Plasma apo CⅢ Levels in Relation to Inflammatory Traits and Metabolic Syndrome in Patients not Treated with Lipid-lowering Drugs Undergoing Coronary Angiography

Objective Assessment of the comprehensive relationship among apolipoprotein CIII（apoCⅢ） levels, inflammation, and metabolic disorders is rare. Methods A total of 1455 consecutive patients not treated with lipid-lowering drugs and undergoing coronary angiography were enrolled in this cross-sectional study. A mediation analysis was used to detect the underlying role of apoCⅢ in the association of inflammation with metabolic syndrome（MetS）. Results Patients with MetS showed higher levels of apoCⅢ [95.1（73.1-131.4） vs. 81.7（58.6-112.4） μg/mL, P 〈 0.001] and inflammatory markers [high sensitivity C-reactive protein, 1.7（0.8-3.4） vs. 1.1（0.5-2.2） mg/L; white blood cell count,（6.48 ± 1.68） vs.（6.11 ± 1.67） × 10~9/L]. The levels of apoCⅢ and inflammatory markers increased with the number of metabolic risk components（all P 〈 0.001）. Furthermore, apoCⅢ levels were associated with virtually all individual MetS risk factors and inflammatory markers（all P 〈 0.05）. Importantly, the prevalence of MetS in each metabolic disorder rose as apoCⅢ levels increased（all P 〈 0.05）. Mediation analysis showed that apoCⅢ partially mediated the effect of inflammation on MetS independently from triglycerides. Conclusion Plasma apoCⅢ levels were significantly associated with the development and severity of MetS, and a role of apoCⅢ in the effect of inflammation on the development of MetS was identified.

Expression of platelet-endothelial cell adhesion molecule-1 in human umbilical vein endothelial cells by exposure to advanced glycosylation end products and inflammatory mediators

Objective To determine whether advanced glycosylation end products modified bovine serum albumin (AGEs-BSA) affects endothelial cell lateral junction protein, platelet-endothelial cell adhesion molecule-1 (PECAM-1) in the presence or absence of inflammatory mediators.Methods Cultured human umbilical vein endothelial cells (HUVECs) were exposed to AGEs-BSA for 6, 12, 24, and 36 hours, and exposed to AGEs-BSA glycosylated with different concentrations of glucose, tumor necrosis factord-α (TNF-α), interferon (IFN-γ), TNF-α + IFN-y and AGEs-BSA + TNF-α for 24 hours, respectively. Expression of PECAM-1 mRNA was measured by semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR) with β-actin as an internal standard, and sequencing of RT-PCR products was performed to confirm the specificity of amplification for PECAM-1 gene. The endothelial cell surface expression of PECAM-1 was determined by flow cytometry (FCM).Results There were no significant changes in the expression of PECAM-1 mRNA and protein when the cells were exposed to AGEs-BSA with different concentrations or periods ( P>0. 05). However, PECAM-1 expression was reduced in the cells treated with TNF-α, IFN-y, TNF-α + IFN-γ and AGEs-BSA + TNF-α. The level of PECAM-1 treated with AGEs-BSA + TNF-α was lower than that of TNF-α treated alone (P<0. 01).Conclusions AGEs-BSA had no effect on the expression of PECAM-1 mRNA and protein in cultured HUVEC. With the presence of inflammatory mediator TNF-α, AGEs-BSA decreased the level of PECAM-1, which might reduce the adhesion interaction between adjacent endothelial cells, enhance the permeability of endothelial cells, and might be implicated in the endothelial dysfunction and pathogenesis of atherosclerosis in patients with diabetes mellitus. The significance of this phenomenon in intracellular signal transduction remains to be determined.

Regulating effects of arsenic trioxide on cell death pathways and inflammatory reactions of pancreatic acinar cells in rats

Background It is accepted that inflammatory cytokines play a key role in the development of acute pancreatitis, so blocking the initiation of inflammatory reactions may alleviate pathological changes of acute pancreatitis. We studied the regulatory effect of arsenic trioxide （As2O3） on apoptosis and oncosis of pancreatic acinar cells in vitro and in vivo and its therapeutic effect on acute pancreatitis. Methods Pancreatic acinar cells were isolated by collagenase digestion method. Apoptosis and oncosis of isolated pancreatic acinar cells were detected with Hoechst 33258＋PI or Annexin V＋PI double fluorescent staining. Amylase and lactate dehydrogenase release were measured. Acute pancreatitis was induced in Wistar rats by intraperitoneal injections of caerulein, and apoptosis was detected with terminal dUTP nick-end labeling method. Tumor necorsis factor α （TNF-α） mRNA, myeloperoxidase, nuclear factor-κB and histological grading of pancreatic damage were measured.Results There was an increased apoptosis but a decreased oncosis of pancreatic acinar cell after the treatment with AS2O3. The levels of lactate dehydrogenase and amylase release were markedly decreased in As2O3 treated group. Myeloperoxidase content, TNF-α mRNA level, nuclear factor-κB activation and pathological score in As2O3 treated group were significantly lower than in the untreated group. Conclusions As2O3 can induce apoptosis and reduce oncosis of pancreatic acinar cell, thus resulting in reduced release of endocellular enzyme of acinar cells, reduced inflammatory cell infiltration and decreased the production of inflammatory cytokines, so that the outcome of alleviated pathological changes was finally achieved.

Clinical study of inflammatory factors in sputum induced early after lung volume reduction surgery

Background The aim of this study was to prospectively study the changes in neutrophil elastase （NE）, fibroblast growth factor 9 （Fgf9）, matrix metalloproteinase-9 （MMP-9）, tissue inhibitor of metalloproteinase 1 （TIMP-1） in sputum induced during the early period after lung volume reduction surgery （LVRS）. Methods From April to October 2005, ten consecutive patients with chronic obstructive pulmonary disease （COPD） underwent LVRS. Ten non-small cell lung cancer patients （stage II-Illa） received Iobectomy as a control group. The induced sputum was collected from both groups at six different times （two weeks before operation and postoperatively at 1, 2, 4, 6 and 10 days）. The level of NE, Fgf9, MMP-9 and TIMP-1 were measured using enzyme-linked immunosorbent assay. Results The pulmonary function （FEV~%） and arterial blood gases （PaO2 and PaCO2） were significantly different belween the groups. There were no significant differences in age, ejection fraction （EF）, and operation duration, but hemoglobin in the LVRS group was statistically higher than in the controls. At certain times, there were significant differences in NE, MMP-9, TIMP-1 and MMP-9/TIMP-1 （P 〈0.05） but not in Fgf9 between the two groups. The levels of NE and TIMP-1 were maximal at 2 days postoperatively and that of MMP-9 and MMP-9/TIMP-1 at 4 days postoperatively in the LVRS group. In the control group, maximal levels of NE and TIMP-1 occurred at 2 days postoperatively and that of MMP-9 and MMP-9/TIMP-1 at 1 day postoperatively. Ten days after surgery, all values of the control group were not significantly different from the baseline. In the LVRS group, the levels were significantly different from the pre-operative values （P 〈0.05） apart from TIMP-1. Conclusion The levels of NE, MMP-9, TIMP-1 and MMP-9/TIMP-1 of the LVRS group were different from those of the control group. The time course of these chanties may be related to LVRS and the underlying process of COPD.

Association between Plasma Leptin Level and Systemic Inflammatory Markers in Patients with Aggressive Periodontitis

Background：Increasing evidence supports an association between periodontitis and systemic diseases.Leptin is involved both in the energy metabolism and inflammatory processes and is suggested to be a link between periodontal infection and systemic health.The present study aimed to evaluate the peripheral leptin concentration in patients with aggressive periodontitis （AgP） and to explore the relationship between leptin and systemic inflammation.Methods：Ninety patients with AgP visiting the Clinic of the Periodontology Department,Peking University School and Hospital of Stomatology between July 2001 and May 2006,and 44 healthy controls （staffand student volunteers in the same institute） were recruited.Plasma levels of leptin and inflammatory cytokines including interleukin （IL）-1β,I L-6,tumor necrosis factor-α （TNF-α） and C-reactive protein （CRP） were measured by enzyme-linked immunosorbent assay.Correlation and multiple linear regression analysis were performed to analyze the association between plasma leptin level and other variables.Results：Plasma leptin level of AgP group was significantly higher than that of the control group （19.7-4.4 ng/ml vs.7.5 ± 1.3 ng/ml,P ＜ 0.01）.After controlling for age,gender,and body mass index,positive correlation was observed between plasma leptin concentration and log-transformed levels of pro-inflammatory cytokines （IL-1β,IL-6,TNF-α and CRP）,and the partial correlation coefficients ranged from 0.199 to 0.376 （P ＜ 0.05）.Log-transformed IL-1β and I L-6 levels entered the final regression model （standardized β were 0.422 and 0.461 respectively,P ＜ 0.01）.Conclusions：Elevated plasma leptin concentration may be associated with increased systemic levels of inflammatory markers in AgP patients.