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.
Objective To investigate the clinical significance of low dose corticosteroid applied in early period after lung volume reduction surgery（LVRS）. Methods From Apr. 2001 to Mar. 2004, 27 patients with chronic obstructive pulmonary disease were undergone video-assisted unilateral LVRS assisted with mini-incision in our department were retrospectively reviewed. According to whether dispensed with postoperative corticosteroid or not, patients were divided into corticosteroid group and non-corticosteroid group. Corticosteroid group received dexamethasone 10mg iv tid for 3 days and then declined to prednisone 5mg qd for 7 days. Both groups were measured and compared the quantity of thoracic drainage flow, duration of chest tube drainage, the time of air leaks and fever, and so on. At same time, blood gas analysis and blood routine test were performed at 1, 3, 7 and 30 d after operation. Results Corticosteroid and non-corticosteroid groups had no statistically differences in the air leaks time （P 〉 0.05）, but the quantity of thoracic drainage flow of corticosteroid group was lower than that of non-corticosteroid group evidently （700±210ml vs. 950±150ml, P = 0.001）. There was significant difference in average duration of chest tube drainage between both groups （9±3 d vs. 12±2 d, P = 0. 05）. Compared with non-corticosteroidgroup, PaO2 of corticosteroid group was higher at 1, 3d after operation （P〈0.05）. The amount of blood leukocyte of corticosteroid group was lower than that of non-corticosteroid group at 3, 7d after operation, there was no statistically significant in two groups （P 〉 0. 05）. At early period after surgery, both groups had no significant infection and death patient. Conclusion The low dose corticosteroid applied in early period after LVRS for short time（10 days in this research） could shorten the duration of chest tube drainage, decrease the quantity of thoracic drainage flow and the extent of inflammation in pleural cavity. In the mean time, this treatment does not increase the occurrence of significant complications during the early postoperative period, and there is no negative influence to the blood gas analysis.
ObjectiveTo analyze the variation of perioperative concentration of mitochondrial DNA (mtDNA) in circulation system after cardiac surgery with cardiopulmonary bypass (CPB). MethodsBetween July and December 2014, 40 continuous patients underwent aortic valve replacement (AVR) and mitral valve replacement (MVR) in Department of Cardiovascular Surgery, West China Hospital, Sichuan University, including 16 males and 14 females with their mean age of 48.7±11.0 years and mean body weight of 59.0±6.9 kg. Perioperative mtDNA concentrations of circulatory blood were tested at different time points:before general anesthesia (T1), 1 min before CPB (T2), reperfusion of the ascending aorta (T3), 6 h after operation (T4), 24 h after operation (T5), 48 h after operation (T6). ResultsAll the surgeries were successfully performed without early death. Postoperative complications were low cardiac output syndrome in 3 cases and acute kidney failure in 1 cases. The concentration of mtDNA in circulation system rising gradually after CPB. The mtDNA concentration of T3, T4 and T5 were significantly higher than T1 (P < 0.05). The peak level was observed at T5 and the mtDNA concentration of T6 was still significantly higher than that of T1 (P < 0.05). ConclusionThe concentration of mtDNA in circulation system was rising after CPB and peak level appeared at 24 h after CPB.
Objective To evaluate the effects of oxidative stress in the airway inflammation and remodeling of high-fat diet induced obese mice with asthma. Methods Sixty female C57 /6J mice were randomly divided into four groups, ie. an asthma group, an obese group, an obese asthma group, and a control group. The mice in the asthma group were sensitized and challenged with ovalbumin ( OVA) and fed with normal diets. The mice in the obese group were fed with high-fat diets. The mice in the obese asthma group were sensitized and challenged as the asthma group, and fed as the obese group. The mice in the control group were sensitized and challenged with normal saline and fed with normal diets. After 12 weeks, bronchoalveolar lavage fluid ( BALF) were collected for total and differential cell count. IL-6 and 8-iso-prostaglandin F2α ( 8-iso-PGF2α) in lung tissue homognate were detected by ELISA. The pathological changes were observed under light microscope by HE staining. Meanwhile the remodeling indices including total bronchial wall area ( WAt) , smooth muscle area ( WAm) , and bronchial basement membrane perimeter ( Pbm) were measured. Results In comparison with the obese group and the asthma group, the leukocytes and eosinophils in BALF, WAt/ Pbm, and IL-6 in lung tissue increased significantly in the obese asthma group ( P lt; 0. 05) . 8-iso-PGF2αin lung tissue increased in sequence of the control group, the obese group, the asthma group, and the obese asthma group significantly. Pearson correlation analysis showed that leukocyte in BALF, WAt/ Pbm, and IL-6 were in positive correlation with 8-iso-PGF2α( r =0. 828, 0. 863, 0. 891, respectively, P lt;0. 01) . Conclusion Oxidative stress is involved in the airway inflammation and remodeling of obese asthma mice with high-fat diets.
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.
Febrile seizures (FS) are one of the most common neurological disorders in pediatrics, commonly seen in children from three months to five years of age. Most children with FS have a good prognosis, but some febrile convulsions progress to refractory epilepsy (RE). Epilepsy is a common chronic neurological disorder , and refractory epilepsy accounts for approximately one-third of epilepsies. The etiology of refractory epilepsy is currently complex and diverse, and its mechanisms are not fully understood. There are many pathophysiological changes that occur after febrile convulsions, such as inflammatory responses, changes in the blood-brain barrier, and oxidative stress, which can subsequently potentially lead to refractory epilepsy, and inflammation is always in tandem with all physiological changes as the main response. This article focuses on the pathogenesis of refractory epilepsy resulting from post-febrile convulsions.
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.
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.
Drusen is one of the early hallmark changes of AMD. The oxidative stress and inflammatory reaction caused by oxidative phospholipids (OxPLs) in drusen can lead to retinal pigment epithelium (RPE) cell death (apoptosis, pyroptosis, etc.) and the formation of choroidal neovascularization, which is the pathogenesis of AMD. Pyroptosis, also known as inflammatory necrosis, is one of the main forms of OxPLs induced cell death. Proinflammatory factors released by pyroptic cells can in turn aggravate the inflammatory reaction, leading to further damage. In order to prevent AMD, inflammatory response and cell death may be reduced by regulating lipid metabolism, reducing OxPLs endocytosis and increasing cholesterol efflux. In-depth understanding effects of OxPLs, inflammation and RPE pyrosis in the pathogenesis of AMD in elucidate the pathogenesis of AMD and to seek new treatment measures has important clinical significance.
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.