Adult ; Anesthetics, Intravenous ; pharmacology ; Cardiopulmonary Bypass ; Heart Valve Prosthesis Implantation ; Humans ; Interleukin-10 ; blood ; Interleukin-6 ; blood ; Interleukin-8 ; blood ; Middle Aged

BACKGROUNDKeratinocytes play a crucial role in the biological function of skin barrier. The relationship between sodium lauryl sulfate (SLS) and keratinocytes has been studied. However, the cytotoxicity and effects of sodium dodecyl benzene sulfonate (SDBS), a common detergent similar to SLS, on keratinocytes are still not known. This study aimed to investigate the effects of SDBS on cytotoxicity and expression of proinflammatory cytokines in cultured human keratinocytes.

METHODSThis study was carried out using the keratinocytes cell line, HaCaT cells. The cytotoxicity of SDBS on HaCaT cells was evaluated with cell counting kit-8 (CCK-8) and phase-contrast microscopy. After exposure to different concentrations of SDBS, the total RNA of the HaCaT cells was extracted for evaluating the relative mRNA expression of IL-1α, IL-6, IL-8, and TNF-α by qPCR. The supernatants of cells were collected for measuring the levels of IL-6 and IL-8 by enzyme-linked immunosorbent assay (ELISA).

RESULTSSDBS at concentrations of 20 µg/ml and over showed direct cytotoxicity and induced morphological changes of the HaCaT cells. The mRNA expressions of IL-1α, IL-6, IL-8, and TNF-a in different concentrations of SDBS at different time were comparable with that of controls. SDBS at concentrations of 5, 10, and 15 µg/ml had no significant effects on IL-6 and IL-8 excretion from HaCaT cells after 24-hour exposure. Moreover, no significant effects on the IL-6 and IL-8 excretion were found after 10 and 15 µg/ml SDBS stimulations for 6, 12, and 24 hours, respectively.

CONCLUSIONSDBS at higher concentrations had cytotoxicity on HaCaT cells but had no effects on the mRNA expression of IL-1α, IL-6, IL-8, and TNF-a, that was different from SLS.

Benzenesulfonates ; pharmacology ; Cell Line ; Enzyme-Linked Immunosorbent Assay ; Humans ; Interleukin-1alpha ; metabolism ; Interleukin-6 ; metabolism ; Interleukin-8 ; metabolism ; Keratinocytes ; drug effects ; metabolism ; Tumor Necrosis Factor-alpha ; metabolism

OBJECTIVETo test the effect of high-mobility group box protein 1 (HMGB1) alone or in synergy with interleukin-1β (IL-1β) on the expression of IL-8 in human airway epithelial cells in vitro.

METHODSHuman airway epithelial 16HBE and A549 cell lines were incubated with HMGB1 (100 ng/ml) in the absence or presence of IL-1β (10 ng/ml) for 24 h, and the changes of IL-8 mRNA and protein expressions were assessed using quantitative PCR and enzyme-linked immunosorbent assay (ELISA).

RESULTSIn the two human airway epithelial cell lines, HMGB1 alone did not produce obvious effect on the expression of IL-8, but in the presence of IL-1β, HMGB1 caused a significant increase of IL-8 expressions at both the mRNA and protein levels.

CONCLUSIONHMGB1 in synergy with IL-1β increases the expression of IL-8 in human airway epithelial cells, which provides new evidence that HMGB1 contributes to neutrophilic airway inflammation by regulating IL-8 expression.

Bronchi ; cytology ; drug effects ; Cell Line ; Epithelial Cells ; drug effects ; metabolism ; HMGB1 Protein ; pharmacology ; Humans ; Inflammation ; Interleukin-1beta ; pharmacology ; Interleukin-8 ; metabolism ; RNA, Messenger

BACKGROUNDStatins are potent lipid-lowering agents widely used in medical practice. There has been growing evidence suggesting the pleiotropic effects of statins in addition to the lipid-lowering effect. However, it is still unclear how rapidly the beneficial effects of statins occur. The transcriptome of peripheral blood cells can be used as a sensor to drug therapy. The purpose of the study was to investigate the acute effects of rosuvastatin both on lipids profile and gene expression of peripheral leukocytes following therapy with a single dose of rosuvastatin.

METHODSThirty healthy Chinese male volunteers were enrolled. The serum lipids, high-sensitivity C-reactive protein, and plasma fibrinogen were determined before and 72 hours after administration of 20 mg of rosuvastatin. The differentially expressed genes of peripheral leukocytes after administration of rosuvastatin were screened using human oligonucleotide microarray gene expression chips. Then four of the differentially expressed genes including ATM, CASP8, IL8RB and S100B were verified by real-time polymerase chain reaction (PCR).

RESULTSRosuvastatin decreased both serum total cholesterol and low-density lipoprotein cholesterol significantly 72 hours after administration of a single dose of 20 mg rosuvastatin. However, no significant changes occurred in blood high-density lipoprotein cholesterol, triglycerides, C-reactive protein and fibrinogen after the treatment. A total of 24 genes were differentially expressed after the treatment. They were involved in important cell biological processes such as cytokine-cytokine receptor interaction, apoptosis signaling, etc.

CONCLUSIONSRosuvastatin rapidly modulates the serum lipids and affects the gene expression of peripheral leukocytes in healthy volunteers. This finding provides some new clues for further studies on its potential pleiotropic effects.

Adult ; Caspase 8 ; genetics ; Fluorobenzenes ; pharmacology ; Gene Expression Profiling ; Humans ; Hydroxymethylglutaryl-CoA Reductase Inhibitors ; pharmacology ; Leukocytes ; drug effects ; metabolism ; Lipids ; blood ; Male ; Polymerase Chain Reaction ; Pyrimidines ; pharmacology ; Receptors, Interleukin-8 ; genetics ; Rosuvastatin Calcium ; Sulfonamides ; pharmacology

AIMTo investigate the effect of interleukin-8 (IL-8) on the differentiation and clonal expansion of 3T3-L1 preadipocyte during the differentiation period.

METHODSThe morphological changes of 3T3-L1 cells during differentiation after the treatment of IL-8 was observed by Oil-Red O staining. Glycerol-3-phosphate dehydrogenase (GPDH) activity was measured by a spectrophotometric method. MTT method and 3H-TdR incorporation were applied to examine the changes of cell proliferation and DNA synthesis in clonal expansion of 3T3-L1 cells. Cell cycle analysis was taken by flow cytometry.

RESULTSIL-8 could inhibit the differentiation and GDPH activity in a dose dependent manner. IL-8 decreased the cell proliferation and DNA synthesis in clonal expansion after induction. Also, the proportion of cells in G1 phase was increased and that of cells in S and G2 phase was declined after the treatment of IL-8.

CONCLUSIONIL-8 inhibits the differentiation of 3T3-L1 preadipocytes by decreasing the clonal expansion of the cells.

3T3-L1 Cells ; Adipocytes ; cytology ; metabolism ; Animals ; Cell Cycle ; Cell Differentiation ; Cell Proliferation ; drug effects ; Interleukin-8 ; pharmacology ; Mice

Inflammatory responses are strictly regulated by coordination of pro-inflammatory and anti-inflammatory mediators. Interleukin-4 (IL-4) and interleukin-10 (IL-10) have typically the biologic anti-inflammatory effects on monocytes, but uncertain effects on polymorphonuclear leukocytes (PMNs). The PMNs are the first line of cellular response for host defense during acute inflammation. To modify hyper-inflammatory reaction with biologic anti-inflammatory mediators, we have determined the biologic anti-inflammatory activities of IL-4 and IL-10 on human PMNs. Human PMNs were pretreated with IL-4 or IL-10 and then stimulated with formyl methionyl leucyl phenylalanine (fMLP) for times indicated. The level of H2O2, interleukin-8 (IL-8) and tumor necrosis factor-alpha (TNF-alpha) were determined in the each cell free supernatants. fMLP plays the role of a typical pro-inflammatory agent and, at least in determined conditions, down-regulated TNF release. IL-4 acts as an anti-inflammatory mediator but IL-10 did not show its anti-inflammatory activities on fMLP-stimulated human PMNs. IL-4 and IL-10 have different anti-inflammatory mechanisms. Perhaps, IL-10 needs co-factors to act as an anti-inflammatory mediator.
Cells, Cultured ; Humans ; Hydrogen Peroxide/metabolism ; Interleukin-10/*pharmacology ; Interleukin-4/*pharmacology ; Interleukin-8/metabolism ; Intracellular Fluid ; N-Formylmethionine Leucyl-Phenylalanine/pharmacology ; Neutrophils/cytology/*drug effects/immunology ; Tumor Necrosis Factor-alpha/metabolism

Animals ; Benzylisoquinolines ; pharmacology ; Brain Ischemia ; metabolism ; Interleukin-1beta ; metabolism ; Interleukin-8 ; metabolism ; Male ; Rats ; Rats, Sprague-Dawley ; Reperfusion Injury ; metabolism ; Tumor Necrosis Factor-alpha ; metabolism

OBJECTIVETo investigate the expression of myeloid differentiation protein-2 (MD-2) in the human endothelial cells and its role in lipopolysaccharide (LPS)-induced NF-kappaB activation in endothelial cells.

METHODSIn vitro cultured human umbilical vein endothelial cells (HUVEC) were employed in the study. The expression of MD-2 mRNA and protein, and the effect of LPS on the expression of its mRNA and protein were assessed with RT-PCR and Western blotting. The role of MD-2 in LPS-induced NF-kappaB activation and IL-8 production were investigated with gene transfection of mutant MD-2 cDNA (0.5, 1.0, 2.0 microg), pEF-BOS vacant vector (2.0 microg) and MD-2 plasmid (2.0 microg) into HUVEC, respectively.

RESULTSThere was MD-2 mRNA and protein expression in HUVECs before LPS stimulation, and it could be obviously upregulated by LPS in time and dose-dependent manner (MD-2 protein absorbency was 25 196 +/- 1 723 without LPS stimulation, which was obviously lower than that stimulated with 0.01 mg/L LPS (58 817 +/- 3 241, P < 0.01) for 6 hours. Transfection of mutant MD-2 cDNA could remarkably inhibit LPS-induced NF-kappaB activation and IL-8 production in endothelial cells.

CONCLUSIONMD-2 might play an important role in the LPS-induced NF-kappaB activation in HUVECs.

Cell Differentiation ; Cells, Cultured ; Endothelial Cells ; metabolism ; Humans ; Interleukin-6 ; genetics ; Interleukin-8 ; metabolism ; Lipopolysaccharides ; pharmacology ; NF-kappa B ; metabolism ; Umbilical Veins ; cytology

OBJECTIVETo study the regulatory role of bacterial lipopolysaccharide (LPS ) in the development of bronchial asthma by examining the effects of LPS on serum IL-4, serum IL-8 and pulmonary vascular endothelial growth factor (VEGF) expression in mice with asthma.

METHODSTwenty-seven BALB/c mice were randomly assigned into control, asthma and LPS-treated asthma groups (n=9 each). Serum IL-4 and IL-8 concentrations were measured using ELISA. VEGF expression in lung tissues was examined using the immunohistochemical method.

RESULTSSerum IL-4 and IL-8 concentrations in the asthma group were significantly higher than in the control group (P<0.05). LPS treatment significantly decreased serum IL-4 and IL-8 concentrations compared with the asthma group (P<0.05), although levels were significantly higher than in the control group (P<0.05). Airway VEGF expression in the asthma group was significantly higher than in the control group (P<0.05). LPS treatment significantly decreased airway VEGF expression compared with the asthma group (P<0.05), although concentrations remained higher than in the control group (P<0.05).

CONCLUSIONSLPS can decrease serum IL-4, serum IL-8 and pulmonary VEGF expression in mice with asthma, and thus can possibly reduce both airway inflammation and airway vascular remodeling.

Animals ; Asthma ; drug therapy ; immunology ; Female ; Interleukin-4 ; blood ; Interleukin-8 ; blood ; Lipopolysaccharides ; pharmacology ; Mice ; Mice, Inbred BALB C ; Vascular Endothelial Growth Factor A ; analysis ; physiology

OBJECTIVETo investigate the protective effects of beta-carotene in rats against the development of chronic bronchitis induced by cigarette smoking.

METHODSForty-two Male Wistar rats were randomly divided into three study groups: (1) control (n = 15), animals underwent no treatment; (2) cigarette smoking (n = 15), animals developed chronic bronchitis through long-term cigarette smoking twice a day for 75 d; (3) beta-carotene plus cigarette smoking animals (n = 12) were given 1 ml or 15 mg/kg beta-carotene orally every day just before cigarette smoking. The levels of IL-6, IL-8, NO, superoxide dismutase (SOD) and lipoperoxide (LPO) in serum, bronchoalveolar lavage fluid (BALF) and lung tissue were measured and the pathological changes to lung tissue were analyzed using light microscopy.

RESULTSLong-term cigarette smoking caused an obvious increase in the amount of IL-6, IL-8 and LPO and a sharp decrease in the levels of NO and SOD in smoking animals compared to controls. beta-carotene intake reversed all the changes induced by smoking and alleviated the pathological changes caused by chronic bronchitis.

CONCLUSIONSQuantitative oral intake of beta-carotene had protective effects against chronic bronchitis induced by long-term cigarette smoking, which was associated with the increased production of NO, the clearance of some oxidative free radicals (OFR) and the alleviation of chronic inflammation.

Animals ; Bronchitis ; blood ; etiology ; prevention & control ; Interleukin-6 ; blood ; Interleukin-8 ; blood ; Male ; Nitric Oxide ; blood ; Rats ; Rats, Wistar ; Smoking ; adverse effects ; Superoxide Dismutase ; blood ; beta Carotene ; pharmacology