Objective To observe the changes of inflammatory cytokines in brain protective methods, study the inflammatory mechanism during cerebral protection tissues in different cerebral Methods Eighteen healthy adult dogs were randomly divided into three groups （6 dogs in each group）： normothermic cardiopulmonary bypass （NCPB group）, deep hypothermic circulatory arrest （DHCA group）, and intermittent selective antegrade cerebral perfusion （ISACP） during DHCA（DHCA＋ISACP group）. After operation the water contents in brain tissue were measured ,the hippocampus were removed, and radio-immunity analysis （RIA） was used to measure the content of interleukin-1β（IL-1β） and tumor necrosis factor-alpha （TNF-α） of the hippocampus tissue. The morphology of the hippocampus were examined by transmission electron （TE） microscopy. Results The contents of IL-1β and TNF-α of DHCA group was higher significantly than those of NCPB group and DHCA＋ISACP group （P〈0.01）, there was no significant difference between NCPB group and DHCA＋ISACP group （P〉0.05）. And the contents of TNF-α and IL-1β were positive linear correlated with degree of edema of brain tissues （r = 0. 987, 0.942; P〈 0.01）. TE examination revealed that the damage of the uhrastructure in the DHCA group was more severe than that in NCPB group and DHCA＋ISACP group. Conclusions This experiment revealed that long duration DHCA can bring some damages to the brain and that ISACP during long-term DHCA has brain protective effects to some extent. IL-1β and TNF-α play an effective role in the brain damage of long-term DHCA.
ObjectiveTo evaluate the effects of N-acetylcysteine (NAC) on lung tissue of Wistar rats, which were tracheally instilled fine particulate matter (PM2.5).MethodsForty-eight male Wistar rats were randomly divided into six groups: two control groups [they were blank group (C1), fake treatment group (C2) separately], four treatment groups [they were PM2.5 group (P), low-dose NAC group (L), medium-dose NAC group (M), high-dose NAC group (H) separately]. C1 received no treatments at all. C2 was instilled with sterile water (1 ml/kg) tracheally once a week for four times. P was instilled equivoluminal PM2.5 suspension (7.5 mg/kg) tracheally once a week for four times. The NAC groups received gavage (10 ml/kg) of different dosage of NAC (125, 250, 500 mg/kg) for six days. At the seventh day, the NAC groups were instilled PM2.5 suspension (7.5 mg/kg) tracheally. The procedures were repeated for three times in the NAC groups. Twenty-four hours later after four weeks or after the last instilling, all rats were sacrificed. Lung tissue was stained by hematoxylin-eosin (HE) staining, and histopathological changes of lung tissue were observed by optical microscope. The levels of C-reactive protein (CRP) as well as tumor necrosis factor-α (TNF-α) of serum, TNF-α of bronchoalveolar lavage fluid (BALF), TNF-α as well as interleukin-1β (IL-1β) of homogenates of lung tissue were detected by enzyme-linked immunosorbent assay. The activity of lactate dehydrogenase (LDH) as well as the levels of malondialhyde (MDA) of serum and BALF were detected by standard colorimetric method.ResultsHE staining showed that the normal structure of lung were destroyed in the groups dealed with PM2.5 and NAC could alleviate these changes. Higher dosage of NAC seemed to provide more powerful protections. Structure of the lung in C1 as well as C2 were nearly normal. The levels of CRP as well as TNF-α of serum, TNF-α of BALF, TNF-α as well as IL-1β of homogenates of lung tissue in the groups of P, L, M, H were higher than that in the groups of C1, C2 (all P<0.05). The levels of CRP as well as TNF-α of serum, TNF-α of BALF, TNF-α as well as IL-1β of homogenates of lung tissue in the groups of L, M, H which groups received NAC treatments were lower than that in P group. More, the groups seemed to have lower levels of CRP, TNF-α, IL-1β when higher dosage of NAC were given. The activity of LDH as well as the levels of MDA of serum, and BALF in the groups of P, L, M, H were higher than that in the groups of C1, C2 (all P<0.05). The activity of LDH as well as the levels of MDA of serum and BALF in the groups of L, M, H which groups received NAC treatments were lower than that in P group (all P<0.05). ConlusionTo some extent, NAC demonstrate antagonistic effects on oxidative stress and inflammatory injury on rats’ lung brought by PM2.5.
ObjectiveTo systematically review the tumor necrosis factor-α (TNF-α) -308G/A polymorphism and the risk of inflammatory bowel disease (IBD).
MethodsAll eligible case-control studies published up to Jan 25th 2015 were identified by searching PubMed, EMbase, CNKI, WanFang Data, CBM and VIP databases. Two reviewers independently screened the studies according to the inclusion and exclusion criteria, extracted data and assessed methodological quality of included studies. Then, meta-analysis was performed using RevMan 5.2 and Stata 12.0 softwares.
ResultsA total of 20 studies involving 2 860 IBD cases and 5 033 controls were included. The results of meta-analysis showed:Compared with the wild genotype GG, genotype GA, AA and genotype GA+AA were associated with susceptibility of ulcerative colitis (UC) (GA vs. GG:OR=1.45, 95%CI 1.02 to 2.07, P=0.04; AA vs. GG:OR=2.01, 95%CI 1.32 to 3.05, P=0.001; GA+AA vs. GG:OR=1.51, 95%CI 1.07 to 2.13, P=0.02); Compared with genotype GA+AA, genotype AA increased the risk of UC (AA vs. GA+GG:OR=1.92, 95%CI 1.26 to 2.91, P=0.002); allele A did not increase the risk of UC; Compared with genotype GG, genotype AA increased the risk of Crohn disease (CD) (AA vs. GG:OR=1.49, 95%CI 1.07 to 2.08, P=0.02); Compared with genotype GA+GG, while genotype AA increased the risk of CD (AA vs. GA+GG:OR=1.50, 95%CI 1.08 to 2.09, P=0.02); genotype GA, GA+AA and allele A did not increase the risk of CD. In stratification analyses by ethnicity, we found that the TNF-α-308G/A was significat associated with IBD in Europeans.
ConclusionCurrent evidence indicates that TNF-α-308G/A polymorphism is associated with the susceptibility of IBD, genotype GA, AA and GA+AA increase the risk of suffering from UC while genotype AA increase the risk of suffering from CD. Due to the limited quantity of the included studies, more researches are needed to verify the above conclusion.
Objective To explore the role of macrophage-stimulating protein ( MSP) and receptor tyrosine kinase RON in the airway inflammation of chronic obstructive pulmonary disease( COPD) , and investigate its possible mechanism. Methods The rat COPDmodel was established by exposing the rats to cigarette smoke daily for three months. Rat alveolar macrophages ( AMs) were isolated in vivo and cultured,and then challenged with different concentrations of MSP for 24 hours. The concentrations of MSP in broncho-alveolar lavage fluid ( BALF) and serum, and the levels of IL-1β, TNF-α, IL-8, and IL-10 in the supernatants were measured by ELISA. The expression of RONmRNA in lung tissue was assessed by reverse transcription-polymerase chain reaction. The levels of RON protein in the lung tissue and AMs cultured in vitro were observed by immunohistochemistry. The activity of superoxide dismutase ( SOD) and malondialdehyde ( MDA) content in the culture solution were measured with chromatometry method. Results Compared with the control group, the concentrations of MSP in serum and BALF of the COPD rats were significantly higher ( P lt;0. 01) . The levels of RONmRNA and RON protein in the COPD rats were also upregulated significantly ( P lt; 0. 01) . MSP evoked the AMs isolated from the normal and COPD rats to generate more content of MDA and caused a reduction in activity of SOD. In addition, MSP stimulated TNF-α, IL-8, IL-1βand IL-10 release fromAMs of the normal and COPD rats dose-dependently. The levels of TNF-α, IL-8, and IL-1βwere higher, while the level of IL-10 and the SOD activity were lower in AMs of the COPD group than those of the control group in the same dose of MSP ( P lt;0. 01) . The more significant increase in the levels of TNF-α, IL-8, IL-1β, and the more notable decrease in the activity of SOD was found in the COPD group compared with the control group. But the degree of increasing MDA and IL-10 in the AMs of the COPD group was lower than that in the control group. Linear correlation analysis showed that the MSP concentration and the RON protein level in the COPD rats were positively associated with the total cellcounts and AM counts in BALF, and were related to the indexes for pulmonary emphysema. Conclusions There is a close correlation between the MSP and receptor tyrosine kinase RON with the airway inflammation of COPD. The mechanism might be that MSP promote the macrophages release inflammatory factors and increase the production of oxygen free radicals.
Objective
To investigate the effects of inflammatory reaction of thymomas with myasthenia gravis (MG) treated by traditional thoracotomy and minimally invasive surgery.
Methods
A total of 40 thymomas patients (Mssaoka Ⅰ or Ⅱ) with myasthenia gravis from August 2014 to June 2015 were treated by traditional thoracotomy (n=20) or video-assisted thoracoscopic surgery (n=20). The serum levels of IL-6, IL-8, TNF-α, CRP and CORT were measured by enzyme-linked immunosorbent assay (ELISA) methods at before anesthesia (T1), after anesthesia (T2), 2 h after skin cut (T3), 24 h post-operation (T4), 48 h post-operation (T5) and 72 h post-operation (T6) respectively. Perioperative parameters were also reported. The statistics analysis was performed by SPSS 17.0 software.
Results
The serum levels of IL-6, IL-8, TNF-α, CRP and CORT had no significant difference between T1 and T2, T2 and T3 (allP value>0.05) in both groups. But the serum levels of these factors after operation were obviously higher than that of before operation, commonly the highest level was reached at T4 (allP value>0.01), and also was higher at T6 than that of before the operation (allP value<0.01), except the level of TNF-α recovered rapidly to the level of before operation (allP value>0.05) in the VATS group. The operation time, postoperative drainage tube indwelling time and incision healing time in the VATS were lower than that in the control group (allP value<0.05).
Conclusion
VATS could be widely applied in clinical practice with lowering operative trauma and reducing the degree of inflammatory reaction.
ObjectiveTo evaluate the clinical effects of segmentectomy versus lobectomy under single utility port video-assisted thoracic surgery on inflammatory factors and immune cells in peripheral blood of non-small cell lung cancer patients, and to analyze the effect of changes of postoperative inflammatory factors and immune cells on the prognosis of the patients.MethodsThe clinical data of 256 patients who underwent segmentectomy or lobectomy under single utility port video-assisted thoracic surgery for non-small cell lung cancer in the First Affiliated Hospital of Hebei North University from January 2016 to October 2020 were retrospectively collected. According to the operation method, they were divided into a segmentectomy group (126 patients with 79 males and 47 females at an age of 63.4±6.2 years) and a lobectomy group (130 patients with 91 males and 39 females at an age of 62.9±5.6 years). The change of inflammatory factors (C reactive protein, interleukin-6, interleukin-8, tumor necrosis factor-α) and immune cells (CD4+T cells, CD8+T cells and natural killer cells) were recorded and analyzed before operation (T0) and 1 day (T1), 3 days (T2), 7 days (T3), 1 month (T4) after the operation between the two groups. According to postoperative recurrence situations, they were divided into a recurrence group and a non-recurrence group, multivariate logistic regression analysis was used to analyze the relationship between the change of postoperative inflammatory factors, immune cells, and the prognosis of patients with non-small cell lung cancer.Results(1) There was no statistical difference in sex ratio, underlying diseases, body mass index, levels of preoperative inflammatory factors or immune cells between the two groups (all P>0.05). (2) The changes of postoperative inflammatory factors in the segmentectomy group were significantly less than those in the lobectomy group at T1-T3 (all P<0.05), and the changes of postoperative immune cells in the segmentectomy group were significantly less than those in the lobectomy group at T1-T4 (all P<0.05). (3) The changes of postoperative inflammatory factors and immune cells on postoperative day 3 in the recurrence group were significantly more than those in the non-recurrence group (all P<0.05). (4) Multivariate logistic regression analysis showed that the changes of postoperative inflammatory factors and immune cells on postoperative day 3 may be the risk factors for postoperative recurrence and metastasis in patients with non-small cell lung cancer (all P<0.05).ConclusionSingle utility port video-assisted thoracic surgery segmentectomy for the treatment of non-small cell lung cancer can reduce the inflammatory response and protect body's immune function, and the change of postoperative inflammatory factors and immune cells in postoperative day 3 may be the risk factors for postoperative recurrence and metastasis in patients with non-small cell lung cancer.
Objective To summarize and review the heterogeneity of bone marrow derived stem cells (BMDSCs) and its formation mechanism and significance, and to analyze the possible roles and mechanisms in intestinal epithel ial reconstruction. Methods The related l iterature about BMDSCs heterogeneity and its role in intestinal epithel ial repair was reviewed and analyzed. Results The heterogeneity of BMDSCs provided better explanations for its multi-potency. The probable mechanisms of BMDSCs to repair intestinal epithel ium included direct implantation into intestinal epithel ium, fusion between BMDSCs and intestinal stem cells, and promotion of injury microcirculation reconstruction. Conclusion BMDSCs have a bright future in gastrointestinal injury caused by inflammatory bowl disease and regeneration.
Objective To identify the effects of single immunoglobin IL-1 receptor related protein （SIGIRR） on inflammation induced by high mobility group box 1 （HMGB1） in A549 derived from human alveolar epithelial cells. Methods Eukaryotic expression vectors pCDNA3.1（+） constructed with SIGIRR cDNA were transiently transfected into A549 cells，in which SIGIRR was forced to be over-expressed. Western blot and RT-PCR were applied to detect the expression level of SIGIRR after transfection. After the stimulation by HMGB1，the transcriptional activity of NF-κB in A549 cells was detected by dual-luciferase reporter assay system，and the protein levels of inflammatory cytokine TNF-α and IL-1β were measured by ELISA. Results The expression level of SIGIRR increased significantly in A549 cells transfected with SIGIRR vectors. The transcriptional activity of NF-κB was enhanced obviously after HMGB1 treatment in A549 cells by dual-luciferase reporter assay system，while the transfection of SIGIRR vectors decreased the activity. The protein levels of TNF-α and IL-1β were down-regulated in A549 cells over-expressing SIGIRR after HMGB1 stimulation compared with the non-transfected cells. Conclusions Up-regulated SIGIRR expression can inhibit HMGB1-induced proinlammatory cytokine release in A549 cells such as TNF-α and IL-1β. The transcriptional activity of NF-κB is dampened by SIGIRR transfection，implying that the anti-inflammatory effects of SIGIRR may be involved in the regulation of NF-κB.
Inflammatory bowel disease (IBD) is characterized by recurrent abdominal pain, diarrhea, and mucopurulent bloody stools as its main clinical manifestations. In recent years, its parenteral manifestations have received increasing attention. Fatigue, as one of the extraintestinal manifestations of IBD, affects the quality of life of patients, and results in considerable distress for patients. The influencing factors of fatigue symptoms in IBD patients include inflammation, psychological comorbidities, sleep disorders, anemia, micronutrient deficiency, changes in microbiota, and metabolomics. The pathogenesis is currently unclear and may be related to disorders in tryptophan metabolism. This article will review the influencing factors and pathogenesis of fatigue symptoms in IBD patients, aiming to provide a basis for the prevention and treatment of IBD fatigue.
Augmenter of liver regeneration (ALR) is a newly discovered cytokine that can promote liver regeneration and proliferation of damaged liver cells. In the renal tissue, ALR is mainly expressed in the cytoplasm of the medullary loops, collecting ducts and distal convoluted tubules in the renal medulla, and is low in the glomerular and cortical tubules. Various stimulation, such as ischemiacal, hypoxia, poisoning and inflammatory stimulation, can induce the expression of ALR in the epithelial cells of proximal tubule regeneration and the damaged areas of cortex, and participate in the repair process. Current studies have found that in acute kidney injury (AKI), exogenous ALR can protect renal tubular epithelial cells by inhibiting apoptosis of renal tubular epithelial cells, promoting proliferation of renal tubular epithelial cells, inhibiting the activities of inflammatory cells, and promoting the reduction of renal injury. This paper intends to review the basic characteristics of ALR and the pathogenesis of AKI, summarize the characteristics of the mechanism of ALR in AKI by combing the relevant literature on ALR and AKI in recent years, and provide knowledge reserve and direction reference for the in-depth study of ALR in kidney in the future.
