Serum Concentrations of Angiotensin, C-Reactive Protein, Interleukin-8, and Tumor Necrosis Factor-α in Train Driver Population

Train drivers are engaged in high-stress job. It may induce sleep, fatigue, and alertness loss at work, and endanger public safety. It’s unclear that cytokines of train driver would be influenced by their job. The research considers the hypothesis that stressful professions, such as train driver, influence the body’s immune system through the long-time and high-pressure working, and change production of neuro-immune factors. Using enzyme linked immunosorbent assay (ELISA), several neuro-immune factors were assayed among train drivers (N = 82) and health blood donors (N = 80) enrolled in the Yunnan Collaborative Innovation Center for Public Health and Disease Control. The concentrations of angiotensin, C-reactive protein (CRP), interleukin-8 (IL-8), and tumor necrosis factor-alpha (TNF-α) were determined. Kruskal-Wallis test and Dunn’s multiple comparisons test were performed for overall comparison between groups and for pairwise comparison, respectively. Statistical significance level was set at P < 0.05. The profession of train driving was not associated with significant increases or decreases in the systemic levels of inflammatory (CRP, IL-8, and TNF-α), but it was associated with the high expression of angiotensin in vivo. These findings suggest that the job of train driving may not be associated with significant alterations in systemic immune condition, but arouse the level of angiotensin.

Xuebijing alters tumor necrosis factor-alpha, interleukin-1beta and p38 mitogen activated protein kinase content in a rat model of cardiac arrest following cardiopulmonary resuscitation

We established a rat model of cardiac arrest by clamping the endotracheal tube of adult rats at expiration. Twenty-four hours after cardiopulmonary resuscitation, nerve cell injury and expression of tumor necrosis factor-α, interleukin-1β, and p38 mitogen activated protein kinase content were increased. Rats injected with Xuebijing, a Chinese herb compound preparation, exhibited normal cellular structure and morphology, dense neuronal cytoplasm, and decreased tumor necrosis factor-α, interleukin-1β, and p38 mitogen activated protein kinase expression at 24 hours following cardiopulmonary resuscitation. These data suggest that Xuebijing can attenuate neuronal injury induced by hypoxia and reperfusion during cardiopulmonary resuscitation.

Helicobacter pylori tumor necrosis factor-α inducing protein promotes cytokine expression via nuclear factor-κB

AIM:To study the effects of Helicobacter pylori(H. pylori)tumor necrosis factor-α(TNF)inducing protein (Tip-α)on cytokine expression and its mechanism. METHODS:We cloned Tip-αfrom the H.pylori strain 26695,transformed Escherichia coli with an expression plasmid,and then confirmed the expression product by Western blotting.Using different concentrations of Tip-αthat affected SGC7901 and GES-1 cells at different times,we assessed cytokine levels using enzyme-linked immunosorbent assay.We blocked SGC7901 cells with pyrrolidine dithiocarbamate(PDTC),a specific inhibitor of nuclear factorκB(NF-κB).We then detected interleukin(IL)-1βand TNF-αlevels in SGC7901 cells. RESULTS:Western blot analysis using an anti-Tip-α antibody revealed a 23-kDa protein,which indicated that recombinant Tip-αprotein was recombined successfully.The levels of IL-1β,IL-8 and TNF-αwere sig-nificantly higher following Tip-αinterference,whether GES-1 cells or SGC-7901 cells were used(P<0.05).However,the levels of cytokines(including IL-1β,IL-8 and TNF-α)secreted by SGC-7901 cells were greater than those secreted by GES-1 cells following treatment with Tip-αat the same concentration and for the same duration(P<0.05).After blocking NF-κB with PDTC, the cells(GES-1 cells and SGC-7901 cells)underwent interference with Tip-α.We found that IL-1βand TNF-αlevels were significantly decreased compared to cells that only underwent Tip-αinterference(P<0.05). CONCLUSION:Tip-αplays an important role in cyto-kine expression through NF-κB.

IL-10 and TNF-α promoter haplotypes are associated with childhood Crohn’s disease location

AIM： To determine the distribution and frequencies of the genotypes and haplotypes of the genes encoding for the glucocorticoid receptor （GR）, the tumor necrosis factor （TNF）-α and the interleukin （IL）-10 in childhood Crohn＇s disease （CD） and to assess the impact of the corresponding DNA variants on clinical and disease phenotypes.METHODS： Ten variants in GR, TNF-a and IL-10 were genotyped in 113 childhood CD cases and 95 healthy subjects, both of French-Canadian origin.RESULTS： For the GR polymorphisms （R23K and N363S） and IL-10 variants in the 5＇flanking region （-1082 G 〉 A, -819 T 〉 C and -592 A 〉 C）, no difference was observed in allele and genotype frequencies between CD patients and controls. At the haplotype level, we found three IL-10 haplotypes previously described in Caucasians （GCC, ACC and ATA） and three novel haplotypes only present in IBD patients. When we analyzed the haplotype distribution with the anatomical location of the disease, the GCC haplotype was associated with the colonic and the ACC haplotype with the terminal ileum location, respectively. The genotyping of five polymorphisms in the promoter region of the TNF-α gene （-1031 T 〉 C, -863 A 〉 C, -857 T 〉 C, -308 A 〉 G and -238 A 〉 G） revealed a significant overrepresentation of homozygous -1031 CC among CD patients （OR = 9.9） and an association with the colonic location. For TNF-α, eleven haplotypes were inferred, including two frequent ones, TCCGG and CACGG, which were significantly observed more frequently in controls and cases, respectively.CONCLUSION： This is one of the first studies investigating the association between haplotype structure and disease location in a CD pediatric cohort. Our results will help to increase our understanding of the genetic determinants of childhood CD.

“Three Methods and Three Points” regulates p38 mitogen-activated protein kinase in the dorsal horn of the spinal cord in a rat model of sciatic nerve injury

Tuina is a traditional Chinese treatment for sensory disturbances caused by peripheral nerve injury and related diseases. Our previous studies showed that tuina regulates relevant regions and indices of the spinal dorsal horn using the Dian, Bo, and Rou method in Yinmen（BL37）, Yanglingquan（GB34）, and Weizhong（BL40）. Treatment prevents muscle atrophy, protects spinal cord neurons, and promotes sciatic nerve repair. The mechanisms of action of tuina for treating peripheral nerve injury remain poorly understood. This study established rat models of sciatic nerve injury using the crushing method. Rats received Chinese tuina in accordance with the principle of ＂Three Methods and Three Points,＂ once daily for 20 days. Tuina intervention reduced paw withdrawal latency and improved wet weight of the gastrocnemius muscle, as well as promoting morphological recovery of sciatic nerve fibers, Schwann cells, and axons. The protein expression levels of phospho-p38 mitogen-activated protein kinase, tumor necrosis factor-α, and interleukin-1β also decreased. These findings indicate that ＂Three Methods and Three Points＂ promoted morphological recovery and improved behavior of rats with peripheral nerve injury.

Silencing the gene encoding C/EBP homologous protein lessens acute brain injury following ischemia/reperfusion

C/EBP homologous protein, an important transcription factor during endoplasmic reticulum stress, participates in cell apoptosis mediated by endoplasmic reticulum stress. Previous studies have shown that C/EBP homologous protein mediates nerve injury during Alzheimer＇s disease, subarachnoid hemorrhage and spinal cord trauma. In this study, we introduced C/EBP homologous protein short hairpin RNA into the brains of ischemia/reperfusion rat models via injection of lentiviral vector through the left lateral ventricle. Silencing C/EBP homologous protein gene expression significantly reduced cerebral infarction volume, decreased water content and tumor necrosis factor-α and interleukin-1β mRNA expression in brain tissues following infarction, diminished the number of TUNEL-positive cells in the infarct region, decreased caspase-3 protein content and increased Bcl-2 protein content. These results suggest that silencing C/EBP homologous protein lessens cell apoptosis and inflammatory reactions, thereby protecting nerves.

Effects of insulin aspart and metformin on gestational diabetes mellitus and inflammatory markers

BACKGROUND Gestational diabetes mellitus(GDM)refers to hyperglycemia caused by insulin resistance or insufficient insulin secretion during pregnancy.Patients with GDM have a high risk of pregnancy complications,which can adversely affect both maternal and fetal health.Therefore,early diagnosis,treatment and monitoring of GDM are essential.In recent years,a new treatment scheme represented by insulin aspart combined with metformin has received increasing attention.AIM To explore the effects of insulin aspart combined with metformin on patients with GDM and inflammatory markers.METHODS From April 2020 to September 2022,124 patients with GDM in Sanya Women and Children’s Hospital Managed by Shanghai Children’s Medical Center were collected and analyzed retrospectively.The control group(CG)comprised 62 patients treated with insulin aspart alone,and 62 patients treated with insulin aspart and metformin formed the observation group(OG).Before and after treatment,improvement of blood-glucose-related indexes[fasting blood glucose(FBG),2-h postprandial glucose(2h PG)and hemoglobin A1c(HbA1c)],serum related factor[serum homocysteine(Hcy)],serum inflammatory cytokines[tumor necrosis factor(TNF)-α,interleukin(IL)-6 and C-reactive protein(CRP)]were compared between the two groups.The clinical efficacy,adverse pregnancy outcomes and incidence of pregnancy complications were compared between the two groups.RESULTS After treatment,the levels of FBG,2h PG,HbA1c,Hcy,TNF-α,IL-6 and CRP in both groups were significantly decreased(P<0.05),and the levels of FBG,2h PG,HbA1c,Hcy,TNF-α,IL-6 and CRP in the OG were lower than in the CG(P<0.05).The total clinical effectiveness in the OG was higher than that in the CG(P<0.05).The total incidence of adverse pregnancy outcomes and complications in the OG was significantly lower than in the CG(P<0.05).CONCLUSION Insulin aspart combined with metformin are effective for treatment of GDM,which can reduce blood-glucoserelated indexes,Hcy and serum inflammatory cytokines,and risk of adverse pregnancy outcomes and complications.

慢性阻塞性肺疾病急性加重期血清瘦素与肺功能关系的临床研究

目的：探讨血清瘦素（ leptin ）与慢性阻塞性肺疾病（ chronic obstructive pulmonary disease， COPD）急性加重期患者肺功能的关系。方法选择COPD急性加重期患者35例、COPD稳定期患者38例及健康志愿者30例，抽取空腹血。用放免法测定血清瘦素、用酶联免疫吸附法（ELISA）测定肿瘤坏死因子-α（TNF-α）及用全自动生化仪检测C-反应蛋白（CRP）；检测肺功能，记录1 s用力呼气量（ FEVl ）、最大通气量（ MVV）、肺一氧化碳弥散量（ DLCO ）等指标、分析COPD急性加重期患者血清瘦素水平与TNF-α、CRP、肺功能等的相关性。结果①COPD急性加重期患者血清瘦素、TNF-α、CRP均明显高于COPD稳定期组和对照组，而FEVl、MVV、DLCO则明显低于后者；②COPD急性加重期患者血清瘦素与TNF-α、CRP呈正相关，与FEVl、MVV、DLCO呈负相关。结论血清瘦素可判断COPD急性加重期预后，可以评估肺功能损害风险。

Adaptive and regulatory mechanisms in aged rats with postoperative cognitive dysfunction

Inflammation may play a role in postoperative cognitive dysfunction. 5＇ Adenosine monophos- phate-activated protein kinase, nuclear factor-kappa B, interleukin-1β, and tumor necrosis factor-a are involved in inflammation. Therefore, these inflammatory mediators may be involved in postoperative cognitive dysfunction. Western immunoblot analysis revealed 5＇ adenosine mo- nophosphate-activated protein kinase and nuclear factor-kappa B in the hippocampus of aged rats were increased 1-7 days after splenectomy. Moreover, interleukin-1β and tumor necrosis fac- tor-α were upregulated and gradually decreased. Therefore, these inflammatory mediators may participate in the splenectomy model of postoperative cognitive dysfunction in aged rats.

Cinnamon extract suppresses experimental colitis through modulation of antigen-presenting cells

AIM:To investigate the anti-inflammatory effects of cinnamon extract and elucidate its mechanisms for targeting the function of antigen presenting cells.METHODS:Cinnamon extract was used to treat murine macrophage cell line(Raw 264.7),mouse primary antigen-presenting cells(APCs,MHCII+) and CD11c+dendritic cells to analyze the effects of cinnamon extract on APC function.The mechanisms of action of cinnamon extract on APCs were investigated by analyzing cytokine production,and expression of MHC antigens and co-stimulatory molecules by quantitative real-time PCR and flow cytometry.In addition,the effect of cinnamon extract on antigen presentation capacity and APC-dependent T-cell differentiation were analyzed by [H3]-thymidine incorporation and cytokine analysis,respectively.To confirm the anti-inflammatory effects of cinnamon extract in vivo,cinnamon or PBS was orally administered to mice for 20 d followed by induction of experimental colitis with 2,4,6 trinitrobenzenesulfonic acid.The protective effects of cinnamon extract against experimental colitis were measured by checking clinical symptoms,histological analysis and cytokine expression prof iles in inflamed tissue.RESULTS:Treatment with cinnamon extract inhibited maturation of MHCII+ APCs or CD11c+ dendritic cells(DCs) by suppressing expression of co-stimulatory molecules(B7.1,B7.2,ICOS-L),MHCII and cyclooxygenase(COX)-2.Cinnamon extract induced regulatory DCs(rDCs) that produce low levels of pro-inflammatory cytokines [interleukin(IL)-1β,IL-6,IL-12,interferon(IFN)-γ and tumor necrosis factor(TNF)-α] while expressing high levels of immunoregulatory cytokines(IL-10 and transforming growth factor-β).In addition,rDCs generated by cinnamon extract inhibited APC-dependent T-cell proliferation,and converted CD4+ T cells into IL-10high CD4+ T cells.Furthermore,oral administration of cinnamon extract inhibited development and progression of intestinal colitis by inhibiting expression of COX-2 and pro-inflammatory cytokines(IL-1β,IFN-γ and TNF-α),while enhancing IL-10 levels.CONCLUSION:Our study suggests the potential of cinnamon extract as an anti-inflammatory agent by targeting the generation of regulatory APCs and IL-10+ regulatory T cells.

Markers of systemic inflammation and colorectal adenoma risk: Meta-analysis of observational studies

To perform a meta-analysis of observational studies on inflammatory markers levels and occurrence of colorectal adenoma.METHODSPubMed and EMBASE databases were searched until March 2016 for the articles reporting on the circulating levels of inflammatory markers, including: C-reactive protein (CRP), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-α) and risk of colorectal adenoma. Random-effects models were used to calculate summary odds ratios (ORs) with 95%CIs for the highest vs lowest category of exposure. Heterogeneity was assessed by using the Q test and I2 statistic. Subgroup analyses were also performed to test for potential source of heterogeneity.RESULTSA total of 14 case-control studies were included. Ten studies on CRP including a total of 3350 cases and 4168 controls showed non-significant summary (OR = 1.23, 95%CI: 0.98-1.54; I2 = 54%, Pheterogeneity = 0.01) in the general analysis, but significant increased odds when considering only advanced adenoma (OR = 1.59, 95%CI: 1.09-2.32; I2 = 44%, Pheterogeneity = 0.15). Subgroup and stratified analyses revealed a potential influence of smoking status and aspirin use on the association between CRP levels and colorectal adenoma. Five studies examined the association between circulating levels of TNF-α and colorectal adenoma risk, including a total of 1,568 cases and 2,832 controls. The summary OR for the highest vs the lowest category of exposure was 1.00 (95%CI: 0.77-1.29). The relationship between circulating IL-6 levels and colorectal adenoma risk was investigated in 7 studies including a total of 1936 cases and 3611 controls. The summary OR for the highest vs the lowest category of exposure was 1.19 (95%CI: 0.92-1.55).CONCLUSIONSummary of current evidence suggests a positive association of CRP levels and advanced colorectal adenoma risk. The role of potential confounding factors should be further evaluated.

Impacts of Mild Hypothermia on LPS-Mediated TLR4/NF-κB Signaling Pathway in Microglia

Background: Existing studies have found that some inflammatory factors cause brain cell damage through the TLR4/NF-κB pathway, and that mild hypothermia has a protective effect on nerve cells. It is not clear whether the mild hypothermic brain protection is achieved through the TLR4/NF-κB pathway in microglia. Objective: To investigate the impacts of mild hypothermia on lipopolysaccharide (LPS)-mediated TLR4/NF-κB signaling pathway in microglia. Method: The cultured microglia cells in vitro were divided into the NS group and the LPS group at 33?C and 37?C, respectively;quantitative RT-PCR was performed to detect the expressions of TLR4 and NF-κB mRNA in the microglia, Western blot was used to detect the expressions of TLR4 and NF-κB protein in the microglia, and ELISA was performed to detect the levels of tumor necrosis factor α (TNF-α) and interleukin-10 (IL-10) in the culture medium. Results: Under the LPS stimulation, the mRNA and protein expressions of TLR4 and NF-κB at different time points had significant changes between the normothermia group and the mild hypothermia group, in which the expressions in the former group were firstly increased and then decreased, while those in the latter showed a continuous increasing trend (P < 0.01);and the expressions of TNF-α in all the groups presented the trend of first-increasing then-decreasing, while IL-10 exhibited one slow linear increasing trend (P Conclusions: Mild hypothermia could inhibit the mRNA and protein expressions of LPS-mediated TLR4/NF-κB signaling pathway in the microglia, and inhibit the production and release of downstream inflammatory cytokines (TNF-α and IL-10).

Visfatin levels in patients with severe pneumonia

BACKGROUND： As a cytokine highly expressed in internal organs, visfatin could be used as a biomarker of systemic inflammation response for chronic obstructive pulmonary diseases, but few studies have reported the use of visfatin in severe pneumonia. The present study was undertaken to determine the plasma levels of visfatin in patients with severe pneumonia. METHODS：A total of 70 patients, including 40 patients with severe pneumonia （group A） and 30 patients with non severe pneumonia （group B） who had been admitted to the ICU from June 2009 to June 2010, were enrolled in this prospective study. And another 30 healthy physical examinees served as healthy controls （group C）. Patients were excluded if they suffered from severe diseases of the heart, brain and kidney, cancers, autoimmune diseases, or received special treatment in the latest month. The plasma levels of visfatin, IL-6, IL-8 and TNF-α were measured by ELISA, while the level of CRP was determined by immuneturbidimetry, and the routine blood test was performed. Blood gas analysis and Acute Physiology and Chronic Health Evaluation II （APACHE II） were performed in patients with pneumonia. Comparisons between the groups were conducted by Student＇s t test, ANOVA or nonparametric test. Correlation analysis was carried out by Pearson＇s correlation test or Spearman＇s rank-order correlation test. RESULTS：The plasma level of visfatin in group A was significantly higher than that in groups B and C （P〈0.001）, and the level of visfatin in group B was significantly higher than that in group C （P〈0.001）. The plasma level of visfatin was positively correlated with CRP, TNF-α, APACHE II and PMN% in patients with severe pneumonia （rho=0.653, r=0.554, r=0.558, r=0.484, respectively, P〈0.05 for all）, while it was negatively correlated with PaO2 and PaO2/FiO2 （rho=-0.422, r=-0.543, respectively, P〈0.05 for all）. CONCLUSION：Visfatin may be involved in the systematic inflammation response in patients with severe pneumonia as a pro-inflammatory cytokine, and it is valuable in assessing the severity of pneumonia..

Immunopathogenesis of reactive arthritis:Role of the cytokines

Reactive arthritis （ReA）, also known as sterile postin-fectious arthritis, belongs to the group of related ar-thropathies known as spondyloarthritis （SpA）. ReA can arise 1-4 wk after a gastrointestinal or genitourinary infection, but once arthritis develops, the microorgan-ism is not found in the joint. The classical microbes as-sociated with ReA development include Gram-negative aerobic or microaerophilic bacteria containing LPS in their outer membrane. The immunopathogenic mechanisms involved in ReA development are still unknown. A hypothesis suggested that the bacteria probably persist outside the joint, at sites such as gut mucosa or lymph nodes, and bacterial antigens might then be transported to the joints. On the other hand, an altered immune response and the unbalanced production of cy-tokines have been reported in subjects with ReA. Currently, there is increased evidence to suggest that both mechanisms would operate in the immunopathogenesis of ReA. In this review we highlight recent advances on the role of cytokines in the ReA. Particularly, we discuss the roles of some pro- and anti-infammatory cytokines involved in the immunopathogenesis of ReA.

Effects of electroacupuncture at lower he-sea points on interleukin-1β and high mobility group box 1 in model rats with ulcerative colitis

Objective To comparatively observe the effect of electroacupuncture at digestive system-related lower he-sea points on the expressions of serum interleukin-1β（IL-1 β）, tumor necrosis factor-α（TNF-α） of colon tissues and high mobility group box 1 protein（HMGB 1） of ulcerative colitis（UC） model rats, and to explore whether there is relative specificity of electroacupuncture at Shàngjùxū（上巨虚 ST 37）, one of lower he-sea points of large intestine, in treatment of bowel diseases. Method A total of 60 SD rats were randomly divided into control group, model group, ST 37 group, Zúsānl？（足三里 ST 36） group, Xiàjùxū（下巨虚 ST 39） group and Yánglíngquán（阳陵泉 GB 34） group. There were ten rats in each group; five were males, and five were females. UC models were established by clysis with 2, 4, 6-trinitrobenzene sulfonic acid/alcohol solution. After modeling, treatment was conducted for ten days, specimens were collected, colonic ulcers and inflammation were inspected visually and scored. The content of serum IL-1β and the expressions of TNF-α and HMGB 1 in colon were detected through ELISA. Results 1 Compared with control group, the scores of colonic ulcers and inflammation, the content of serum IL-1β and the expressions of TNF-α（except ST 37 group） and HMGB 1 were all higher（P〈0.05, P〈0.01）; 2 compared with model group, the scores of colonic ulcers in ST 36 group and ST 37 group were lower obviously（P〈0.05, P〈0.01）; the expressions of IL-1β, TNF-α and HMGB 1 in the four treatment groups were lower obviously（P〈0.01）; 3 compared with ST 37 group, the expressions of IL-1β, TNF-α and HMGB 1 in other three treatment groups were higher obviously（P〈0.05, P〈0.01）; and the scores of colonic ulcers in ST 39 group and GB 34 group were higher obviously（P〈0.05）. Conclusion 1 The score of colonic ulcers can be reduced through electroacupuncture at ST 37, ST 36, ST 39 and GB 34, which can also reduce the content of serum IL-1β and the expressions of TNF-α and HMGB 1, and effectively inhibit inflammatory response of colon caused by UC; 2 the effect trend of the four acupoints in treatment of UC is： ST 37ST 36ST 39GB 34, and electroacupuncture at ST 37 has the best effect with relative specificity.

EFFECT OF ASPIRIN PLUS CLOPIDOGREL ON INFLAMMATORY MARKERS IN PATIENTS WITH NON-ST-SEGMENT ELEVATION ACUTE CORONARY SYNDROME

Background Aspirin can inhibit inflammatory reactions and platelet aggregation, but little is known about the effects of the combination of aspirin plus clopidogrel, a new antiplatelet agent, on inflammation. The purpose of this study was to determine whether aspirin plus clopidogrel can further suppress inflammation in patients with non-ST-segment elevation acute coronary syndrome （NSTEACS）. Methods One hundred and fifteen patients with NSTEACS were randomized into two groups： group A （aspirin alone, n=58） and group B （aspirin plus clopidogrel, n=57）. Patients in group A received a loading dose of 300 mg aspirin, then 100 mg per day. The patients in group B received a loading dose of 300 mg aspirin and 300 mg clopidogrel, then 100 mg aspirin and 75 mg clopidogrel per day. Serum high sensitivity C-reactive protein （hs-CRP） and tumor necrosis factor-α （TNF-α ） were measured in all patients at baseline prior to any drug treatment after admission, and at 7 and 30 days after beginning drug treatment. Thirty healthy volunteers on no medications were enrolled as controls （group C）. Results Baseline levels of hs-CRP and TNF-α in group A and group B were significantly higher than those in group C. Seven days after administration, the levels of hs-CRP in both group A and group B decreased significantly [Group A： （6.15 ± 1.39） mg/L vs （9.18 ± 1.62） rag/L, P 〈0.01; Group B：（4.99 ± 1.62） mg/L vs （10.29 ± 1.47） rag/L, P〈0.01]. Similarly, levels of TNF-α in both groups decreased at 7 days compared to baseline [Group A： （90.99 ± 28.91） pg/ml vs （117.20 ± 37.13） pg/ml, P 〈0.01; Group B： （74.32± 21.83） pg/ml vs （115.27 ± 32.11） pg/ml, P 〈0.01]. Thirty days after administration, the levels of hs-CRP in both group A and group B decreased further to （3.49 ± 1.53） rag/L, and （2.40 ± 1.17） mg/L respectively （P 〈0.01 for both comparisons）. Levels of TNF-α in groups A and B also decreased significantly between 7 and 30 days, to 63.28 ± 29.01 pg/ml （group A） and （43.95 ± 17.10） pg/ml （group B; P 〈0.01 for both comparisons）. Significantly lower levels of hs-CRP and TNF-α were observed in group B compared to Group A at thirty days after initiating drug treatment （P 〈0.05）. Conclusions Aspirin plus clopidogrel treatment reduced levels of serum hs-CRP and TNF-α in patients with NSTEACS significantly more than aspirin alone. Because both aspirin and clopidogrel produce important anti-inflammatory effects, these results suggest the possibility that long-term treatment with aspirin plus clopidogrel may produce greater clinical benefits compared to treatment with aspirin alone.

Effect of moxibustion plus Duhuo Jisheng decoction on hs-CRP,IL-1β and TNF-α levels in middle-aged and elderly patients with knee osteoarthritis

Objective： To observe the clinical effect of moxibustion combined with Duhuo Jisheng decoction for middle-aged and elderly patients with knee osteoarthritis（KOA） and its impact on serum high sensitive C-reactive protein（hs-CRP）,interleukin-1β（IL-1β） and tumor necrosis factor-α（TNF-α） levels.Methods： A total of 90 eligible KOA patients were randomized into an observation group（n=45） and a control group（n=45）.Cases in the observation group received moxibustion plus oral administration Duhuo Jisheng decoction, while cases in the control group received Duhuo Jisheng decoction. Then the hs-CRP, IL-1β and TNF-α levels were examined and the clinical effect was evaluated.Results： Before treatment, the hs-CRP, IL-1β and TNF-α levels showed no between-group statistical differences（all P〉0.05）. After 8 weeks of treatment, the hs-CRP, IL-1β and TNF-α levels all dropped significantly in both groups（P〈0.01 or P〈0.05）, and the treatment group showed more substantial changes than the control group（all P〈0.05）. The total effective rate was 97.8% in the treatment group, versus 86.7% in the control group, showing a statistical difference（P〈0.05）.Conclusion： Moxibustion plus Duhuo Jisheng decoction has a good clinical effect for middle-aged and elderly KOA patients,and the effect may relate to the decreased hs-CRP, IL-1β and TNF-α levels.