TNF-alpha), interleukin 6, 8 and 10 (IL-6, IL-8, IL-10) in arterial blood were measured at 5 time points in the process of CPB, namely, anesthetic induction (T1), 10 min after the clamp of the ascending aorta (T2), 10 min, 2 h and 12 h after the Clamped aorta is unclamped (T3, T4 and T5).. All the above-mentioned indexes (TNF-alpha, IL-6, IL-8 and IL-10) gradually increased after beginning CPB, reached the peak at T4, then lowered gradually but still presented the higher levels at T5 than those at T1 (P < 0.05). Comparison between the two groups showed that levels of TNF-alpha, IL-6 and IL-8 were significantly lower (P < 0.05 or P < 0.01) and level of IL-10 was higher in the PP group than those in the control group respectively at all the time points (P < 0.01).. Injecting puerarin before CPB could effectively suppress the pro-inflammatory cytokines like TNF-alpha, IL-6 and IL-8; and enhance the expression of anti-inflammatory cytokines like IL-10, thus to alleviate the inflammatory reaction induced by CPB.

Topics: Adolescent; Adult; Cardiopulmonary Bypass; Female; Heart Diseases; Humans; Interleukin-10; Interleukin-6; Interleukin-8; Ischemic Preconditioning; Isoflavones; Male; Middle Aged; Perioperative Period; Postoperative Period; Treatment Outcome; Tumor Necrosis Factor-alpha; Young Adult

Atherosclerosis (AS) is the main cause of cardiovascular and cerebrovascular diseases.. The. By feeding a high-fat diet to 8-week-old apolipoprotein E knockout mice, an atherosclerosis model was created. H&E and IHC staining were used to analyse the histopathology of mice. CCK-8, TUNEL, and scratch tests were used to detect cell proliferation, apoptosis, and migration after 24 h treatment, respectively. ELISA was performed to evaluate the level of IL-6 and IL-8. The target miRNA and its downstream target gene were screened by the bioinformatics method; RT-qPCR has conducted to analyse the expression of these genes.. In the aortic tissue and serum of AS mice, puerarin can lower the expression of α-SMA and the inflammatory proteins IL-6 and IL-8. Puerarin (200 M) decreased hVSMC proliferation, migration, and IL-6 and IL-8 secretion by more than half. The inhibitory impact of puerarin on hVSMC was decreased by overexpression of miR-29b-3p. IGF1 was miR-29b-3p's downstream target gene. IGF1 expression increased almost 3-fold in AS mice and hVSMC, but miR-29b-3p mimic inhibited it. The effect of miR-29b-3p on hVSMC was reversed when IGF1 was overexpressed.. Puerarin inhibits the proliferation and inflammation of vascular smooth muscle in AS through the miR-29b-3p/IGF1 pathway. Puerarin may have a beneficial effect in the treatment of atherosclerosis and offer a novel therapy option.

Topics: Animals; Atherosclerosis; Cell Proliferation; Inflammation; Interleukin-6; Interleukin-8; Mice; MicroRNAs; Muscle, Smooth, Vascular; Pueraria

In the present study, we investigated effects of Puerarin on the early oxidative and inflammatory responses in the lung triggered by acute cigarette smoking (ACS). C57BL/6 mice were exposed to ACS for 1 hr in the presence or absence of Puerarin and harvested at 2, 6, and 24 hours. ACS induced significant increases in superoxide production in mouse lungs at 2 and 6 hours; and superoxide production was also elevated in a time and concentration dependent manner in cigarette smoke extract (CSE) stimulated human small airway epithelial cells (HSAECs), which was dose-dependently abrogated by Puerarin. ACS exposure upregulated NOX1, NOX2, and NOX4 protein expression in mouse lungs. Likewise, NOX1 and NOX4 were upregulated in CSE-stimulated HSAECs. These responses were significantly or completely attenuated by Puerarin. ACS induced significant infiltrations of neutrophils and macrophages in mouse lung parenchyma and BAL fluid, which were completely or significantly abrogated by Puerarin, so was the activation of the NF-

Topics: Animals; Cyclooxygenase 2; Inflammation Mediators; Interleukin-8; Isoflavones; Mice; Mice, Inbred C57BL; NADPH Oxidases; Nicotiana; Oxidation-Reduction; Oxidative Stress; Pulmonary Disease, Chronic Obstructive; Reactive Oxygen Species; Signal Transduction; Superoxides

Acute lung injury (ALI) is a critical illness syndrome with high morbidity and mortality in patients. Inflammation has been known to be involved in the development of ALI. The purpose of this study was to investigate the effect of puerarin on lipopolysaccharide (LPS)-induced ALI in mice. The pro-inflammatory cytokines TNF-α, IL-6 and IL-1β were determined by ELISA. Western blot analysis was used for detecting the expression of NF-κB, IκBα, and LXRα. And myeloperoxidase (MPO) activity, lung wet/dry (W/D) ratio, and histopathological examination were also detected in lung tissues. The results showed that puerarin significantly inhibited LPS-stimulated MPO activity in lung tissues. Meanwhile, puerarin attenuated lung histopathological changes and lung wet/dry (W/D) ratio. We also found that the expression of pro-inflammatory cytokines, TNF-α, IL-6 and IL-1β were inhibited by puerarin. Puerarin also inhibited LPS-induced TNF-α in RAW264.7 cells and IL-8 in A549 cells. From the results of western blotting, puerarin significantly suppressed LPS-stimulated NF-κB activation. And the expression of LXRα was dose-dependently increased by treatment of puerarin. The inhibition of puerarin on TNF-α production in RAW264.7 cells and IL-8 production in A549 cells were blocked by LXRα inhibitor geranylgeranyl pyrophosphate (GGPP). These results suggested that puerarin attenuated ALI by activating LXRα, which subsequently inhibited LPS-induced inflammatory response.

Topics: A549 Cells; Acute Lung Injury; Animals; Cytokines; Humans; Inflammation; Interleukin-1beta; Interleukin-6; Interleukin-8; Isoflavones; Lipopolysaccharides; Liver X Receptors; Lung; Mice; Mice, Inbred BALB C; NF-kappa B; NF-KappaB Inhibitor alpha; Peroxidase; Polyisoprenyl Phosphates; RAW 264.7 Cells; Tumor Necrosis Factor-alpha

In the present study, we aimed to explore the effects of puerarin on vascular endothelial cell injury induced by lipopolysaccharide (LPS) and its underlying mechanisms.. The cell viability and morphological changes were assessed using the cell counting kit-8 (CCK-8) assay and 4´,6-diamidino-2-phenylindole (DAPI) staining, respectively. The levels of tumor necrosis factor-alpha (TNF-α), interleukin-1β (IL-1β), monocyte/macrophage chemotactic protein-1 (MCP-1), IL-8, intercellular cell adhesion molecule-1 (ICAM-1), thrombomodulin (TM) and plasminogen activator inhibitor-1 (PAI-1) in cell culture supernatant were determined by the enzyme-linked immunosorbent assay (ELISA). The neutrophils adhesion to endothelial cells were examined by myeloperoxidase activity assay. The nuclear translocation of nuclear factor-κB p65 (NF-κB p65) was assessed by immunofluorescence analysis.. Compared with the control group, LPS challenge significantly injured human umbilical vein endothelial cells (HUVECs) and increased the levels of TNF-α, IL-1β, MCP-1, IL-8, ICAM-1, TM and PAI-1 in the cell culture supernatants. The neutrophils adhesion to endothelial cells were significantly increased in LPS-challenged HUVECs. Moreover, LPS challenge increased the nuclear translocation of NF-κB p65. However, puerarin pre-treatment attenuated the vascular endothelial injury and reduced the levels of TNF-α, IL-1β, MCP-1, IL-8, ICAM-1, TM and PAI-1 in cell supernatants of LPS-challenged HUVECs. In addition, the neutrophils adhesion to HUVECs induced by LPS were also decreased by puerarin pre-treatment. Furthermore, puerarin pre-treatment reduced the nuclear translocation of NF-κB p65 elicited by LPS.. Puerarin prevented LPS-induced vascular endothelial injury, the mechanism of which might be related to the suppression of NF-κB activation and subsequently altered levels of inflammatory factors and coagulation-related factors.

Topics: Cell Survival; Cells, Cultured; Chemokine CCL2; Gene Expression Regulation; Human Umbilical Vein Endothelial Cells; Humans; Intercellular Adhesion Molecule-1; Interleukin-1beta; Interleukin-8; Isoflavones; Lipopolysaccharides; NF-kappa B; Plasminogen Activator Inhibitor 1; Signal Transduction; Tumor Necrosis Factor-alpha

To investigate the effect of puerarin on interleukin (IL)-8 mRNA expression and the protein release in the co-culture of human bronchial epithelial (BEAS-2B) cells and human neutrophils.. BEAS-2B cells and neutrophills were cultured separately and co-cultured with puerarin (50, 100, and 200 μg/mL) for a predetermined time. Cytokines in culture supernatant were evaluated by protein array and IL-8 quantified by enzyme-linked immunosorbent assay (ELISA). IL-8 mRNA expression was evaluated by real-time quantitative polymerase chain reaction (real-time qPCR).. The co-culture of BEAS-2B cells and neutrophils exhibited synergistic effects on IL-8 mRNA expression in BEAS-2B cells, but not in neutrophils after 12 h incubation (P<0.01), as compared with that in BEAS-2B cells or neutrophils alone. IL-8 protein release in the culture supernatant was obviously elevated when BEAS-2B cells were co-cultured with human neutrophils as compared with that in the supernatant of BEAS-2B cells or neutrophils alone after incubated for 2, 6, 12, and 18 h (P<0.01). Treatment with puerarin could significantly down-regulate the expression of IL-8 mRNA in BEAS-2B cells and IL-8 release in the supernatant of the co-culture of BEAS-2B cells and neutrophils (P<0.01).. Puerarin could exhibit anti-inflammatory activity by suppressing IL-8 production from the co-culture of human bronchial epithelial cells and neutrophils.

Topics: Adult; Bronchi; Cell Communication; Cell Line; Coculture Techniques; Epithelial Cells; Fluorescence; Gene Expression Regulation; Humans; Interleukin-8; Isoflavones; Neutrophils; Real-Time Polymerase Chain Reaction; RNA, Messenger