ObjectiveTo summarize the advance of triggering receptor expressed on myeloid cells-1 (TREM-1). MethodsLiteratures about the recent studies on the TREM-1 were reviewed. ResultsTREM1 was a mediator of inflammation. It could amplify the inflammation and lead to overexpression of inflammation in final. ConclusionTREM-1 is very important in development of many diseases and provide a new molecule target to cure.
ObjectiveTo establish a cell inflammation model induced by tumor necrosis factor-α (TNF-α) in human bronchus epithelial cells, and investigate the effects of glutathione S-transferase mu 5 (GSTM5) on the inflammation and oxidative stress. Methods16HBE cells were treated with TNF-α (10 ng/mL, 24 h) in the absence or presence of the constructed GSTM5 eukaryotic expression vector (1 μg/mL). The concentration of malondialdehyde (MDA) and total antioxidation capacity (T-AOC) were detected by colorimetric method. The survival rate of cells was assessed by the methyl thiazolyl tetrazolium (MTT) assay. The transcription level of NADPH oxidase-1 (NOX1), NOX2, NOX3, NOX4, NOX5, dual oxidase-1 (DUOX1) and DUOX2 were evaluated by RT-PCR. Western blot was performed to investigate the protein levels of NOX1 and NOX2. ResultsTNF-α simulation significantly increased the level of MDA in cells, and decreased the level of T-AOC and survival rate of 16HBE. When transfected with the GSTM5 eukaryotic expression vector, the concentration of MDA significantly decreased (P < 0.05), and the activation of T-AOC increased dramatically (P < 0.05). Consequently, the survival rate of 16HBE in the GSTM5 group improved (P < 0.05). The 16HBE cells transfected with the constructed GSTM5 eukaryotic expression vector had a lower transcription and protein levels of NOX1 and NOX2 (all P < 0.01). There were no significant changes in the mRNA expressions of NOX3, NOX4, NOX5, DUOX1 or DUOX2. ConclusionGSTM5 may down-regulate the transcription level of NOX1 and NOX2 to reduce the inflammation and oxidative stress induced by TNF-α.
【Abstract】ObjectiveBy using multidetectorrow spiral CT (MDCT), to investigate the CT imaging features of inflammatory diseases in retroperitoneal space with correlation of radiological anatomy.MethodsThe clinical and laboratory dada of 30 patients with proven inflammatory diseases of retroperitoneal space were collected. All patients underwent MDCT plain scanning and portal venous acquisition. CT imaging data generated at portal venous phase were processed with coronal, sagittal and oblique multiplanar reformation (MPR) technique.ResultsAcute pancreatitis and various types of renal infection were the two main sources of retroperitoneal inflammation. Depending on the specific anatomic locations, retroperitoneal inflammation of different subspaces demonstrated characteristic imaging features. Spreading of inflammatory process across subspaces was also quite common.ConclusionMDCT is the imaging method of choice to depict comprehensively and clearly the inflammatory diseases of various retroperitoneal spaces.
ObjectiveTo explore the relationship of the level of inflammation and nutritional status with the occurrence and prognosis of refractory diabetic foot.MethodsA total of 70 patients with refractory diabetic foot between August 2015 and August 2017 were randomly selected as the observation group. Another 70 patients with diabetes mellitus (without foot ulcer) who visited the hospital in the same period were set as the control group. The observation group was subgrouped into the non-amputation group and the amputation group according to the follow-up endpoint events, and into the grade Ⅲ, Ⅳ, and Ⅴ groups according to Wagner classification method. The blood levels of inflammatory markers and nutritional markers between groups were compared.ResultsIn the observation group, vascular cell adhesion molecule-1 (VCAM-1), fibroblast growth factor 2 (FGF2), fibrinogen (FIB), tumor necrosis factor-α (TNF-α), interleukin (IL)-6, IL-18, lipoprotein phospholipase A2 (LP-PLA2), C-reactive protein (CRP) levels were significantly higher than those in the control group, and albumin (ALB), prealbumin (PA), and transferrin (TRF) levels were significantly lower than those in the control group, with statistically significant differences (P<0.01). The blood levels of FGF2, FIB, IL-6, IL-18, LP-PLA2, and CRP in the amputation group were significantly higher than those in the non-amputation group, and the levels of TRF, ALB, and PA were significantly lower than those in the non-amputation group (P<0.01). There were statistically significant differences in the levels of FGF2, FIB, IL-6, IL-18, LP-PLA2, CRP, TRF, ALB, and PA in patients with diabetic foot with different Wagner grades (P<0.05). The result of multiple logistic regression analysis showed that IL-6 [odds ratio (OR)=1.487, 95% confidence interval (CI) (1.023, 2.120), P<0.001], IL-18 [OR=1.274, 95%CI (1.052, 1.665), P<0.001], LP-PLA2 [OR=1.478, 95%CI (1.126, 1.789), P<0.001], and CRP [OR=2.085, 95%CI (1.574, 2.782), P<0.001] were independent risk factors for the occurrence of refractory diabetic foot, and TRF [OR=0.645, 95%CI (0.002, 0.898), P<0.001], ALB [OR=0.838, 95%CI (0.429, 0.923), P<0.001], and PA [OR=0.478, 95%CI (0.201, 0.984), P<0.001] were independent protective factors for the occurrence of refractory diabetic foot.ConclusionIn the clinical treatment of diabetic foot, we should pay attention to the monitoring of the level of inflammatory factors and nutritional status, and it is necessary to timely carry out anti-inflammatory treatment and appropriate nutritional support treatment.
Objective To explore the relationship between the structure and function of galectin-3， lipid metabolism disorders， and investigate the expression of galectin-3 in the occurrence and progress of lower limb arteriosclerosis block disease. Methods Related articles were reviewed. Results Galectin-3 participates in inflammatory reaction and lipid metabolism disorders， regulates the cell growth， differentiation， adhesion， apoptosis， and angiogenesis， and palys a role in the occurrence and progress of arteriosclerosis obliterans. Conclusion Galectin-3 is correlation with the occurrence， progress， and the prognosis of arteriosclerosis obliterans.
ObjectiveTo investigate the effect of curcumin on lipopolysaccharide (LPS)-induced inflammation and apoptosis in alveolar macrophage via microRNA-132 (miR-132)/high mobility group protein B1 (HMGB1).MethodsThe cultured mouse alveolar macrophage line (RAW264.7 cells) were divided into the control group, the LPS group, the LPS+50 μmol/L curcumin group, and the LPS+100 μmol/L curcumin group. Forty-eight hours after drug treatment, the levels of miR-132/HMGB1, inflammatory mediator and apoptotic were detected. Secondly, the empty vector, synthetic miR-132 mimics and inhibitors were transfected into another cultured mouse alveolar macrophage line (RAW264.7 cells) to detect the inflammation and apoptosis of alveolar macrophage after transfection.ResultsCompared with the control group, in the LPS group, the apoptosis of alveolar macrophage, the levels of interleukin (IL)-6, IL-8 and tumor necrosis factor (TNF)-α, and the expression of miR-132 increased, while the expression of HMGB1 decreased (P<0.05); compared with the LPS group, in the two curcumin groups, the apoptosis of alveolar macrophage, the levels of IL-6, IL-8 and TNF-α, and the expression of miR-132 decreased, while the expression of HMGB1 increased (P<0.05); and the greater the drug concentration, the more obvious the effect (P<0.05). In addition, up-regulation of miR-132 reduced the expression of HMGB1 in alveolar macrophage, increased inflammatory factor, and induced apoptosis in alveolar macrophage; however, down-regulation of miR-132 increased the expression of HMGB1 in alveolar macrophage, reduced inflammatory factor, and inhibited apoptosis in alveolar macrophage (P<0.05).ConclusionCurcumin could decrease LPS-induced inflammation and apoptosis in alveolar macrophage via decreasing miR-132 and increasing HMGB1.
There is a close relationship between inflammation and coagulation response. Inflammation and coagulation are activated simultaneously during cardiopulmonary bypass, which induce postperfusion syndrome. Leukocyte depletion filter can inhibit inflammation by reducing neutrophils in circulation. But, its effects on blood conservation are limited. Aprotinin is a serine protease inhibitor, and can prevent postoperative bleeding by anti-fibrinolysis and protection of platelet function. But its effects on anti-inflammation and protection of organs are subjected to be doubted. The combination of leukocyte depletion filter and aprotinin can inhibit inflammation as well as regulate coagulation, and may exert a good protective action during cardiopulmonary bypass.
The application of gene therapy in ocular diseases is gradually expanding from mono-gene inherited diseases to multigene, multifactorial, common and chronic diseases. This emerging therapeutic approach is still in the early exploratory stage of treating diseases, and the expected benefits and risks remain highly uncertain. In the delivery process of gene therapy drugs, viral vector is currently one of the most mature and widely used vectors. The occurrence of vector-associated immunity will affect the short-term and long-term effects of gene therapy, and even cause permanent and serious damage to visual function. Therefore, gene therapy vector-associated immunity is the focus and challenge for the safety and long-term efficacy of gene therapy. During the perioperative and follow-up of gene therapy, attention should be paid to the monitoring of vector-associated immune inflammation, and appropriate measures should be taken to deal with the corresponding immune response, so as to achieve the best visual benefits for patients.
ObjectiveTo study on the relationship of serum apelin level with inflammation in patients with atrial fibrillation (AF). MethodsWe recruited 58 patients with valvular heart disease who admitted in our hospital between October 2014 and December 2014 and planned to undergo surgery, including 29 patients with persistent AF (an AF group) and 29 patients with sinus rhythm (a SR group). There were 14 males and 15 females in the AF group at an average age of 57±8 years. There were 20 males and 9 females in the SR group at an average age of 54±10 years. The left atrial diameter (LAD) and ejection fraction (EF) were detected by echocardiography. The levels of serum apelin and interleukin-6 (IL-6) were measured by enzyme linked immuno sorbent assay, and the level of high-sensitivity C-reactive protein (hs-CRP) were determined by turbidimetric inhibition immuno assay. ResultsCompare with the SR group, the serum apelin level (201.94±71.96 pg/ml vs. 286.72±129.33 pg/ml) and EF (54.52%±3.94% vs. 56.41%±2.85%) were significantly lower in the AF group, while the hs-CRP (5.58±12.90 mg/L vs. 1.89±3.55 mg/L), IL-6 (2.59±0.64 pg/ml vs. 2.26±0.55 pg/ml) and LAD (57.10±11.69 mm vs. 43.07±5.31 mm) were significantly higher in the AF group (P<0.05). Correlation analysis showed that the apelin level was negatively correlated with hs-CRP and LAD (r=-0.308, P=0.019; r=-0.313, P=0.017), and were positively correlated with EF (r=0.265, P=0.044). ConclusionSerum apelin level is significantly lower in patients with AF and levels of inflammation makers are significantly higher. Apelin may be closely related to AF and inflammation, and may take part in the occurrence and maintenance of AF through the regulation of inflammatory processes.
The hallmark lesions of age-related macular degeneration (AMD) are drusen and basal linear deposit which are lipid substances deposited in Bruch membrane or the compartment on the Bruch membrane. There is a prevailing hypothesis that lipid and its oxidized derivant deposited in retina may have important roles in the pathogenesis of AMD. Lipid oxidation products are toxic, may affect the adjacent cells, induce inflammation, and trigger neovascularization.7-ketocholestoral (7KCh), a naturally occurring oxidized form of cholesterol, had been found to be toxic to retinal cells and able to induce chronic inflammation, which may play a critical role in the development of AMD. However the precise mechanism remains to be elucidated. Thus we will make a brief review of 7KCh and its association with AMD.