Objective To investigate the impacts of cytokines （interleukin-4，IL-4；tumor necrosis factor-α，TNF-α） and medications of bronchial asthma （dexamethasone，aminophylline，salbutamol） on the activity of histamine N-methyltransferase（HMT） in tracheal epithelial cells.Methods BEAS-2B bronchial epithelial cells were cultured and treated with different concentration of TNF-α, IL-4, dexamethasone, salbutamol and aminophylline respectively. The activity of HMT in BEAS-2B cells was determined by high performance liquid chromatography.Results The activity of HMT in tracheal epithelial cells was (50±7) pmol?min-1?mg pro-1.TNF-α and IL-4 lowered the activity of HMT significantly at the concentration equal to or higher than 1 ng/mL and 5 ng/mL respectively，and reached the maximum inhibitory effect at the level of 10 ng/mL.Dexamethasone and aminophylline could ameliorate distinctly the inhibitory effect of TNF-α on the activity of HMT, while salbutamol had no significant inhibitory effect.Conclusions TNF-α and IL-4 exert the lowering effect on the activity of HMT，which would be one important cause of airway hyperreactivity.Glucocorticoids and theophyllines are administered to treat asthma partly due to its relieving mechanism of TNF-α negative effects on HMT.
ObjectiveTo investigate the effects and clinical significance of edaravone on serum tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and intercellular adhesion molecule-1 (ICAM-1) in elderly patients with obstructive sleep apnea hypopnea syndrome (OSAHS).MethodsA total of 90 elderly patients with moderate to severe OSAHS confirmed by polysomnography were recruited from North China University of Science and Technology Affiliated Hospital in February 2016 to October 2017. According to random number table method the OSAHS patients were randomly divided into group A (n=30), group B (n=30) and group C (n=30). Group A received continuous positive airway pressure treatment for six months, group B received edaravone therapy and continuous positive airway pressure treatment for six months, and group C only received edaravone therapy for six months. The changes of serum TNF-α, IL-6 and ICAM-1 were detected by enzyme-linked immunosorbent assay before and after treatment.ResultsThe differences of serum TNF-α, IL-6 and ICAM-1 before treatment in the three groups were not statistically significant (P>0.05). Compared with before treatment, the levels of serum TNF-α, IL-6 and ICAM-1 decreased in the three groups (P<0.05). After six months of treatment, the levels of serum TNF-α, IL-6 and ICAM-1 decreased in group A and group B compared with group C (P<0.05), and decreased significantly in group B compared with group A (P<0.05).ConclusionEdaravone can inhibit the expressions of serum TNF-α, IL-6 and ICAM-1 in elderly patients with moderate to severe OSAHS, and thereby reduce vascular endothelial dysfunction and injury.
Objective To observe the levels of malonaldehyde (MDA) , interleukin-8 (IL-8) and tumor necrosis factor-α(TNF-α) in lung tissues of subjects with or without chronic obstructive pulmonary disease (COPD) , and investigate their roles in the the pathogenesis of COPD. Methods The content of MDA, IL-8 and TNF-αin lung tissues of smokers with COPD (n=9) , ex-smokers with COPD (n=8) , non-smokers with COPD (n=7) , healthy smokers (n=9) , healthy ex-smokers (n=8) and healthy nonsmokers (n=6) was measured with enzyme-linked immunosorbent assay ( ELISA) and corrected by creatinine. Results The levels of MDA, IL-8 and TNF-α in lung tissues of the COPD patients were significantly higher than those in the healthy subjects (Plt;0.05) , which were also significantly higher in the smokers when compared with the non-smokers (Plt;0.05) , whether suffering from COPD or not. In the COPD patients, not the levels of IL-8 but MDA and TNF-αin lung tissues of the smokers were significantly higher than those in the ex-smokers (Plt;0.05) ; whereas in the healthy cases, no statistical significance was revealed between the smokers and the ex-smokers on the levels of MDA and IL-8 in lung tissues except TNF-α( Pgt;0.05) . Conclusion The abnormal increase of MDA, IL-8 and TNF-αin lung tissues caused by chronic smoking may play an important role in the the pathogenesis of COPD.
Objective To investigate the effects of ginkgo biloba extract （GBE） on expressions of IL-1β, IL-6,and TNF-α in the pancreas and brain tissues of rats with severe acute pancreatitis （SAP）, and further to explore the pathogenesis of SAP and the efficacy of GBE on brain injury. Methods Fifty-four Winstar rats were randomly divided into normal control group, model group, and treatment group, with 18 rats for each group. For rats in the normal control group, only conversion of pancreas was performed by abdomen opening , followed by wound closure immediately. For rats in the model group and treatment group, 5% sodium taurocholate hydrate were injected under pancreatic capsule to establish SAP model, and then GBE and normal saline were infected into intra-abdomen repeatedly every 8 hours, respectively. At 6 h, 12 h, and 24 h after the model establishment, experimental samples were extracted and serum amylase was detected. Pathogenic scoring for pancreas tissues was performed under light microscopy, and immunohistochemistry method was employed to detect the expression levels of IL-1β, IL-6, and TNF-α in pancreas and brain tissues. Results For the treatment group, both serum amylase and pancreas scoring were significantly lower than those of the model group （P＜0.01）. At 24 h after model establishment, the expressions of IL-1β, IL-6, and TNF-α of pancreas tissues in model group were significantly higher than those at 6 h and 12 h （P＜0.05 or P＜0.01）, but no significant differences wereobserved in treatment group （P＞0.05）. The expressions of IL-1β, IL-6, and TNF-α of brain tissues in model group were significantly higher than those at 6 h and 12 h （P＜0.05 or P＜0.01）, but in treatment group decreased （P＜0.05 or P＜0.01）. The expressions of IL-1β, IL-6, and TNF-α in the treatment group were significantly lower than those of the model group at same time （P＜0.01）. Conclusions During SAP, the expressions of IL-1β, IL-6 and TNF-α in pancreas and brain tissues increased obviously. GBE showed suppressing and scavenging effects on IL-1β, IL-6 and TNF-α in pancreas and brain tissues.
ObjectiveTo explore the mechanism of liver capillary permeability in rats with severe acute pancreatitis (SAP). MethodsTotally 40 healthy Sprague-Dawley (SD) rats were randomly divided into two groups: sham operation (SO) group and SAP group, SAP group were divided into four subgroups according to sampling time (3 h， 6 h, 12 h， and 24 h). The model was established by injecting 5% sodium taurocholate retrogradely into pancreaticobiliary ducts. The changes of tumor necrosis factor-α (TNF-α), pathohistology, and tissue moisture content were compared among different groups. Liver occludin protein expression was analyzed by immunohistochemistry method, and occludin mRNA was measured by RT-PCR. ResultsThere was no significant pathological changes of liver tissue in the SO group. Typical pathological changes of SAP， such as interstitial edema, vasodilatation, infiltration of inflammatory cells, were found in the SAP group. TNF-α level and tissue moisture content of each phase increased gradually, and the highest level appeared at 24 h within the observing period. The two above indicators at different time point in subgroups were significantly different from each other and higher than those in the SO group (Plt;0.05)． In the SAP group, the expression of occludin and it’s mRNA began to decrease at 3 h to the bottom at 6 h and rebounced significantly at 12 h, 24 h compared with those at 6 h (Plt;0.05), but still lower than those in the SO group (Plt;0.05). ConclusionUpregulation in TNF-α and subsequent downregulation in occludin protein and mRNA maybe bly related to the severe liver capillary permeability in rats with SAP.
Objective To investigate the effects of tobacco smoke exposure on histone deacetylase 2 (HDAC2),interleukin-8(IL-8)and tumor necrosis factor-α(TNF-α)expression in peripheral blood of patients with lung adenocarcinoma and analyze the relationships among them. Methods Seventy-three cases diagnosed as lung adenocarcinoma were collected in the First Affiliated Hospital and Affiliated Tumor Hospital of Guangxi Medical University from April 2014 to March 2015.All patients underwent lung function test preoperatively.Fourteen healthy volunteers without tobacco smoke exposure and chronic obstructive pulmonary disease (COPD)were recruited as healthy control.According to the lung function and tobacco smoke exposure,all cases were divided into four groups,ie. a healthy control group (group A,14 cases),a group without tobacco smoke exposure and COPD(group B,19 cases),a group with tobacco smoke exposure and without COPD(group C,33 cases),and a group with tobacco smoke exposure and COPD(group D,21 cases).The expressions of HDAC2 mRNA,IL-8 mRNA and TNF-α mRNA in peripheral blood mononuclear cells (PBMCs)were detected by real-time polymerase chain reaction (PCR).The contents of IL-8 and TNF-α in serum were detected by ELISA. Results Compared with group A,the HDAC2 mRNA expression in PBMCs had no difference in group B(P>0.05),and was down-regulated significantly in group C and D (P<0.05),which in group D was the most obvious.Compared with group A,the expressions of IL-8 mRNA and TNF-α mRNA in PBMCs and the contents of IL-8 and TNF-α in serum were significantly higher in all lung adenocarcinoma patients(all P<0.05),and the up-regulation was more obvious in group D.The relative expression of HDAC2 mRNA in PBMCs showed no significant difference with respect to age,gender or TNM stage (P>0.05).IL-8 and TNF-α in PBMCs and serum showed no significant difference with respect to age and gender (P>0.05),and were higher in the patients with TNM stage Ⅲ lung adenocarcinoma than those with stage Ⅰ and Ⅱ(P<0.05),with no obvious difference between stage Ⅰ and stage Ⅱ (P>0.05). Conclusion Tobacco smoke exposure causes lower expression of HDAC2 and over-expression of IL-8 and TNF-α in peripheral blood of patients with lung adenocarcinoma,can aggravate inflammatory response especially when complicated with COPD,which may be related to the prognosis of lung adenocarcinoma.
【Abstract】ObjectiveTo explore the effects of p38 mitogenactivated protein kinase (MAPK) on apoptosis of small intestinal epithelial cells after transplantation in rats. MethodsSmall intestinal transplantation was performed in SD and Wistar rats. The recipients were divided into three groups: isograft group (Wistar→Wistar group), allograft group (SD→Wistar group) and allograft+cyclosporine A group (SD→Wistar+CsA group). The grafts were harvested on day 1, 3, 5 and 7 after operation. All graft samples were subjected to histological examination. The apoptosis of graft epithelial cells was detected by TUNEL method. p38 MAPK was measured by Westernblotting method and serum TNFα was determined by ELISA. ResultsMild, moderate and severe rejection reaction occurred in the SD→Wistar group, it was showed that the number of apoptotic cells increased with the severity of the rejection reaction by TUNEL. In SD→Wistar group, the numbers of apoptotic cells were significantly higher than those of the other two groups （P＜0.01）. The severity of rejection reaction in SD→Wistar+CsA group was less than that of SD→Wistar group and the number of apoptotic cells increased with the severity of the rejection reaction (P＜0.01). The level of serum TNFα varied with the apoptotic degree of small intestinal epithelial cells in SD→Wistar group and SD→Wistar+CsA group （P＜0.01）. The expression of p38 MAPK increased with the number of the apoptotic cells in SD→Wistar group and SD→Wistar+CsA group （P＜0.01）, but there was no evident change in Wistar→Wistar group （Pgt;0.05）. The expression of p38 MAPK and the level of serum TNFα were positively correlated with apoptosis in small intestinal rejection after transplantation （r=0.875， P＜0.01； r=0.837， P＜0.01）. p38 MAPK and TNFα were also positively correlated （r=0.826，P＜0.01）. ConclusionApoptosis plays an important role in small intestinal rejection. p38 MAPK is involved in apoptosis and is an important regulator in signal pathway of cell apoptosis.
Objective To investigate the changes of 8-isoprostane ( 8-isoPG) , leukotriene B4 ( LTB4 ) , TNF-α, IL-10 and hypersensitive C-reactive protein( Hs-CRP) in serum of patients with obstructive sleep apnea hypopnea syndrome ( OSAHS) . Methods Forty OSAHS patients ( 20 cases underwent therapeutic Auto-CPAP or UPPP treatment for over three months) and 30 normal controls were included in the study. Serum 8-isoPG, LTB4, TNF-α and IL-10 were measured by ELISA. Hs-CRP was detected by automatic biochemistry analyzer. Results ①The serum levels of 8-isoPG, LTB4, TNF-α, Hs-CRP were significantly higher and IL-10 was considerably lower after sleep in 40 OSAHS patients [ ( 36. 59 ±14. 89) ng/L, ( 14. 75 ±6. 25) μg/L, ( 1022. 13 ±97. 57 ) ng/L, ( 2. 46 ±1. 58 ) mg/L, ( 4. 68 ±3. 42) ng/L, respectively ] than those in the normal controls [ ( 19. 91 ±7. 76 ) ng/L, ( 1. 43 ±0. 72) μg/L, ( 540. 00 ±78. 70) ng/L, ( 0. 30 ±0. 16) mg/L, ( 7. 41 ±4. 49) ng/L, respectively] ( P lt;0. 01) . ② Serum 8-isoPG, LTB4, TNF-α, and Hs-CRP levels elevated gradually following the severity of OSAHS while serum IL-10 level was decreased( P lt; 0. 05) . ③Serum 8-isoPG, LTB4, TNF-α, and Hs-CRP levels in OSAHS patients after sleep were correlated positively with AHI ( r =0. 863, 0. 746, 0. 868, 0. 842,all P lt; 0. 01) and negatively with LSpO2 ( r = - 0. 623, - 0. 524, - 0. 618, - 0. 562, all P lt; 0. 01) and MSpO2 ( r = - 0. 654, - 0. 573, - 0. 537, - 0. 589, all P lt;0. 01) . SerumIL-10 level in OSAHS patients was correlated negatively with AHI ( r = - 0. 722, P lt; 0. 01) and positively with LSpO2 ( r = 0. 564, P lt; 0. 01) and MSpO2 ( r = 0. 505, P lt; 0.01) . ④ After three months of auto continuous positive air pressure( Auto-CPAP) or uvulopalatopharyngoplasty( UPPP) treatment, serum 8-isoPG, LTB4, TNF-α, and Hs-CRP levels of the OSAHS patients after sleep were obviously decreased [ ( 23. 10 ±9. 54) ng/L, ( 4. 02 ±2. 15) μg/L, ( 810. 25 ±135. 85) ng/L, ( 0. 79 ±0. 60) mg/L, respectively] , and serum IL-10 level was obviously increased[ ( 6. 93 ±3. 91) ng/L] ( P lt; 0. 01) . ⑤ serum 8-isoPG and IL-10 had no statistics difference and serum LTB4, TNF-α, Hs-CRP levels were higher in OSAHS underwent therapy compared with the normal controls. Conclusions The results suggest that inflammation and oxidative stress are activated and antiflammatory cytokines are decreased in the OSAHS patients. The serum levels of 8-isoPG, LTB4 , TNF-α, Hs-CRP and IL-10 may prove to be useful in severity monitoring and intervention efficacy judgement in OSAHS patients.
Objective To study the role of hydrogen sulfide （H2S） in prophase of acute peritoneal cavity infection. Methods NaHS was taken as a donor of H2S. Seventy-two Sprague-Dawley rats were divided into 4 groups randomly：control group， cecal ligation and puncture （CLP） and treated with natural saline group，CLP and treated with NAHS group， and CLP and treated with DL-propargylglycine （PAG， an inhibitor of H2S formation） group. Selected 6 rats at 2h， 6h， and 12h after treatment in each group. The contents of TNF-αand H2S in serum and the content of MPO in intestinal tissue were measured， respectively. The histopathological change of ileum tissues were observed at 6 h after treatment in each group. Results The H2S could alleviate CLP-induced inflammation obviously， decrease the content of TNF-α in serum when inflammation，and attenuate the infiltration of neutrophilic granulocyte in small intestine. Conclusion The H2S has anti-inflammation effect in prophase of acute peritoneal cavity infection.
Abstract: Objective To investigate the effect of modified ultrafiltration on attenuating the inflammatory reaction and endothelial cell activation or damage after cardiopulmonary bypass (CPB). Methods Forty patients undergoing cardiac operation with CPB were randomly divided into two groups. Ult rafiltration group ( n = 20) : patients underwent modified ultrafiltration after CPB; control group ( n = 20 ) : without ultrafiltration. Plasma concentrations of soluble intercellular adhesion molecules-1 ( s ICAM -1) and tumor necrosis factor-α (TNF-α) were determined with enzyme linked immunosorbent assay and radioimmunity pre-operat ively (baseline) , at the end of CPB, 4h and 24h post-operatively in both groups. Results The concentrations of sICAM -1 in the cont rol group at 4h and 24h po st-operatively were higher than those pre-operatively (P lt; 0. 01). The concentrations sICAM -1 in the ultrafiltrat ion group in pre-operatively and at the end of CPB were not significantly different from that of the control group, but they were lower at 4h and 24h post-operatively (269. 6±33. 8Lg/L vs. 409. 6±37. 3Lg/L , 245. 9±32. 2Lg/L vs. 379. 3±35. 7Lg/L ; P lt; 0. 01). In the ultrafiltration group, the concentration of TN F-α at the end of CPB and 4h post-operatively were higher than that pre-operatively (P lt; 0. 01). The concent rations of TNF-α in the ultrafiltration group at 24h post-operatively recoved to the pre-operative level (0. 177±0. 024Lg/L vs. 0. 172±0. 030Lg/L ; P gt;0.05). In the control group, the concentration of TN F-α was higher at the end of CPB than that pre-operatively (P lt;0.01) , and decreased slightly at 4h and 24h post-operatively, but remained higher than those pre-operat ively (0. 264±0.045Lg/L vs. 0.174±0.033Lg/L , 0.218±0.028Lg/L vs. 0.174±0. 033Lg/L ; P lt; 0. 05). Conclus ion CPB is known to induce inflammatory reaction and endothelial cell activation or damage. Modified ultrafiltration appears to attenuate these adverse reactions and is beneficial to postoperative convalescence.