ObjectiveTo explore the relationship among plasma cytokines’ level, adhesion molecules expression and skin damage in patients with chronic venous insufficiency (CVI) of lower extremities.MethodsIn 32 patients with CVI and 8 normal individuals as control, blood TNFα, IL1β and IL2R were assayed with ELISA method; serum endothelial cellintercellular adhesion molecule1(ECICAM1), polymorphonuclearCD18(PMNCD18) and polymorphonuclearCD11b(PMNCD11b) were assayed with immunohistochemical method; and ultrastructure of diseased veins was examined by electroscope.ResultsThe results showed that the level of plasma TNFα and IL1β increased remarkably in Class 2-3 compared with Class 1 and control (P＜0.05), IL2R had no difference in Class 1,2,3(Pgt;0.05). The index of ECICAM1 and PMNCD11b positively expression increased remarkably in Class 2-3 compared with that in Class 1 and control. The index of PMNCD18 expression in Class 2-3 and Class 1 was greatly higher than that in control (P＜0.05). The expression of ICAM1 was positively correlated with that of CD11b/CD18. Electron microcopy showed that the change in microvessel was mainly PMN adhesion with endothelial cells (ECs) and trapped in microvessels.ConclusionThe results suggest that activated monocyte may release TNFα and IL1β, upregulate ICAM1 and CD11b/CD18 expression, and mediate the PMN adhesion to ECs, thus causing ECs and tissue damage. It may be one of important mechanism of venous ulcer.
ObjectiveTo determine the nuclear factor kappa B (NFkB) activity in peripheral blood mononuclear cells (PBMC) in patients with acute cholangitis of severe type (ACST) and correlate the degree of NFkB activation with severity of biliary tract infection and clinical outcome.MethodsTwenty patients with ACST were divided into survivor group (14 cases) and nonsurvivor group (6 cases). Other 10 patients undergoing elective gastrectomy or inguinal hernia repair were selected as control group. Peripheral blood samples were taken 24 hours after operation, PBMC was separated and nuclear proteins were isolated from PBMC, and NFkB was determined with electrophoretic mobility shift assay (EMSA). The levels of TNFα, IL6 and IL10 in plasma were determined by using an enzymelinked immunoassay (ELISA). ResultsThe NFkB activity was 5.02±1.03, 2.98±0.51 and 1.02±0.34 respectively in three groups. It was increased in all patients with ACST, versus the control group (P＜0.05), and the patients of nonsurvivor group had higher levels of NFkB activation than those of survivor group (P＜0.05). The levels of TNFα and IL6 were (496.28±52.35) ng/L and (578.13±67.72) ng/L in nonsurvivor group; (284.47±39.41) ng/L and (318.67±34.92) ng/L in survivor group; (89.43±10.39) ng/L and (101.27±13.47) ng/L in control group. All patients with ACST had increased levels of TNFα and IL6, which were many fold greater than that of control group, and there was an evidence of significantly higher levels in nonsurvivor group than in survivor group (P＜0.05). All patients had also increased levels of IL10 as compared to control group (P＜0.05), but the IL10 concentrations in plasma were not significantly higher in nonsurvivors than that of in those survivors (Pgt;0.05). ConclusionNFkB activation in PBMCs in patients with ACST
【Abstract】Objective To investigate the protective effect of improving the pancreatic ischemia and calcium channel blockers on preventing the progression of acute pancreatitis. Methods Twenty-four patients with mild acute pancreatitis were randomly divided into two groups： control group and treated group. Within the first 72 hours from the onset of AP, routine conservative managements were performed in control group, improving the pancreatic ischemia and preventing Ca2+ overload were performed in treated group for two weeks. The hemorrheological parameters were measured at 1,4,7,14 days after adimission, simultanously, serum TNFα, IL-1β, C-reactive protein and plasma TXB2, 6-keto-PGF1α levels were determined with ELISA methods. Results The hemorrheological changes were improved in treated group, serum TNFα, IL-1β, C-reactive protein and plasma TXB2, 6-keto-PGF1α levels were significantly decreased each time point in treated group as compared with control group. Conclusion Improving the pancreatic ischemia and calcium channel blockers have protective effect through reducing the generation of cytokines and inflammatory mediators on preventing the progression of acute pancreatitis.
The aim of this study was to investigate the role of tumor necrosis factor (TNF), interleukin-6(IL-6), C-reactive protein (CRP) in pancreatitis and its systemic complications. Thirty six patients with acute pancreatitis were studied, 12 with mild disease, and 24 severe disease, of whom 9 developed systemic complications. TNF, IL-6, CRP in these patients with pancreatitis was assessed during the first, 4th, 8th days of admission. The serum concentration of TNF, IL-6, CRP were significantly increased, and significantly higher in complicated group than in mild group and severe group. These findings suggest that proinflammatory cytokines play a central role in the pathophysiology of the disease, the host systemic response to pancreatic inflammation and the level of the response did relate to the development of organ dysfunction.
The serum activities of 3 cytokines (TNF,IL-1 and IL-6) were observed in 23 patients admitted within 4 days of onset of acute pancreatitis (AP). The results showed that the serum level of 3 cytokines raised in all of the AP patients, significant difference between TNF and IL-1 was abserved at admission and IL-6 did after one week of admission, suggesting that proper cytokine criteria are useful in predicting severity of the disease but the relationship between cytokines and MOF had not established.
Objective To investigate the effects of high dose ambroxol on patients with acute lung injury（ALI） after liver transplantation.Methods Thirty patients with ALI after liver transplantation were divided randomly into an ambroxol group and a control group.On the base of routine treatment，the patients were treated by intravenous infusion with high dose ambroxol of 15 mg/kg once a day for 7 days in the ambroxol group and with normal saline of same volume in the control group.The arterial blood gas analysis was performed and IL-1，IL-10 and TNF-α were measured before and 1 day，3 day and 7 day after the treatment.Length of stay in ICU were recorded and death rate in one year were followed-up.Results After the 1 days，3 days and 7 days of treatment，PaO2 and PaO2/FiO2 were improved in both groups with more significant improvement in the ambroxol group（Plt;0.05）.Before treatment，no differences of IL-1，IL-10 and TNF-α level were found between the two groups.But the level of IL-1 and TNF-α decreased significantly in the ambroxol group compared with the control group after 1 day treatment，and no differences were found after 3 day and 7 day.The level of IL-10 increased in both groups，but significantly in the ambroxol group after 1 day.The lenght of ICU stay in the ambroxol group was shorter than that in the control group[（8.2±5.6）d vs（11.4±6.5）d，Plt;0.05].Two died in the ambroxol group and 3 in the control group with no significant difference.Conclusion High dose ambroxol can improve blood gas exchange and decrease the lenght of ICU stay in ALI patients after liver transplantation，through its inhibitory effects on inflammatory response by down-regulation of IL-1，TNF-α and up-regulation of IL-10.
Objective To observe the protective effects of ambroxol hydrochloride ( AMB) on rabbit model of acute lung injury ( ALI) induced by oleic acid and explore its mechanisms. Methods The ALI model of rabbit was induced by oleic acid. Twenty-four Japanese white rabbits were divided into three groups randomly, ie. a normal saline group ( NC group) , an ALI group and an ALI plus ambroxol injection group ( AMB group) . The pathological changes and apoptotic index ( AI) in lung tissue, Caspase-3 activity in lung tissue homogenate were observed 6 hours after the intervention. Serum activity of superoxide dismutase ( SOD) and serum levels of malonaldehyde ( MDA) , interleukin-1β( IL-1β) , and tumor necrosis factor-α ( TNF-α) were measured simutanously. Results The pathological injury of lung in the AMB group was milder than that in the ALI group. Both the AI in lung tissue and Caspase-3 activity in homogenate in the AMB group were lower than those in the ALI group significantly ( P lt;0. 01, P lt;0. 05 respectively) , butwere higher than those in the NC group( both P lt; 0. 01) . The activity of SOD in serum measured 6 hours after AMB intervention was higher while the serum levels of MDA, IL-1βand TNF-αin serum were lower ( P lt;0. 01) than those in the ALI group significantly ( all P lt;0. 01) . Conclusions Ambroxol hydrochloride has protective effects on oleic acid-induced acute lung injury. The mechanisms may be related to inhibition of oxidative stress and suppression of cytokines synthesis ( IL-1βand TNF-α) , the activity of the Caspase-3,and the apoptosis of lung tissue.
Objective By using small interfering RNAs ( siRNAs) specific for spleen tyrosine kinase ( Syk) , to evaluate the role of Syk in maturation of bone marrow-derived dendritic cells. Methods The fragments of 21-23 bp siRNAs specific for mice Syk were chemo synthesized and transfected into the asthmatic murine bone marrow-derived dendritic cells ( BMDCs) by Lipofectamine 2000 transfection system for 48 hours. Then BMDCs were co-cultured with T cells from the normal mice spleen for 48 hours. The cytokines including IL-4, IL-13, IL-2 and INF-γin supernatant were detect by ELISA. The expression of Syk protein was measured by Western Blot to determine whether the Syk gene was silenced. Results The expression of Syk protein was obviously decreased in the siRNA-interference group. The secretions of IL-4 and IL-13 were significantly inhibited by siRNA interference ( P lt; 0. 05) , but the secretions of IL-2 and INF-γwere not interfered signficantly ( P gt;0. 05) . Conclusion Syk specific siRNA fragments can block the antigen presentation function of dendritic cells and block the activation and differentiation of T cells.
Objective To investigate the protective effects of ulinastatin on acute lung injury ( ALI)induced by seawater drowning in rats. Methods Thirty male SD rats were randomly divided into three groups, ie. a control group, a model group, and an ulinastatin treatment group. The rats in the model group and the ulinastatin treatment group received intratracheal artificial seawater ( 4 mL/kg) instillation. Then the ulinastatin treatment group received ulinastatin ( 100 000 U/kg) injection after infusion of seawater while the model group received an injection of same amount of saline. The rats were sacrificed at 4 hours after instillation. The pathological changes of lung were evaluated by hematoxylin-eosin stain under light microscope. Lung wet/dry weight ratios were measured to assess the level of pulmonary edema.Concentrations of tumor necrosis factor ( TNF) -α, interleukin ( IL) -1β, IL-6, and IL-10 in bronchoalveolar lavage fluid ( BALF) were detected by enzyme-linked immunosorbent assay ( ELISA) . The myeloperoxidase activity in lung tissue homogenates were measured by colorimetric method. Results Ulinastatin treatmentsignificantly relieved the decline of PaO2 and lung pathological changes, inhibited myeloperoxidase activity,and reduced lung wet/dry weight ratios. Ulinastatin also inhibited the release of TNF-α, IL-1β, and IL-6,whereas increased the expression of IL-10 simultaneously. Conclusion Ulinastatin attenuates seawater induced ALI, which may be related to its inhibitory effects on inflammation reaction through regulating cytokine secretion.
Objective To investigate the expression levels of osteoprotegerin (OPG) and receptor activator of nuclear factor kappa B l igand (RANKL) mRNAs in BMSCs in patients suffering glucocorticoid-induced necrosis of the femoral head (GNFH), and to discuss the relationshi p between OPG/RANKL system and GNFH. Methods The bone tissue and BMSCs of femoral head were collected from 35 patients suffering GNFH (experimental group) and from 21 patients suffering fracture of femoral neck (control group). The ratio of men to women was 4 ∶ 3 in two groups, aged 41 to 70 years (mean 55.34years in the experimental group and mean 55.33 years in the control group). The patients of experimental group received over 3 weeks’ glucocorticoid treatment or more than 1 week’s high-dose glucocorticoid therapy in recent 2 years, but patients of the control group did not receive more than 1 week’s hormone therapy. In 2 groups, the microstructure of bone tissue of femoral head was detected by HE staining. The BMSCs were isolated and cultured by adherent-wall method; the expression levels of OPG and RANKL mRNAs were examined by real-time quantitative polymerase chain reaction and the ratio of OPG mRNA to RANKL mRNA was caculated. Results Bone trabeculae and bone units were replaced by interrupted bone fragments, which were surrounded by inflammation and granulation tissue and few osteocytes were seen in bone lacunae in the experimental group. In control group, bone trabeculae and bone units were made by complete lamellar bone which surrounded blood vessels and osteocytes were seen in lacunae. The expression levels of OPG mRNA in the experimental group (0.37 ± 0.12) was significantly lower than that in the control group (0.47 ± 0.13), and the levels of RANKL mRNA in the experimental group (1.12 ± 0.39) was significantly higher than that in the control group (0.84 ± 0.24), showing statistically significant difference (P lt; 0.05). The ratio of OPG mRNA to RANKL mRNA in the experimental group (0.37 ± 0.17) was significantly lower than that in the control group (0.61 ± 0.26, P lt; 0.05). Conclusion The GNFH may be related to the expression levels of OPG mRNA and RANKL mRNA in BMSCs.