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.
ObjectiveTo investigate the effect of etomidate and propofol on inflammatory cytokines and cortisol for patients with lung adenocarcinoma. MethodSixty patients scheduled for lung cancer surgery under general anesthesia were studied. All patients were randomly divided into an etomidate total intravenous anesthesia group (group E, 30 patients, 16 males and 14 females at age of 58.0±5.0 years) and a propofol total intravenous anesthesia group (group P, 30 patients, 17 males and 13 females at age of 55.0±5.0 years), with 30 patients in each group. ResultsThe concentration of IL-6 in serum of patients in the two groups at time points T1, T2 and T3 was significantly higher than those at time point T0 (P < 0.01). The concentration of IL-10 and TNF-α in serum of patients at time points T1 and T2 was significantly higher than those at time point T0 (P < 0.01). And the difference of the concentration of TNF-α in serum of patients at time points T0 and T3 was not statistically significant (P > 0.05). The level of Cor of patients in the group E at time point T0 was slightly higher than those at time point T1, but lower than that at time points T2 and T3. There was no statistical difference in the concentration of IL-6 and TNF-α in serum of patients between the two groups. The level of IL-10 of patients in the group E at time points T2 and T3 was lower than those in the group P (P < 0.05), but no significant difference was observed at the other time points. The concentration of Cor in the patients in the group E at time point T1 was lower than that in the group P (P < 0.01), but no significant difference was observed either at the other time points. ConclusionThe effect of etomidate used for maintenance of general anesthesia on the inflammatory factors is essentially similar to that of propofol.
Osteochondral defects is a common clinical joint disease. The complexity of cartilage-bone interface and the poor self-repair capacity of cartilage are both reasons for current relatively limited clinical treatments. The introduction of tissue engineering provides a new treatment method for osteochondral repair. This paper reviews three main elements of cartilage-bone tissue engineering: seed cell source and culture method, cytokines regulation and synergistic effect, and scaffold components and type. We mainly focused on current status quo and future progress of cartilage-bone repair scaffolds. This paper provides some reference for the further development of osteochondral tissue engineering.
ObjectiveTo summarize the research status and progress of interleukin-6 (IL-6) in Takayasu arteritis (TAK). MethodRecent literature published at home and abroad about the study of IL-6 in the TAK was reviewed and analyzed. ResultsIL-6 was a pro-inflammatory cytokine secreted by a variety of cells, which participated in a variety of inflammatory and immune reactions, and played an important role in the progress of TAK. The expression levels of IL-6 in the peripheral blood and vascular wall tissues of patients with TAK were increased. The gene polymorphism of IL-6 might be related to the occurrence of TAK. Tocilizumab, an IL-6 receptor antagonist, was effective and safe in the treatment of TAK. ConclusionsIL-6 can be used as one of the monitoring indicators for the active phase and recurrence of TAK. IL-6 receptor antagonist can be used as the treatment choice of TAK, but the application results in different stages of TAK are still worth expecting.
Objective To investigate the mRNA and protein expression of human β-defensin-2 (hBD-2) induced by lipopolysaccharide (LPS)，IL-1β and TNF-α in human airway primary epitheliums.Methods The bronchial primary epitheliums from human were stimulated with LPS，IL-1β and TNF-α respectively and then were harvested for hBD-2 expression detection.The mRNA expression of hBD-2 was detected by RT-PCR，and the protein expression by immunocytochemistry and western blot.Results There was a small expression of hBD-2 mRNA in human airway primary epitheliums before stimulation.The hBD-2 mRNA expression was significantly increased after 3 hours of LPS，IL-1β and TNF-α stimulation respectively and the expression increasement was in a dose dependent manner.The hBD-2 protein could be detected in cytoplasm after 4 hours of LPS (0.1 μg/mL)，IL-1β (1 ng/mL) and TNF-α (10 ng/mL) stimulation.Conclusions LPS and proinflammatory cytokines can induce the mRNA and protein expression of hBD-2 in a short time.The expression of hBD-2 may play an initial defense role against bacterial invasion.
【摘要】 目的 观察胎羊宫内心脏介入手术胎羊血气及血浆炎性细胞因子的变化。方法 8只怀孕双胎山羊,双胎之一为实验组,在相同麻醉条件下,实验组进行胎羊心脏介入治疗,并抽取血样标本。监测胎羊的心率、血气、乳酸值,运用ELISA法检测治疗组及对照组胎羊白介素(IL)1、IL6、IL8及肿瘤坏死因子(TNFα)。结果 2只胎羊因手术中发生心包填塞死亡,存活的6只胎羊手术前pH值较手术后有明显下降(Plt;005),手术前后乳酸浓度上升(Plt;005),PCO2、PO2差异无统计学意义(Pgt;005),手术前血浆IL1、IL6、IL8的浓度较手术后高(Plt;005),手术前后TNFα的浓度变化无统计学意义(Pgt;005)。结论 胎羊宫内心脏介入手术可引起胎羊血浆pH值下降,乳酸浓度上升,及细胞因子IL1、IL6、IL8浓度上升。【Abstract】 Objective To observe the change of blood gas and inflammatory cytokines during intrauterine cardiac intervention surgery on the fetal lambs. Methods Eight pregnant goats with two fetal in each goat were included. With the same anesthesia condition, one of the twin fetus was chose to perform the intrauterine cardiac intervention surgery. The fetal heart beating rate was monitored, and blood samples of the fetus were taken to do the blood gas analysis and to detect the concentration of inflammatory cytokines (IL1, IL6, IL8, and TNFα). Results Two of the eight fetal lambs which was died in the operation because of pericardial tapenade. In the other six survived fetus, the PH was lower than after the surgery, and the concentrations of lactic acid, IL1, IL6, and IL8 are higher than after the surgery. There was no significant difference of PCO2,PO2 and TNFα between before and after the surgery. Conclusion The intrauterine cardiac intervention surgery can make the PH of fetal plasma lower and the concentrations of lactic acid and IL1, IL6, IL8 higher.
Abstract： Objective To investigate the acute cardioprotective effect of 17b-estradiol (17b-E2) against severe myocardial ischemia/reperfusion (I/R) injury in rabbits and the mechanism of the effect. Methods We established the model of myocardial I/R in vivo by occluding the left anterior descending coronary artery of the rabbits (who underwent coronary occlusion for 40 minutes followed by 3 hours of reperfusion). Twentyfour New Zealand white male rabbits were randomly divided into two groups with 12 in each group. Before coronary occlusion, 1 ml of ethanol or 17b-E2 at 10 μg/kg was administered intravenously to the rabbits in the control group and the experimental group respectively. The serum levels of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) were measured by enzymelinked immunosorbent assay (ELISA) at the following time points: before occlusion, 40 minutes after occlusion, 1 hour, 2 hours and 3 hours after reperfusion. Activation of p38 mitogen activated protein kinase(MAPK) was determined by Western blotting analysis, and apoptosis of cardiocytes was identified by terminal deoxynucleotidlyl transferase mediated deoxyuridinebiotin dUTP Nick End Labeline (TdT)mediated dNTP nick end labeling (TUNEL) staining. Results During myocardial ischemia, TNF-α decreased significantly in the experimental group compared with the control group (F=0.007,P=0.001), while there was no difference in IL-6 between the two groups (F=0.616,P=0.095). During the process of reperfusion, the levels of TNF-α and IL-6 in the experimental group were significantly lower than those in the control group (Plt;0.01). Besides, the activation of p38 MAPK and apoptotic index for the experimental group were also lower (45.07%±2.73% vs. 61.25%±2.41%, t＝－15.398, P=0.000; 11.21%±3.85% vs. 22.02%±4.49%, t＝－6.332, P=0.000). Conclusion The cardioprotective effect of 17b-E2 against myocardial I/R may be attributed to its antiinflammatory and antiapoptotic properties, which is probably associated with the inhibition of 17bE2 on p38MAPK activity.
Objective To investigate the effects of glutathione S-transferase M5 (GSTM5) on the inflammation in human bronchial epithelial 16HBE cells and its possible molecular mechanisms. Methods Acute lung injury cell model was constructed with 16HBE cells induced by tumour necrosis factorα (TNF-α, 10 ng/mL). The cells were devided into a control group, a TNF-α group (TNF-α), a GSTM5 group (GSTM5+TNF-α), a negative control group (negative control plasmid+TNF-α). GSTM5-GFP plasmid and negative control plasmid were respectively transfected to the cells of the GSTM5 group and the negative control group using Lipofectamine2000. The contents of interleukin-6(IL-6), IL-8, IL-10 in the cell supernatant were measured by ELISA.The expression of nuclear factor-κB (NF-κB) mRNA was detected by RT-PCR, and the expression of NF-κB, phospho-NF-κB, p38, phospho-p38 protein were detected by Western blot. Results The GSTM5-GFP eukaryotic expression vector was successfully constructed and transfected successfully confirmed by fluorescence microscope. The contents of IL-6, IL-8, IL-10 in the TNF-α-induced cell supernatant were significantly higher than those in the control group(P < 0.05), and the contents of IL-6, IL-8, IL-10 in the GSTM5 group were lower than those in the TNF-α group (P < 0.05)with statistically significant difference. At the same time, the total NF-κB mRNA, phospho -NF-κB and phospho-p38 protein were increased in TNF-α stimulated cells compared with the control group (P < 0.05), while the GSTM5 group was lower than that in the TNF-α group and the negative control group (P < 0.05). Conclusion Overexpression of GSTM5 inhibits the phosphorylation of p38MAPK and NF-κB and down-regulates the inflammation of TNF-α-induced human bronchial epithelial 16HBE cells.
ObjectiveTo explore the potential causal relationship between 91 inflammatory factors and the risk of lung cancer (LC). MethodsBy extracting related data of inflammatory factors and LC and its subtypes from public databases of genome-wide association studies (GWAS), bidirectional, repeated, multivariable Mendelian randomization (MR) and subgroup MR methods were used for analysis. The inverse variance weighted method was mainly used for causal inference, and a series of sensitivity analyses were applied to verify the strength of the results. ResultsHigher levels of CD5, interleukin-18 (IL-18), and oncostatin-M (OSM) were causally associated with a lower risk of LC, while nerve growth factor-β (NGF-β) and S100 calcium-binding protein A12 (S100A12) were associated with an increased risk of LC. Subgroup MR analysis results showed that IL-18 had a causal relationship with a reduced risk of lung adenocarcinoma, while NGF-β and S100A12 had a causal relationship with an increased risk of lung adenocarcinoma; CD5 and OSM had a causal relationship with a reduced risk of lung squamous cell carcinoma; NGF-β had a causal relationship with an increased risk of small cell lung cancer. ConclusionFive inflammatory factors, including CD5, IL-18, OSM, NGF-β, and S100A12 have a causal correlation with the risk of LC, providing potential targets for early screening of LC patients and development of therapeutic drugs.
Myocardial remodeling is a common pathological physiology change for a variety of heart diseases under stimulation such as stress or ischemia. The engine body will release a lot of cytokines to promote the change of myocardial structure and ultimately lead to heart failure. Myocardial remodeling includes myocardial cells remodeling and the extracellular matrix remodeling. In recent years, we find that the function of adipose tissue is not only about energy storage, buffering to protect, supporting and filling, but also has a powerful function of secretion. Adipose tissue can secrete various adipocytokines, such as leptin, adiponectin, visfatin, omentin, angiotensin Ⅱ, and so on. Current studies have shown that adipocytokines and myocardial remodeling are intimated. And this article will summarize the function of adipocytokines on myocardial remodeling.