ObjectiveTo review the research progress of the role of seed cells and related cytokines in angiogenesis of the vascularized tissue engineered bone. MethodsThe latest literature of tissue engineered bone angiogenesis was reviewed, including the common source of seed cells, biological characteristics, transformation mechanism, related cytokines, and signaling pathways in re-vascularization. ResultsMicrosurgery technique, genetic technique, and co-culture system of vascularized tissue engineered bone have developed to a new level. Moreover, both the induction of introduced pluripotent stem cells and vascular endothelial growth factor-angiopoietins 1 transfected mesenchymal stem cells and endothelial progenitor cells have some advantages for bone regeneration and vascularization. However, all the techniques were not used in clinical practice. ConclusionUsing techniques of genetically modified seed cells, related cytokines, and scaffolds may have bright prospects for building vascularized tissue engineered bone.
Objective To explore the possible anti-inflammatory mechanism of intensive insulin therapy （IIT） by studying the effect of IIT on the levels of TNF-α, IL-6, C-reactive protein （CRP） and APACHE Ⅱ score in biliary pyemia. Methods Twenty eight patients with biliary pyemia who were admitted by our department and given an operation within 24 h form Jan. 2005 to Dec. 2008 were randomly divided into two groups by using random number table numbers: one group treated with IIT （IIT group, n=14） and another group treated with routine insulin therapy （RIT group, n=14）. The inflammatory factors, such as TNF-α, IL-6 and CRP were detected dynamically and the APACHEⅡ score was calculated. ResultsThe level of CRP and APACHEⅡ score on day 5 and 7 and the levels of TNF-α and IL-6 on day 3, 5 and 7 after operation in IIT group were significantly lower than those in RIT group （P＜0.05, P＜0.0１）. Compared with preoperative levels, the IL-6 and APACHEⅡ score in IIT group commenced to decrease on day 3 after operation （P＜0.05）, that was earlier than control group. Conclusion The treatment with IIT can suppress the composition of TNF-α, IL-6 and CRP, protect impaired hepatic cells, and reduce APACHEⅡ score, the degree of systemic inflammation and incidence of MODS.
Objective To summarize the role of nuclear factor kappa B (NF-κB) in the occurrence and progression of various sorts of liver injury. Methods Literatures on the structures, property of molecular biology and function of NF-κB, as well as its relationships with liver injury were collected and reviewed. Results NF-κB was an important nuclear factor existed in cells widely distributed in most cell types. The activation of NF-κB was induced by various sorts of liver injury. The activated NF-κB could affect the liver injury by regulating cytokines, adhesion molecules, and activating factor involving in immunologic reaction， inflammatory reaction and the apoptosis. Conclusion NF-κB plays an important role during the occurrence and progression of liver injury， and may become a new target in the treatment of liver injury.
Objective To study the significance of the levels of plasma inflammatory cytokines (IL-6，IL-8，IL-10 and TNF-α) in patients with acute deep venous thrombosis (DVT) of lower extremity. Methods Forty untreated DVT cases were selected as the subjects in the DVT group, while thirty healthy subjects, whose ages and genders showed no significant difference with the DVT patients, were collected as the control group. The plasma levels of IL-6, IL-8 and TNF-α were detected by radioimmunoassay (RIA), and the plasma level of IL-10 was measured by enzyme-linked immunosorbent assay (ELISA). Correlation analysis was used to investigate the relationships between the levels of different inflammatory cytokines within DVT group. Results The levels of plasma cytokines in the DVT group were all significantly higher than those in control group (P＜0.001). The results of the correlation analysis showed that there were positive correlations between IL-6 and TNF-α (r=0.383, P＜0.05), IL-10 and TNF-α (r=0.390, P＜0.05), respectively, within the DVT group; whereas there were no correlations between IL-6 and IL-8, IL-6 and IL-10, IL-8 and IL-10, and IL-8 and TNF-α. Conclusion The levels of plasma cytokines increased significantly in patients of DVT. Inflammatory cytokines may play an important role in acute DVT by accelerating the pace of thrombosis, intensifying the inflammatory reaction around thrombus and aggravating the injured blood vessel.
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
bjectiveTo observe the effecacy of immunosuppressive agents on modulation of the disorders of inflammatory and antiinflammatory cytokines in acute pancreatitis, and to investigate the mechanism of treatment of acute pancreatitis with immunosuppressive agents. MethodsSD male rats were divided into 6 groups: group 1, the normal control group (n=6); group 2, acute pancreatitis induced by ductual injection of 5%sodium cholate sulfur at the volume of 1.0 ml/kg without treatment (n=8). After the pancreatitis were induced, the rest rats were injected intravenously with 5Fu 40 mg/kg (group 3, n=6); or methylprednisolone 30 mg/kg (group 4, n=6); or cyclophosphamide 20 mg/kg (group 5, n=6); or methotrexate 1.2 mg/kg (group 6, n=6). Twentyfour hours afteroperation, the animals were killed, the blood samples were taken for measurement of TNFα, IL1, IL6 (by bioassay), and IL10, TGFβ (by ELISA) as well as amylase. ResultsThe inflammatory cytokines (TNFα,IL1,IL6 ) and the antiinflammatory cytokines (IL10 and TGFβ), in blood of acute pancreatitis were increased significantly. After treated with immunosuppressive agents, both the inflammatory and antiinflammatory cytokines were decreased in different degrees. Some indexes of the severity of acute pancreatitis, such as amylase and pancreatic weight were improved obviously.ConclusionImmunosuppressive agents can regulate inflammatoryassociated cytokines increased remarkably in the acute pancreatitis. Therefore, improvement of acute pancreatitis can be achieved through rectifying the abnormal immunity and relieving the pathophysiological disorders of the acute pancreatitis by immunosuppressive agents.
Objective To research the changes in plasma endothelin, LPS, TNF-α, IL-6 and IL-8 in the patients with obstructive jaundice (OJ) and non-obstructive jaundice (NOJ) after surgery. Methods The plasma ET, LPS, TNF-α, IL-6 and IL-8 were measured in 15 patients without jaundice as controls. Results As compared with NOJ, the postoperative changes of ET, LPS, TNF-α, IL-6 and IL-8 in OJ group increased significantly at multiple time points (P＜0.05). Conclusion There is interaction between ET,LPS, TNF-α, IL-6 and IL-8 and damage to multiple organ function in patients with OJ after surgery.
【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.
To observe the change in plasma endotoxin and cytokine during the early period of intra-abdominal infection (IAI) complicated by multiple system organ dysfunction (MSOD) in animals. Twenty rabbits were randomly divided in to two groups. One group received the operation of cecal ligation plus puncture (CLP) inducing IAI complicated by MSOD, and another group received sham operation as a control. All animals were placed in metabolic cages and maintained with intravenous infusion for one week. Plasma levels of endotoxin and cytokine (TNF, IL-1, IL-6) were determined seperately at the beginning (0 hour) or 1, 2, 3, 4, 5, 6 and 24 hours after CLP. Blood bacteria cultures and pathological examination of several organs were made when the animal was dead or killed. Results: The levels of plasma endotoxin, TNF and IL-6 were found to be significantly increased at one or two hours after CLP, the incidence rate of bacteriemia was 80% and the pathological alterations in the abdomen and organs were remarkale, with an average survival time of 84.1±39.0 hours in CLP group. No change in plasma IL-1 level was found in the CLP group. Conclusion: The plasma levels of endotoxin and cytokine (TNF and IL-6) do increase in the early period of IAI complicated by MSOD, and the change in plasma IL-1 is not obvious.