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Effect of Jiawei Shenfu decoction on tumor necrosis factor-alpha and nuclear factor-kappa B in patients who have chronic heart failure with syndromes of deficiency of heart Yang
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作者 Yu Mei Guo Hangyuan +3 位作者 Ye Lingling Bian Jiaping Ma Lijuan Zheng Chunli 《中医杂志:英文版》 SCIE CAS CSCD 2019年第3期418-424,共7页
OBJECTIVE:To examine the clinical efficacy of Jiawei Shenfu decoction on tumor necrosis factor-alpha (TNF-cα) and nuclear factor-kappa B (NF-KB) levels in patients who have chronic heart failure with syndromes of def... OBJECTIVE:To examine the clinical efficacy of Jiawei Shenfu decoction on tumor necrosis factor-alpha (TNF-cα) and nuclear factor-kappa B (NF-KB) levels in patients who have chronic heart failure with syndromes of deficiency of heart Yang.METHODS:A total of 63 patients with syndromes of deficiency of heart Yang (chronic heart failure)were enrolled.Patients were randomly divided into the control group and Jiawei Shenfu group.All patients received standard medications for treatment of chronic heart failure.Patients in the Jiawei Shenfu group were additionally provided Jiawei Shenfu decoction one dose daily.Treatments continued for 4 consecutive weeks.The primary endpoint was the change in plasma B-type natriuretic peptide (BNP),NF-KB,and TNF-cα levels during 4 weeks of treatment.RESULTS:At the 4-week follow-up,a significant reduction in BNP levels compared with baseline was observed in both groups,but the Jiawei Shenfu decoction group showed a significantly greater reduction than did the control group.The Jiawei Shenfu group also showed superior performance regarding the Minnesota Living with Heart Failure Questionnaire score,the Chinese medicine syndrome score,heart rate,left ventricular ejection fraction,and 6-min walking distance compared with the control group.The degree of changes in NF-KB and TNF-α levels in the Jiawei Shenfu group was more significant than that in the control group.CONCLUSION:Routine medicine combined with Jiawei Shenfu decoction for patients with heart Yang deficiency syndrome in chronic heart failure can improve the left ventricular ejection fraction and cardiac function,and reduce BNP levels.The mechanism may be related to inhibition of pro-inflammatory cytokines and the NF-KB-induced kinase pathway,leading to amelioration of the inflammatory response. 展开更多
关键词 HEART failure NATRIURETIC peptide brain Tumor necrosis FACTOR-ALPHA NF-KAPPA B Heart-Yang DEFICIENCY Jiawei SHENFU decoction
Effects of etanercept on the apoptosis of ganglion cells and expression of Fas, TNF-α, caspase-8 in the retina of diabetic rats
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作者 Qin Ye Yu-Ni Lin +5 位作者 Mao-Song Xie Yi-Hua Yao Shu-Min Tang Yan Huang Xiao-Hui Wang Yi-Hua Zhu 《国际眼科杂志:英文版》 SCIE CAS 2019年第7期1083-1088,共6页
AIM: To evaluate the effects of etanercept on the expression of Fas, tumor necrosis factor-alpha(TNF-α) and caspase-8 in the early stage of the apoptotic pathway in diabetic rats, and to explore the therapeutic effec... AIM: To evaluate the effects of etanercept on the expression of Fas, tumor necrosis factor-alpha(TNF-α) and caspase-8 in the early stage of the apoptotic pathway in diabetic rats, and to explore the therapeutic effect of etanercept on diabetic retinopathy.METHODS: A total of 60 Sprague-Dawley(SD) rats were randomly and evenly divided into 3 groups with 20 rats each, including control group, and diabetic groups with or without treatment. Streptozotocin(STZ)-induced diabetic rats were established for diabetic groups. Blood glucose and body weight were measured weekly. All the rats were sacrificed at the 12 wk after treatment. The expressions of Fas, TNF-α and caspase-8 in rat retina were quantitatively detected by PCR and Western blot. The leakage of Evan blue was adopted to measure the retinal vascular leakage quantitatively, and to compare it among different groups. TUNEL method was used to compare the amount of apoptotic bodies quantitatively in rat retina ganglion cells under electron microscope.RESULTS: The expressions of Fas, TNF-α and caspase-8 in each group were compared via PCR and Western blot, in which the diabetic group with treatment was lower than those without treatment(P<0.01), but all the diabetic groups were higher than the control group(P<0.01). Evans blue leakage in the diabetic treatment group was lower than those without treatment(P<0.01), but those in the control group was the lowest compared with the other two groups(P<0.01). TUNEL method showed that the apoptoticbodies of retina in the diabetic treatment group was lower than those without treatment(P<0.01), while those in the control group was the lowest compared with the other two groups(P<0.01). CONCLUSION: Etanercept can effectively reduce the expression of Fas, TNF-α and caspase-8, as well as the retinal leakage and retinal cell apoptosis in diabetic rats. 展开更多
关键词 ETANERCEPT GANGLION cells FAS tumor necrosis FACTOR-ALPHA CASPASE-8 APOPTOSIS diabetes rat
Three Tiaobu Feishen therapies protect human alveolar epithelial cells against cigarette smoking and tumor necrosis factor-α-induced inflamation by nuclear factor-kappa B pathway
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作者 Chen Yulong Wu Yaosong +8 位作者 Li Jiansheng Feng Suxiang Hao Lili Liu Xuefang Zheng Wanchun Dong Haoran Qin Yanqin Yin Sugai Zhao Peng 《中医杂志:英文版》 SCIE CAS CSCD 2019年第1期45-49,共5页
OBJECTIVE: To investigate the efficacy of Tiaobu Feishen formulae(TBFS), including Bufei Jianpi formula(BJF), Bufei Yishen formula(BYF), and Yiqi Zishen formula(YZF), on inflammatory response, protease-anti-protease i... OBJECTIVE: To investigate the efficacy of Tiaobu Feishen formulae(TBFS), including Bufei Jianpi formula(BJF), Bufei Yishen formula(BYF), and Yiqi Zishen formula(YZF), on inflammatory response, protease-anti-protease imbalance and collagen deposition in rats.METHODS: In present work, we used an in vitro model of cigarette smoking extract(CSE)-and tumor necrosis factor-α(TNF-α)-induced A549 cellsto examine the efficacy of BJF, BYF and YZF on the production of inflammatory cytokines, including TNF-α and interleukin(IL)-8, IL-6, matrix metalloproteinases(MMP)-9, and IL-10 in CSE or TNF-ls. And their related transcripα-induced A549 celtion factors and signaling pathway were also analyzed.RESULTS: The results showed that BJF, BYF and YZF could significantly decrease the expression levels of the pro-inflammatory cytokines induced by CSE or TNF-α. Furthermore, BJF, BYF and YZF could suppress CSE-or TNF-α-induced activation of nuclear factor-kappa B(NF-κB) transcription factors and its corresponding pathways. Taken together, these data implied that BJF, BYF and YZF effectively inhibited CSE-or TNF-α-induced inflammatory response in alveolar epithelial cell, which was due to their inhibition effect on NF-κB pathways.CONCLUSION: Our findings suggest that the Tiaobu Feishen therapies may protect human alveolar epithelial cells against cigarette smoking and TNF-α-induced inflammation. NF-κB pathway may involve in the actions. 展开更多
关键词 Chinese medical formula CIGARETTE SMOKING Tumor NECROSIS FACTOR-ALPHA A549 cells
Systematic review and meta-analysis on the association of tuberculosis in Crohn’s disease patients treated with tumor necrosis factor-αinhibitors(Anti-TNFα) 预览
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作者 Brent L Cao Ahmad Qasem +2 位作者 Robert C Sharp Latifa S Abdelli Saleh A Naser 《世界胃肠病学杂志:英文版》 SCIE CAS 2018年第25期2764-2775,共12页
AIM To perform a meta-analysis on the risk of developing Mycobacterium tuberculosis(TB)infection in Crohn’s disease(CD)patients treated with tumor necrosis factoralpha(TNFα)inhibitors.METHODS A meta-analysis of rand... AIM To perform a meta-analysis on the risk of developing Mycobacterium tuberculosis(TB)infection in Crohn’s disease(CD)patients treated with tumor necrosis factoralpha(TNFα)inhibitors.METHODS A meta-analysis of randomized,double-blind,placebocontrolled trials of TNFαinhibitors for treatment of CD in adults was conducted.Arcsine transformation of TB incidence was performed to estimate risk difference.A novel epidemiologically-based correction(EBC)enabling inclusions of studies reporting no TB infection cases in placebo and treatment groups was developed to estimate relative odds.RESULTS Twenty-three clinical trial studies were identified,including 5669 patients.Six TB infection cases were reported across 5 studies,all from patients receiving TNFαinhibitors.Eighteen studies reported no TB infection cases in placebo and TNFαinhibitor treatment arms.TB infection risk was significantly increased among patients receiving TNFαinhibitors,with a risk difference of 0.028(95%CI:0.0011-0.055).The odds ratio was 4.85(95%CI:1.02-22.99)with EBC and 5.85(95%CI:1.13-30.38)without EBC.CONCLUSION The risk of TB infection is higher among CD patients receiving TNFαinhibitors.Understanding the immunopathogenesis of CD is crucial,since using TNFαinhibitors in these patients could favor mycobacterial infections,particularly Mycobacterium avium subspecies paratuberculosis,which ultimately could worsen their clinical condition. 展开更多
关键词 TUBERCULOSIS Tumor NECROSIS FACTOR-ALPHA INHIBITORS Crohn’s Disease META-ANALYSIS Systematic review
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Role of inflammatory response in liver diseases:Therapeutic strategies 预览
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作者 JoséA Del Campo Paloma Gallego Lourdes Grande 《世界肝病学杂志:英文版(电子版)》 2018年第1期1-7,共7页
Inflammation and tumorigenesis are tightly linked pathways impacting cancer development.Inflammasomes are key signalling platforms that detect pathogenic microorganisms,including hepatitis C virus(HCV)infection,and st... Inflammation and tumorigenesis are tightly linked pathways impacting cancer development.Inflammasomes are key signalling platforms that detect pathogenic microorganisms,including hepatitis C virus(HCV)infection,and sterile stressors(oxidative stress,insulin resistance,lipotoxicity)able to activate pro-inflammatory cytokines interleukin-1βand IL-18.Most of the inflammasome complexes that have been described to date contain a NOD-like receptor sensor molecule.Redox state and autophagy can regulate inflammasome complex and,depending on the conditions,can be either pro-or antiapoptotic.Acute and chronic liver diseases are cytokinedriven diseases as several proinflammatory cytokines(IL-1α,IL-1β,tumor necrosis factor-alpha,and IL-6)are critically involved in inflammation,steatosis,fibrosis,and cancer development.NLRP3 inflammasome gain of function aggravates liver disease,resulting in severe liver fibrosis and highlighting this pathway in the pathogenesis of non-alcoholic fatty liver disease.the other hand,HCV infection is the primary catalyst for progressive liver disease and development of liver cancer.It is well established that HCV-induced IL-1βproduction by hepatic macrophages plays a critical and central process that promotes liver inflammation and disease.In this review,we aim to clarify the role of the inflammasome in the aggravation of liver disease,and how selective blockade of this main pathway may be a useful strategy to delay fibrosis progression in liver diseases. 展开更多
关键词 Caspase-1 Fibrosis Hepatitis C virus INFLAMMASOME INTERLEUKIN-1Α INTERLEUKIN-1Β LIVER DISEASE Non-alcoholic fatty LIVER DISEASE NLRP3 Tumor necrosis FACTOR-ALPHA
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Role of leptin in the progression of psoriatic,rheumatoid and osteoarthritis 预览
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作者 Jessica Mounessa Iryna Voloshyna +1 位作者 Amy D Glass Allison B Reiss 《世界风湿病学杂志》 2016年第1期9-15,共7页
Leptin,an adipokine responsible for body weight regulation,may be involved in pathological processes related to inflammation in joint disorders including rheumatoid arthritis(RA),osteoarthritis,and psoriatic arthritis... Leptin,an adipokine responsible for body weight regulation,may be involved in pathological processes related to inflammation in joint disorders including rheumatoid arthritis(RA),osteoarthritis,and psoriatic arthritis(PsA).These arthropathies have been associated with a wide range of systemic and inflammatory conditions including cardiovascular disease,obesity,and metabolic syndrome.As a potent mediator of immune responses,leptin has been found in some studies to play a role in these disorders.Furthermore,current potent biologic treatments effectively used in PsA including ustekinumab(an interleukin 12/23 blocker)and adalimumab(a tumor necrosis factor-alpha blocker also used in RA)have been found to increase leptin receptor expression in human macrophages.This literature review aims to further investigate the role leptin may play in the disease activity of these arthropathies. 展开更多
关键词 Psoriatic ARTHRITIS RHEUMATOID ARTHRITIS LEPTIN USTEKINUMAB Tumor necrosis FACTOR-ALPHA
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大骨节病、骨关节炎软骨细胞分泌IL-1β、TNF-α及透明质酸对其影响实验研究 预览 被引量:13
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作者 高宗强 郭雄 +3 位作者 陈君长 段琛 马玮娟 顾其胜 《陕西医学杂志》 CAS 2015年第7期774-778,共5页
目的:探讨在不同剂量透明质酸作用下,人大骨节病(KBD )软骨细胞和骨关节炎(O A )软骨细胞对IL‐1β、T N F‐α合成分泌的影响,为临床上透明质酸钠治疗O A及KBD提供实验依据。方法:将符合临床诊断标准的KBD及O A 患者与从遭遇... 目的:探讨在不同剂量透明质酸作用下,人大骨节病(KBD )软骨细胞和骨关节炎(O A )软骨细胞对IL‐1β、T N F‐α合成分泌的影响,为临床上透明质酸钠治疗O A及KBD提供实验依据。方法:将符合临床诊断标准的KBD及O A 患者与从遭遇意外事故的病人作为正常对照,分离、体外培养三组患者关节软骨细胞,分别给予100μg/ml(H100组)、500μg /ml(H500组)不同剂量的透明质酸钠(HA )干预及阴性对照(0.00μg /ml ,H0组),通过放免测定细胞培养上清液中IL‐1β、TNF‐α的含量变化。结果:与正常组比较,KBD和OA 组软骨细胞IL‐1β、TNF‐α明显增高;HA干预随其剂量增高抑制IL‐1β、TNF‐α合成增强,对TNF‐α的抑制有统计学意义。结论:骨关节炎和大骨节病患者软骨细胞合成分泌IL‐1β、T N F‐α明显增加;应用透明质酸后,可降低两种炎性因子的分泌。 展开更多
关键词 透明质酸 大骨节病 骨关节炎 软骨细胞 白细胞介素-1Β 肿瘤坏死因子-α
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Psoriasis:Biologic treatment and liver disease 预览
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作者 Eva Vilarrasa Luis Puig 《世界皮肤病学杂志》 2014年第4期76-85,共10页
Patients with moderate or severe psoriasis have a high prevalence of chronic liver disease.Chronic liver disease in these patients is related to metabolic syndrome,alcohol abuse or viral infections.Therefore,treatment... Patients with moderate or severe psoriasis have a high prevalence of chronic liver disease.Chronic liver disease in these patients is related to metabolic syndrome,alcohol abuse or viral infections.Therefore,treatment of these patients is challenging.Classic systemic treatments may be contraindicated because of their immunosuppressive and hepatotoxic potential.First-line therapy in this setting is generally ultraviolet B phototherapy combined with topical treatment,but its feasibility and efficacy are sometimes limited.The therapeutic options are further restricted by concomitant psoriatic arthritis.Biologic treatments have shown to be effective in psoriasis and psoriatic arthritis,and they are largely devoid of liver toxicity.Anti-tumor necrosis factor-alpha(TNF-α)treatments have proven to be effective and safe in patients with chronic hepatitis C virus(HCV)infections and other non-infectious chronic liver disorders,including alcoholic and non-alcoholic liver diseases.However,in chronic hepatitis B virus(HBV),anti-TNF-αtreatments carry a high risk of HBV reactivation.Anti-interleukin-12/23 treatments are also effective in patients with psoriasis,but data regarding their safety in chronic hepatitis infections are still limited.Safety reports in patients with psoriasis and chronic HCV infection are contradictory,and in chronic HBV evidence indicate a potential risk of viral reactivation.Moreover,concerns remain about the long-term safety of both TNF-αantagonists and ustekinumab.Non-viral liver diseases such as alcoholic and non-alcoholic liver diseases are more prevalent in patients with psoriasis than in the general population.TNF-αantagonists have also been prescribed in these patients.Although data are still scarce in this setting,results suggest a favorable profile in patients with psoriasis and non-alcoholic liver diseases.We review the literature regarding all these aspects. 展开更多
关键词 PSORIASIS LIVER DISEASE BIOLOGIC Antitumor necrosis factor-alpha Ustekinumab Chronic HEPATITIS C Chronic HEPATITIS B ALCOHOLIC LIVER DISEASE Non-alcoholic fatty LIVER DISEASE
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水通道蛋白1和肿瘤坏死因子α在变应性鼻炎黏膜中的表达 被引量:3
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作者 程波 邹祖圣 +3 位作者 陈世汉 刘国斌 李康 张志茂 《中国耳鼻咽喉头颈外科》 北大核心 2009年第8期461-462,共2页
常年变应性鼻炎(allergicrhinitis,AR)是临床的常见病和多发病,迄今为止,其腺体的过度分泌的发生机制仍无定论。水通道蛋白(aquaporin,AQP)是一组与水转运有关的细胞膜转运蛋白,参与水的分泌,吸收及细胞内外水的平衡。肿瘤坏... 常年变应性鼻炎(allergicrhinitis,AR)是临床的常见病和多发病,迄今为止,其腺体的过度分泌的发生机制仍无定论。水通道蛋白(aquaporin,AQP)是一组与水转运有关的细胞膜转运蛋白,参与水的分泌,吸收及细胞内外水的平衡。肿瘤坏死因子-α【(tumor necrosis factor-alpha,TNFα】)是由单核巨噬细胞产生的一种多肽,是细胞因子家族中最强效的炎症介质。目前,AQP和炎症介质TNF-α【在变应性疾病的腺体分泌及组织水肿的相关报道甚少,本实验检测两者在常年AR鼻黏膜组织中的表达及分布,初步探讨两者与该病临床病理特征之间的关系,以及AQP与TNF-α的相关性。 展开更多
关键词 鼻炎 变应性 常年性(Rhinitis Allergic Perennial) 水孔蛋白类(Aquaporins):肿瘤坏死因子α (Tumor Necrosis Factor-alpha)
子宫内膜异位症腹腔液中细胞因子的测定 预览 被引量:3
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作者 高虹 户瑞丽 王世进 《中国优生与遗传杂志》 2007年第2期 19-20,共2页
目的探讨腹腔液中细胞因子在子宫内膜异位症(内异症)发病中的作用。方法采用酶联免疫吸附试验检测37例内异症患者,19例非内异症患者(对照)腹腔液中白细胞介素6(IL-6)、白细胞介素8(IL-8)及肿瘤坏死因子α(TNFα)的含量,并对... 目的探讨腹腔液中细胞因子在子宫内膜异位症(内异症)发病中的作用。方法采用酶联免疫吸附试验检测37例内异症患者,19例非内异症患者(对照)腹腔液中白细胞介素6(IL-6)、白细胞介素8(IL-8)及肿瘤坏死因子α(TNFα)的含量,并对内异征患者腹腔液中细胞因子浓度与美国生育协会修正标准分期(R-AFS)进行相关性分析。结果内异征患者腹腔液中IL-6含量(2.0±0.4)明显高于对照组(1.1±0.5);Ⅲ、Ⅳ期异位征患者腹腔液中IL-8、TNFα含量明显高于对照组及Ⅰ、Ⅱ期。IL-6、IL-8及TNFα与R-AFS评分有显著相关性。结论内异征患者腹腔液中异常水平的IL-6、IL-8及TNFα是腹腔免疫动态环境失衡的部分原因。 展开更多
关键词 子宫内膜异位征 腹水液 白细胞介素-6 白细胞介素-8 转化生长因子a
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Interleukin-1 receptor antagonist intervenes in signaling between different types of synoviocytes in rats with adjuvant arthritis
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作者 Yong-qiu ZHENG Wei WEI +3 位作者 Min DAI Lei ZHU Xiao-yi JIA Yuan WANG 《中国药理学报:英文版》 SCIE CAS CSCD 2006年第1期111-118,共8页
瞄准:在辅助关节炎(AA ) 的治疗调查 interleukin-1 受体对手(IL-1ra ) 的机制。方法:AA 被治疗与 Freunds 完全的助手(农业信贷) 在老鼠导致。老鼠被给 IL-1ra 的 intracutaneous (2.5, 10, 40 mg/kg, 3 每天预定) 从 d 14 到 d ... 瞄准:在辅助关节炎(AA ) 的治疗调查 interleukin-1 受体对手(IL-1ra ) 的机制。方法:AA 被治疗与 Freunds 完全的助手(农业信贷) 在老鼠导致。老鼠被给 IL-1ra 的 intracutaneous (2.5, 10, 40 mg/kg, 3 每天预定) 从 d 14 到 d 21 在免疫以后。Synoviocyte 增长和 IL-1 的活动被使用 MTT 试金决定。肿瘤坏死因素高山哈(TNF-alpha ) 并且前列腺素 E (2 )(PGE (2 )) 集中被放射性免疫测定测量。synoviocytes 的超微结构被使用一台传播电子显微镜观察。c6 月 N 终端激酶(JNK ) 的磷酸化,细胞外的调整激酶(英皇家空军之阶级最低之兵) 和 p38 激酶被西方的污点分析检测。结果:IL-1ra (10 和 40 mg/kg, ic, d 14-21 ) 调制了第二等的炎性反应(P 【 0.01 ) , synoviocytes 的超微结构和激活 mitogen 的蛋白质在 AA 老鼠的激酶(MAPK ) 磷酸化。IL-1ra 的管理(10 和 40 mg/kg, ic, d 14-21 ) 在 AA,老鼠显著地减少了由像巨噬细胞的 synoviocytes (MLS ) 的 IL-1, PGE2 和 TNF-alpha 的生产(P 【 0.01 ) 。IL-1ra (2.5 mg/kg ) 也减少了 PGE2 的生产(P 【 0.01 ) 并且 TNF-alpha (P 【 0.05 ) 由在 AA 老鼠的 MLS。在 MLS 的上层清液在 AA 老鼠刺激的像成纤维细胞的 synoviocytes (FLS ) 的 MAPK 和房间增长的增加的磷酸化被 IL-1ra 也禁止(10 和 40 mg/kg, ic, d 14-21 ) 。结论:因为它调制 synoviocytes 的超微结构, IL-1ra 有反煽动性的效果,减少由 MLS 的支持 inflammatory 调停人的生产,并且在 FLS 禁止 MAPK 的磷酸化。 展开更多
关键词 关节炎 试验性 动物 房间增长 Dinoprostone Freund 的助手 INTERLEUKIN-1 男性 激活 Mitogen 的蛋白质激酶 Kinases 磷酸化 老鼠 老鼠 Sprague-Dawley 受体 Interleukin-1 研究支持 Non-U.S. Gov't Sialoglycoproteins 滑液膜 肿瘤坏死 Factor-alpha
Tumor necrosis factor-alpha and interleukin-6 production by astrocytes in vitro:regulation by other cytokines
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作者 袁汉娜 朱涛 陆伯刚 《中华医学杂志:英文版》 SCIE CAS CSCD 1998年第10期26-26,共1页
Tumor necrosis factor-alpha and interleukin-6 production by astrocytes in vitro:regulation by other cytokines@袁汉娜@朱涛@陆伯刚...
关键词 INTERLEUKIN-6 ASTROCYTES by TUMOR FACTOR-ALPHA and NECROSIS other production CYTOKINES
2型糖尿病血管病变患者TIPE2与TF的检测及临床意义 预览
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作者 熊石龙 吴一行 +1 位作者 龚芳 何伟 《天津医药》 CAS 北大核心 2019年第9期958-962,共5页
目的观察2型糖尿病(T2DM)血管病变患者外周血单个核细胞(PBMCs)内肿瘤坏死因子α诱导蛋白8样分子2(TIPE2)、组织因子(TF)的表达与血浆肿瘤坏死因子(TNF)-α和TF水平的变化,并探讨其与T2DM血管病变的相关性。方法收集广州医科大学附属第... 目的观察2型糖尿病(T2DM)血管病变患者外周血单个核细胞(PBMCs)内肿瘤坏死因子α诱导蛋白8样分子2(TIPE2)、组织因子(TF)的表达与血浆肿瘤坏死因子(TNF)-α和TF水平的变化,并探讨其与T2DM血管病变的相关性。方法收集广州医科大学附属第二医院番禺院区2015年5月-2016年5月收治并确诊为T2DM患者78例,根据是否合并有血管病变分为血管病变(T2DM+V)组36例和非血管病变(T2DM)组42例,另择40例同期行健康体检者为对照(CON)组。收集患者年龄、性别等一般资料,采用高效液相色谱法测定糖化血红蛋白(HbA1c);全自动生化分析仪检测总胆固醇(TC)、三酰甘油(TG)、高密度脂蛋白胆固醇(HDL-C)、低密度脂蛋白胆固醇(LDL-C)等生化指标;实时荧光定量PCR检测PBMCs中TIPE2、TF mRNA的表达水平;ELISA法测定血浆TF和TNF-α浓度。比较3组间各指标的差异并分析TIPE2 mRNA与TF mRNA、TF及TNF-α的相关性。结果 3组间性别、年龄、血脂方面差异无统计学意义(P>0.05);CON组、T2DM组和T2DM+V组HbA1c依次升高,PBMCs中TIPE2 mRNA表达依次下降,TF mRNA表达则依次升高(P<0.05);血浆TF、TNF-α水平依次增高(均P<0.05);T2DM+V组内TIPE2 mRNA与TF mRNA及TNF-α均呈负相关(r分别为-0.340和-0.342,P<0.05)。结论 T2DM血管病变的发生发展与TIPE2的下降及TF的升高有关。 展开更多
关键词 糖尿病 2型 糖尿病血管病变 肿瘤坏死因子Α 炎症 组织因子 肿瘤坏死因子α诱导蛋白8样分子2
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白细胞介素-4负调控NF-κB通路抑制炎症反应的机制研究 预览
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作者 黄洁媛 刘文明 《天津医药》 CAS 北大核心 2019年第10期1025-1029,共5页
目的探讨白细胞介素(IL)-4对于脂多糖(LPS)诱导的Ana-1细胞髓样分化因子88(MyD88)/核因子(NF)-κB信号通路的影响。方法将小鼠巨噬细胞Ana-1分为LPS组(给予50μg/LLPS刺激)和LPS+IL-4组(10μg/LIL-4预培养1h后,给予LPS刺激)。在0、0.5、... 目的探讨白细胞介素(IL)-4对于脂多糖(LPS)诱导的Ana-1细胞髓样分化因子88(MyD88)/核因子(NF)-κB信号通路的影响。方法将小鼠巨噬细胞Ana-1分为LPS组(给予50μg/LLPS刺激)和LPS+IL-4组(10μg/LIL-4预培养1h后,给予LPS刺激)。在0、0.5、1和2h时收集细胞培养上清液。采用RT-PCR检测MyD88和NF-κBmRNA的相对表达水平;Westernblot法检测MyD88、NF-κB总蛋白、NF-κBp65蛋白表达水平;ELISA法检测NF-κBp65胞核/胞浆比例,以及细胞培养上清液中IL-6和肿瘤坏死因子(TNF)-α含量。结果随着细胞培养时间的延长,LPS组MyD88、NF-κBmRNA和蛋白表达水平,NF-κBp65胞核/胞浆比例,IL-6和TNF-α水平均呈逐渐升高的趋势(P<0.05);而LPS+IL-4组MyD88mRNA表达水平无明显变化(P>0.05),MyD88蛋白表达水平、NF-κBmRNA和蛋白表达水平、NF-κBp65胞核/胞浆比例、IL-6和TNF-α水平则均呈先升高后降低的趋势(P<0.05);LPS+IL-4组MyD88mRNA和蛋白表达水平、NF-κBp65胞核/胞浆比例、IL-6和TNF-α水平在1h和2h时显著低于LPS组(P<0.05),而2组不同时间点NF-κBmRNA和蛋白表达水平比较差异均无统计学意义(P>0.05)。结论IL-4发挥抗炎作用可能与抑制MyD88/NF-κB信号通路活化有关,IL-4可下调促炎细胞因子IL-6和TNF-α的表达。 展开更多
关键词 白细胞介素4 白细胞介素6 脂多糖类 肿瘤坏死因子α 髓样分化因子88 NF-ΚB 炎症
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病毒性心肌炎患儿血清炎性细胞因子和高迁移率族蛋白1水平变化 预览
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作者 王茜 姜红 +1 位作者 朱聚 熊海英 《中国实验诊断学》 2019年第5期826-828,共3页
目的观察病毒性心肌炎患儿血清转化生长因子-β1(TGF-β1)、肿瘤坏死因子-α(TNF-α)和高迁移率族蛋白1(HMGB1)水平变化,探讨临床意义。方法选择我科收治的病毒性心肌炎患儿共96例,根据其病程分为急性期组、恢复期组,各48例。另选择40... 目的观察病毒性心肌炎患儿血清转化生长因子-β1(TGF-β1)、肿瘤坏死因子-α(TNF-α)和高迁移率族蛋白1(HMGB1)水平变化,探讨临床意义。方法选择我科收治的病毒性心肌炎患儿共96例,根据其病程分为急性期组、恢复期组,各48例。另选择40名同期健康体检儿童为对照组。采用双抗体夹心酶联免疫分析法定量检测各组患儿血清TGF-β1、TNF-α和HMGB1水平。结果与对照组比较,急性期组的TGF-β1、HMGB1升高,TNF-α升高更显著(P<0.01),恢复期组TGF-β1较急性期稍低,但差异无统计学意义(P>0.05);TNF-α、HMGB1明显低于急性期组,仍高于对照组(P<0.05)。TGF-β1第3d、7d无显著变化,第14d时明显降低(P<0.05);TNF-α和HMGB1第3d、7d、14d依次降低,各时间点间差异有统计学意义(P<0.05)。结论病毒性心肌炎急性期炎性因子升高,恢复期虽降低,但仍存在心肌纤维化的危险,联合检测病毒性心肌炎患儿血清TGF-β1、TNF-α和HMGB1有助于病情判断及预后评估。 展开更多
关键词 病毒性心肌炎 转化生长因子-Β1 肿瘤坏死因子-Α 高迁移率族蛋白1
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血清TNF-α、TGF-β1及调节性T淋巴细胞亚群水平与胸部恶性肿瘤患者放射性肺病的相关性 预览
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作者 陈建江 吴刚 《中国现代医药杂志》 2019年第8期32-35,共4页
目的 探讨血清肿瘤坏死因子-α(TNF-α)、转化生长因子-β1(TGF-β1)及T淋巴细胞亚群水平与胸部恶性肿瘤患者放射性肺病的相关性。方法 选择2016年1月~2018年1月在我院进行放疗的70例胸部恶性肿瘤患者,按照其放射性肺损伤的程度分为重... 目的 探讨血清肿瘤坏死因子-α(TNF-α)、转化生长因子-β1(TGF-β1)及T淋巴细胞亚群水平与胸部恶性肿瘤患者放射性肺病的相关性。方法 选择2016年1月~2018年1月在我院进行放疗的70例胸部恶性肿瘤患者,按照其放射性肺损伤的程度分为重损伤组和轻损伤组;利用酶联免疫吸附法检测血清TNF-α、TGF-β1水平,利用流式细胞术检测T淋巴细胞亚群,探讨这些指标与放射性肺病的相关性。结果 将全部患者分为轻损伤组(0~1级,49例)和重损伤组(2~5级,21例),其中发生1级及以上放射性肺损伤42例(60.00%)。两组患者放疗前的血清TNF-α、TGF-β1、总T细胞比例、CD4^+CD25^+T细胞比例差异均无统计学意义(t=-0.458,-0.652,0.551,0.618,P>0.05);放疗后,两组患者的血清TNF-α、TGF-β1、CD4+CD25+T细胞比例均显著上升,总T细胞比例显著降低,与放疗前相比,差异均具有统计学意义(t=-17.580,-8.020,4.249,-3.133,-11.981,-8.680,6.287,-5.364,P<0.05)。放疗后,两组患者TNF-α水平差异无统计学意义(t=-1.214,P>0.05),重损伤组的TGF-β1水平和CD4+CD25+T细胞比例均显著高于轻损伤组,总T细胞比例低于轻损伤组,差异均具有统计学意义(t=-4.748,3.391,-3.931,P<0.05);放疗前后,患者CD4+CD25+T细胞比例与血清TGF-β1浓度均呈正相关(r=0.452,0.461,P<0.05)。结论 相当比例胸部肿瘤患者会发生放射性肺损伤,血清TGF-β1浓度、CD4+CD25+T和总T细胞水平可能反映损伤的程度。 展开更多
关键词 肿瘤坏死因子-α 转化生长因子-Β1 淋巴细胞 放射性肺病
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急性脑出血患者血管内皮生长因子和肿瘤坏死因子-α检验结果分析 预览
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作者 康文慧 《世界最新医学信息文摘》 2019年第45期14-15,共2页
目的研究急性脑出血患者血管内皮生长因子和肿瘤坏死因子-α检验结果。方法收集符合自发性脑出血诊断标准的急性脑出血患者30例作为观察组,选健康体检者10例作为对照组,对各组的血管内皮生长因子和肿瘤坏死因子-α进行检验,并对比检验结... 目的研究急性脑出血患者血管内皮生长因子和肿瘤坏死因子-α检验结果。方法收集符合自发性脑出血诊断标准的急性脑出血患者30例作为观察组,选健康体检者10例作为对照组,对各组的血管内皮生长因子和肿瘤坏死因子-α进行检验,并对比检验结果,计算水肿面积及水肿指数,分析水肿面积与血管内皮生长因子、肿瘤坏死因子-α含量的相关性。结果观察组急性脑出血患者的血管内皮生长因子和肿瘤坏死因子-α含量均高于对照组,差异具有统计学意义(P<0.05);观察组组内不同时间点同一指标进行比较差异具有统计学意义(P<0.05);水肿体积大小与血管内皮生长因子和肿瘤坏死因子-α均呈正相关(P<0.05),肿瘤坏死因子-α与血肿量大小存在相关性(P<0.05)。结论在急性脑出血发生后,患者的血清血管内皮生长因子和肿瘤坏死因子-α呈动态变化趋势,且均与血肿周围水肿体积存在相关性,表明两种指标均与急性脑出血进程相关。 展开更多
关键词 急性脑出血 血管内皮生长因子 肿瘤坏死因子-Α
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重组人粒细胞集落刺激因子对急性肝衰竭大鼠模型的作用 预览
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作者 哈福双 韩涛 +2 位作者 梁宁 聂新华 朱争艳 《临床肝胆病杂志》 CAS 北大核心 2019年第7期1565-1569,共5页
目的评价重组人粒细胞集落刺激因子(rhG-CSF)对于D-氨基半乳糖(D-GalN)诱导的急性肝衰竭大鼠模型的作用。方法将105只雄性SD大鼠随机分为正常对照组、肝衰竭模型组、rhG-CSF组,每组35只。采用腹腔内注射D-GalN (1400mg/kg)建立急性肝衰... 目的评价重组人粒细胞集落刺激因子(rhG-CSF)对于D-氨基半乳糖(D-GalN)诱导的急性肝衰竭大鼠模型的作用。方法将105只雄性SD大鼠随机分为正常对照组、肝衰竭模型组、rhG-CSF组,每组35只。采用腹腔内注射D-GalN (1400mg/kg)建立急性肝衰竭模型。观察建立模型后12、24、48、72及120 h的肝脏ALT、TBil水平、外周血白细胞计数、肝脏组织病理变化;测定TNFα阳性细胞率。并观察建立模型后120 h生存率。计量资料多组间比较用单因素方差分析,进一步两两比较采用LST-t检验。结果 rhG-CSF组与肝衰竭模型组相比,肝脏HE染色提示除造模后120 h外,其余各个时间点肝细胞变性坏死均更严重;造模后120 h rhG-CSF组的肝脏HE染色提示肝小叶结构恢复相对更完全。rhG-CSF组在5个时间点TNFα阳性细胞率较肝衰竭模型组均有增高趋势。rhG-CSF组ALT及TBil水平在5个时间点均有高于肝衰竭模型组的趋势,两组内比较,ALT水平在造模后24 h差异有统计学意义(P <0. 05),TBil水平在造模后24、48、120 h差异有统计学意义(P <0. 05)。在5个时间点,rhG-CSF组外周血白细胞计数水平均高于肝衰竭模型组,差异均有统计学意义(P值均<0. 05)。rhG-CSF组和肝衰竭模型组相比,120 h生存率差异无统计学意义(P> 0. 05)。结论在急性肝衰竭的急性炎症反应期应用rhG-CSF可能加重肝脏炎症反应。 展开更多
关键词 肝功能衰竭 急性 重组人粒细胞集落刺激因子 D-氨基半乳糖 肿瘤坏死因子-Α 大鼠 Sprague-Dawley 疾病模型 动物
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NOX1与NF-κB对TNF-α诱导A549细胞氧化损伤的影响
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作者 周舫 任亚南 +5 位作者 王娜 翟若南 夏艳秋 薛腾 张恺 姚武 《中国职业医学》 CAS 北大核心 2019年第2期188-193,共6页
目的探讨酰胺腺嘌呤二核苷酸磷酸氧化酶1(NOX1)和核转录因子-κB(NF-κB)在肿瘤坏死因子-α(TNF-α)诱导A549细胞发生氧化损伤中的关系。方法①以质量浓度为0.0、10.0、25.0和50.0μg/L的TNF-α刺激A549细胞,采用CCK-8实验检测各组细胞... 目的探讨酰胺腺嘌呤二核苷酸磷酸氧化酶1(NOX1)和核转录因子-κB(NF-κB)在肿瘤坏死因子-α(TNF-α)诱导A549细胞发生氧化损伤中的关系。方法①以质量浓度为0.0、10.0、25.0和50.0μg/L的TNF-α刺激A549细胞,采用CCK-8实验检测各组细胞抑制率,选择合适的TNF-α刺激浓度。②取对数生长期A549细胞分为空白对照组、溶剂对照组、TNF-α组、二亚苯基碘(DPI)组和TNF-α+DPI组进行NOX1抑制实验。取对数生长期A549细胞分为空白对照组、TNF-α组、BAY11-7082组和TNF-α+BAY11-7082组进行NF-κB抑制实验。以蛋白印迹法检测各组细胞NOX1和p65相对表达水平,以流式细胞术检测细胞内活性氧(ROS)相对表达水平。结果①随着TNF-α剂量的增加,A549细胞的抑制率增加(P<0.05),选择25.0μg/L作为后续实验TNF-α刺激剂量。②TNF-α组细胞NOX1、p65蛋白及ROS相对表达水平分别高于空白对照组、溶剂对照组和DPI组(P<0.05);TNF-α+DPI组细胞上述指标均低于TNF-α组(P<0.05),但高于DPI组(P<0.05)。TNF-α组细胞NOX1、p65蛋白及ROS相对表达水平分别高于空白对照组和BAY11-7082组(P<0.05),TNF-α+BAY11-7082组细胞上述指标均低于TNF-α组(P<0.05)。结论抑制NOX1或NF-κB均可减轻TNF-α诱导的A549细胞氧化损伤。 展开更多
关键词 A549细胞 酰胺腺嘌呤二核苷酸磷酸氧化酶1 核转录因子-ΚB 肿瘤坏死因子-α 活性氧 氧化损伤
莪术醇对子宫内膜异位症模型大鼠炎症因子的影响 预览
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作者 聂晓博 马怡坤 +3 位作者 赵娜 胡彬 刘姣 刘晓兰 《天津医药》 CAS 北大核心 2019年第9期913-917,共5页
目的研究莪术醇对子宫内膜异位症(EMS)模型大鼠腹腔液中炎症因子的影响,探讨本药对EMS的治疗机制。方法取成年雌性SD大鼠,以自体移植法制备EMS模型。将造模成功的大鼠随机分为模型组、莪术醇组(20mg/kg),另设假手术组,每组10只。各组大... 目的研究莪术醇对子宫内膜异位症(EMS)模型大鼠腹腔液中炎症因子的影响,探讨本药对EMS的治疗机制。方法取成年雌性SD大鼠,以自体移植法制备EMS模型。将造模成功的大鼠随机分为模型组、莪术醇组(20mg/kg),另设假手术组,每组10只。各组大鼠每日灌胃给药1次,连续4周。末次给药后,大鼠麻醉,收集腹腔液,检测其中巨噬细胞趋化蛋白-1(MCP-1)、巨噬细胞游走抑制因子(MIF)、肿瘤坏死因子(TNF)-α、白细胞介素(IL)-1β和IL-6含量,假手术组大鼠取在位子宫,EMS大鼠取异位子宫内膜组织,HE染色观察病理变化,并以免疫组化染色检测内膜组织中TNF-α表达,Real-time PCR检测内膜组织中成纤维细胞生长因子2(FGF-2)mRNA表达。结果与模型组相比,莪术醇组大鼠异位内膜萎缩,腹腔液中MCP-1、MIF、TNF-α、IL-1β、IL-6含量和内膜组织中TNF-α表达、FGF-2 mRNA表达水平均明显降低(P<0.05)。结论莪术醇能够改善实验性大鼠EMS,其作用机制可能与抑制腹腔微环境中炎症反应有关。 展开更多
关键词 子宫内膜异位症 莪术醇 趋化因子类 巨噬细胞游走抑制因子 成纤维细胞生长因子2 肿瘤坏死因子α 白细胞介素1Β 白细胞介素6
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