Objective To explore the association of macrophages with carcinogenesis and development of gastric cancer. Method The related literatures at home and abroad were consulted and reviewed. Results The microenvironment of gastric cancer could induce the polarization of macrophages，and then the activated macrophages，especially the tumor associated macrophages，could in turn motivate the growth，invasion，and metastasis of tumor cells by secreting a series of active substances. Conclusions Macrophages，especially the tumor associated macrophages play an importantrole in the carcinogenesis and development of gastric cancer. Investigating the macrophages and their interaction with gastric cancer may lead to a profound understanding of carcinogenesis of gastric cancer as well as opening up a new prospectfor treatment.
Objective To study the effect of water soluble chitosan (WSC) on the apoptosis of peritoneal macrophage induced by lipopolysaccharides (LPS), and discuss the mechanism. Methods Peritoneal macrophages were divided to three groups: phosphate buffered saline (PBS) group, LPS group and LPS plus WSC group. At hour 24, apoptosis cell and active caspase-3 were detected by flow cytometry; nitric oxide (NO) was determined with Griess reagent. Results There were more apoptosis cells in the LPS group than the PBS group. The percentage of apoptosis cells was significantly decreased in the LPS plus WSC group than the LPS group. The expression of active caspase-3 and the secretion of NO were also inhibited by WSC after LPS intervention. Conclusion WSC inhibits apoptosis of peritoneal macrophage induced by LPS.
Retinal macrophages and (or) microglial cells play important roles in regulating inflammation, angiogenesis and tissue repairing, thus affect the development and prognosis of ischemic retinal disease, ocular immune diseases and ocular tumors. Reversing the polarization imbalance of these cells may provide new therapeutic strategies for ischemic retinal disease and ocular immune diseases. The duality of the polarization direction of these cells is still controversial in the inflammatory reaction and pathological angiogenesis of ischemic retinal disease. Meanwhile, the plasticity and diversity of the function need to be further studied and discussed.
Objective To explore the effects of several immunosuppressants on the cell numbers of cultured rat macrophages and Schwann’s cells. Methods The macrophages and Schwann’s cells were cultured from the newborn Wistar rats. Different concentrations of methylprednisolone(10-3, 10－4,10－6 and 10－8 mol/L), CsA(10－5, 10－6, 10－7 and 10－8 mol/L) and FK506(10-6, 10－7, 10－8 and 10－9 mol/L) were administrated to the cells, while control group was given no drugs. Twentyfour, 48 and 72 hours after administration, the cells from different concentrations were measured with MTT methods respectively. Theresults were compared and analyzed statistically. Results Only high concentration methylprednisolone (10-4 mol/L) and a certain range of concentrations of CsA (10-6，10-7 and 10-8 mol/L) and FK506 (10-7,10-8 and 10-9 mol/L) can provide protection to culturedrat macrophages. Under most concentrations, CsA and FK506 had no effects onthe cell number of cultured rat Schwann’s cell. Only with high concentration CsA (10-5 mol/L) and methylprednisolone (10-3 mol/L) could significantly decreased the cell number of Schwann’s cell. Long time (72 hours) and low dosage (10-8 mol/L) administration of methylprednisolone could significantlyprotect Schwann’s cell. Conclusion High concentration methylprednisolone and some certain concentration CsA and FK506 can protect cultured rat macrophages. But high concentration CsA and methylprednisolone prohibit the proliferation of Schwann’s cells. Only long time and low dosage methylprednisolonecan protect cultured rat Schwann’s cells.
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 role of macrophage stimulating protein (MSP) in the pathogenesis of chronic obstructive pulmonary disease (COPD). Methods Ninety subjects were recruited from health examination center, outpatient or inpatient department in Affiliated Hospital of North Sichuan Medical College from July 2013 to December 2013. They were divided intoahealthy control group, a stable COPD group, and an acute exacerbation of COPD (AECOPD) group with 30 subjects in each group. The levels of MSP, interleukin-6 (IL-6), IL-8 and tumor necrosis factor-α (TNF-α) in the plasma of all subjects, as well as the levels of MSP in the induced sputum of the AECOPD and the stable COPD patients were assessed by enzyme-linked-immuno-sorbent assay. Results The concentrations of MSP, IL-6, IL-8 and TNF-α in the plasma of the patients with COPD were obviously higher than those of the healthy controls (P<0.05) while much higher in AECOPD patients than those in stable COPD patients (P<0.01).The concentration of MSP in the induced sputum of the patients with AECOPD was higher than that in the stable COPD patients (P<0.01). The concentrations of MSP in the serum and induced sputum as well as serum levels of IL-6, IL-8 and TNF-α in the patients with COPD were negatively correlated with the level of FEV1%pred. The concentrations of MSP in the serum and induced sputum in the COPD patients were positively correlated with the concentrations of IL-6, IL-8 and TNF-α. Conclusions The concentrations of serum and induced sputum MSP, and the serum concentrations of IL-6, IL-8 and TNF-α in COPD patients are related to the severity of the disease. MSP may play an important role in the pathogenesis of COPD. The mechanism might be mainly involved in the regulation of airway inflammation.
ObjectiveTo interpret the mechanisms of vascular repair disorders in steroid-induced avascular necrosis of the femoral head (SANFH) via detection of the changes of proliferation, migration, and macrophage migration inhibitory factor (MIF)/vascular endothelial growth factor (VEGF) expressions of endothelial cells (ECs) under hypoxia/glucocorticoid. MethodsAccording to culture conditions, human umbilical vein ECs (HUVECs) at passage 3 were divided into group A (normal), group B (1.0×10-6 mol/L dexamethasone), group C (hypoxia), and group D (hypoxia+1.0×10-6 mol/L dexamethasone). The cell activity was detected by AlamarBlue; the number of viable cells was detected in live/dead cell staining; the cell morphology was observed after cytoskeleton staining; cell migration ability was compared by scratch test; and the levels of MIF and VEGF expressions were detected by ELISA. ResultsAt 24 hours after culture, the cell activity and the number of living cells in group C were significantly higher than those in the other 3 groups, showing significant difference between groups (P < 0.05), and group D had the worst cell activity and least living cells. Cytoskeleton staining showed that cells had normal morphology in groups A and B; cells had rich cytoskeleton and secretion granules in group C; cytoskeleton form disorder and nucleus pyknosis were observed in group D. Scratch test showed that the cell migration ability of group C was strongest while cell migration ability of group D was weakest. Accumulated concentration of MIF and VEGF in 4 groups significantly increased with time extending. Accumulated concentration of MIF in group C were significantly higher than that in other 3 groups at each time point (P < 0.05). Within 24 hours after intervention, stage concentration of MIF during 1-8 hours was significantly lower than that during 0-1 hour and 8-24 hours in every group (P < 0.05). Stage concentration of MIF in group C was significantly higher than other groups during 0-1 hour and 8-24 hours (P < 0.05). Within 2 hours after intervention, stage concentration of MIF in 4 groups during 0.5-1 hour was significantly higher than that during other stages (P < 0.05). Accumulated concentration of VEGF in group C was significantly higher than that in other groups at 8 and 24 hours (P < 0.05). The stage concentration of VEGF in groups C and D during 8-24 hours was significantly higher than that during 0-1 hour and 1-8 hours (P < 0.05). There was no significant difference in the stage concentration of VEGF within and among group A, B, C, and D at every stage within 2 hours after intervention (P > 0.05). ConclusionIn hypoxia environment, the proliferation and migration of ECs is enhanced, and the secretion of VEGF and MIF is increased. High concentration of dexamethasone will suppress the process above, which induces vascular repair disorders and aggravating SANFH.
Eight patients with macromastia were treated with spoialy designed dermis preserved crossingmammary pedicle flap. A crossed curved scar situated below the edge of the breast was left behind andwas covered by the breast ofter operation. The breast had a good appearlance, mammary mecrosisdidn t occur in any cases. In four patients who had been followed up for six months of longer, thesensation of the nipple and areola had completely recovered in two patients, partially recovered in oneand h...
Objectives To explore the expression of macrophage inflammatory protein-1beta (MIP-1β) in patients with none-small cell lung cancer (NSCLC) of different pathological types and its association with cancer clinical stages and metastasis of lymph nodes.Methods MIP-1β mRNA from fresh lung tissue of 38 NSCLC patients was amplified by RT-PCR and half-quantified.Immunohistochemical technique was performed to find out the expression of MIP-1β in paraffin-embedded lung tissue from 66 patients with NSCLC.The area and degree of stain were evaluated to determine the positive rate，which was compared between with or without metastasis of lymph nodes，different pathological types and TNM clinical stages.Results MIP-1β protein was found in cytoplasm of malignant cells of squama cell cancer and adenocarcinoma without significant difference between them，while not found in bronchus-alveolus cell cancer.The MIP-1β mRNA expression in squama cell cancer and adenocarcinoma were significant higher than which in bronchus-alveolus cell cancer without significant difference between each other.The positive rates of MIP-1β in lung cancer of Ⅰ，Ⅱ and Ⅲ stages were 74.2%，29.4% and 85.7% respectively，which of Ⅰ and Ⅲ stages cancer were significant higher than Ⅱ stage without significant difference between each other.The positive rates of MIP-1β in lung cancer with or without metastasis of lymph nodes were 45.8% and 76.3% respectively with significant difference between them.Conclusion MIP-1β is expressed in lung cancer cells and relates to the pathological type，TNM stage and the metastasis of lymph nodes.
PURPOSE: To investigate the activation and immune respones of lymphocytes in epiretinal membranes (ERMs)and subretinaI membranes (SRMs). METHODS: A panel of morioclonal antibodies against CD23 (activated B cell), CD25 (activated T cell), CD68(macrophages) and HLA-DR (human leukocyte antigen II antigen)were used for the study of 20 specimens of ERMs from 20 patients with proliferative vitreoretinopathy (PVR),traumatic PVR and secondary traction retinal detachment,and 2 SRMs from PVR and traumatic PVR, with positive and negative reaction specimens as controls. RESULTS:Four cases of ERMs were found to be CD23 and CD25 positive respectively,and one case of SRMs to be CD23 and CD25 positive respectively. All the specimens of ERMs and SRMs revealed CD68 and HLA-DR positive in this series. CONCLUSIONS :There might be an aberrant immunoreaction mediated by T and B cells in the ERMs and the SRMs,and they might play an important role in the patbogenesis of PVR,traumatic PVR and secondary traction retinal detachments. （Chin J Ocul Fundus Dis,1996,12: 147-150）