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Clinicopathologic significance of expression of Nuclear factor-kB RelA and its target gene products in gastric cancer patients

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World Journal of Gastroenterology 2012年第34期18卷 4744-4750页

作者： Hyuk-Chan Kwon Sung-Hyun Kim Sung Yong Oh Suee Lee Ji Hyun Lee Jin Seok Jang Min Chan Kim Ki Han Kim Su-Jin Kim Seong-Geun Kim Hyo-Jin Kim Department of Internal Medicine Dong-A University College of MedicineBusan 602-715South Korea Department of Surgery Dong-A University College of MedicineBusan 602-715South Korea Department of Pathology Dong-A University College of MedicineBusan 602-715South Korea Research Institute for Convergence of Biomedical Science and Technology Pusan National University Yangsan HospitalBusan 602-715South Korea

AIM:To assess the prognostic significance of Nuclear factor-kB (NF-kb) and its target genes in gastric cancer. METHODS:The tumor tissues of 115 patients with gastric cancer were immunohistochemically evaluated using monoclonal antibodies against NF-kb RelA. Preoperative serum levels of vascular endothelial growth factor (VEGF), interleukin-6 (IL-6) were assessed via enzyme-linked immuno-sorbent assay. C-reactive protein (CRP) and serum amyloid A (SAA) were measured via immunotrubidimetry. RESULTS:Positive rate of NF-kb RelA was 42.6%. NF-kb RelA expression in tumor tissues was also related to serum levels of IL-6 (P = 0.044) and CRP (P = 0.010). IL-6, SAA, CRP were related to depth of invasion, VEGF and SAA were correlated with lymph node metastasis. IL-6, VEGF, SAA and CRP were related to the stage. Univariate analysis demonstrated that immunostaining of NF-kb RelA, levels of IL-6, VEGF, SAA were significantly related with both disease free survival and over-all survival (OS). Multivariate analysis verified that NF-kb RelA [hazard ratio (HR): 3.40, P = 0.024] and SAA (HR: 3.39, P = 0.045) were independently associated with OS. CONCLUSION: Increased expression of NF-kb RelA and high levels of serum SAA were associated with poor OS in gastric cancer patients.

关键词： Nuclear factor-kB Vascular endothelial growth factor Interleukin-6 C-reactive protein Serum amyloid A Stomach Carcinoma

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Hyperbaric Oxygen Treatment Improves Hearing Level via Attenuating TLR4/NF-κB Mediated Inflammation in Sudden Sensorineural Hearing Loss Patients

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Biomedical and Environmental Sciences 2020年第5期33卷 331-337页

作者： LIU Xue Hua LIANG Fang JIA Xing Yuan ZHAO Lin ZHOU Yan YANG Jing Department of Hyperbaric Oxygen Medicine Beijing Chaoyang HospitalCapital Medical UniversityBeijing 100020China Institute of Basic Medicine Sciences Beijing Chaoyang HospitalCapital Medical UniversityBeijing 100020China Department of Hyperbaric Oxygen Medicine Beijing Pinggu HospitalBeijing 101200China

Objective Hyperbaric oxygen treatment(HBOT)has demonstrated efficacy in improving hearing levels of patients with idiopathic sudden sensorineural hearing loss(ISSHL);however,the underlying mechanisms are not well understood.HBOT alleviates the inflammatory response,which is mediated by Toll-like receptor(TLR)4 and nuclear factor(NF)-κB.In this study we investigated whether HBOT attenuates inflammation in ISHHL patients via alteration of TLR4 and NF-κB expression.Methods ISHHL patients(n=120)and healthy control subjects(n=20)were enrolled in this study.Patients were randomly divided into medicine group treated with medicine only(n=60)and HBO group receiving both HBOT and medicine(n=60).Audiometric testing was performed pre-and posttreatment.TLR4,NF-кB,and TNF-αexpression in peripheral blood of ISSHL patients and healthy control subjects was assessed by ELISA before and after treatment.Results TLR4,NF-κB,and TNF-αlevels were upregulated in ISSHL patients relative to healthy control subjects;the levels were decreased following treatment and were lower in the HBO group than that in the medicine group post-treatment(P<0.05 and P<0.01).Conclusion HBOT alleviates hearing loss in ISSHL patients by suppressing the inflammatory response induced by TLR4 and NF-κB signaling.

关键词： Hyperbaric oxygen treatment Sudden sensorineural hearing loss Toll-like receptor 4 Nuclear factor-kB

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Hepatic Cyp1a2 Expression Reduction during Inflammation Elicited in a Rat Model of Intermittent Hypoxia

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Chinese Medical Journal 2017年第21期130卷 2585-2590页

作者： Li-Xia Shi Xing Wang Qi Wu Xin Sun Zhen Wan Li Li Kuan Li Xue Li Yu Li Qiu-Yang Zhang Jun-Ping Wu Huai-Yong Chen Department of Respiratory Medicine Haihe Clinical College of Tianjin Medical University Tianjin 300350 China Key Research Laboratory for Infectious Disease Prevention for State Administration of Traditional Chinese Medicine Tianjin Haihe Hospital Tianjin 300350 China Department of Basic Medicine Tianjin Institute of Respiratory Diseases Tianjin Haihe Hospital Tianjin 300350 China

Background： Intermittent hypoxia （IH） is a key element of obstructive sleep apnea （OSA） that can lead to disorders in the liver. In this study, IH was established in a rat model to examine its effects on the expression of hepatic cytochrome P450 （CYP） and CYP regulators, including nuclear receptors. Methods： Hematoxylin and eosin staining was conducted to analyze the general pathology of the liver of rats exposed to IH. The messenger RNA （mRNA） expression levels of inflammatory cytokines, CYPs, nuclear factor-κB （NF-κB）, and nuclear factors in the liver were measured by quantitative reverse transcription polymerase chain reaction. Results： We found inflammatory infiltrates in the liver of rats exposed to IH. The mRNA expression level of interleukin-1beta was increased in the liver of the IH-exposed rats （0.005 ± 0.001 vs. 0.038 ± 0.008, P = 0.042）, whereas the mRNA expression level of Cyp1a2 was downregulated （0.022 ± 0.002 vs. 0.0050 ± 0.0002, P = 0.029）. The hepatic level of transcription factor NF-κB was also reduced in the IH group relative to that in the control group, but the difference was not statistically significant and was parallel to the expression of the pregnane X receptor and constitutive androstane receptor. However, the decreased expression of the glucocorticoid receptor upon IH treatment was statistically significant （0.056 ± 0.012 vs. 0.032 ± 0.005, P = 0.035）. Conclusions： These results indicate a decrease in expression of hepatic CYPs and their regulator GR in rats exposed to IH. Therefore, this should be noted for patients on medication, especially those on drugs metabolized via the hepatic system, and close attention should be paid to the liver function of patients with OSA-associated IH.

关键词： Cytochrome P450 Glucocorticoid Receptor Inflammation Intermittent Hypoxia Nuclear factor-kB

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Dose-dependent effects of lanthanum chloride on wear particle-induced aseptic inflammation in a murine air-pouch model

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Journal of Rare Earths 2013年第4期31卷 420-427页

作者：江川邹飏刘翔尚江荫子程明戴闽 Department of Orthopaedics the First Affiliated HospitalNanchang University

To investigate the effects of local injection of different doses of lanthanum chloride （LaCl3） on aseptic inflammation in mice stimulated by wear particles from artificial joints, the particles were prepared by vacuum ball mill in vitro and air-pouch models were performed with 45 male BALB/c mice that were randomly divided into blank control group, wear particle group and wear parti- cle ＋ LaCl3 （0.1, 0.9 and 8.1 μmol） group. All animals were sacrificed and tissue specimens were harvested 7 days after treatment. Hematoxylin and eosin （H＆E） staining, enzyme-linked immunosorbent assay （ELISA）, reverse transcription-polymerase chain reac- tion （RT-PCR） and western blot were applied to observe inflammatory reaction and detect the expression of pro-inflammatory cyto- kines （TNF-et, IL-1β） and nuclear factor-κB （NF-κB） in mRNA and protein levels in air-pouch membrances. The results showed that wear particles could stimulate aseptic inflammation in vivo effectively; 0.9 μmol LaCl3 could significantly inhibit wear parti- cle-induced gene and protein expression of pro-inflammatory cytokines and NF-Id3 （P〈0.05）; 0.1 and 8. 1 μmol LaCl3 did not exert an inflammation-inhibiting effect and even caused adverse effects at 8.1 μmol. In conclusion, LaC13 played a protective role against wear particle-induced aseptic inflammation dose-dependently, which was involved in NF-κB related signaling pathways.

关键词： lanthanum chloride wear particle aseptic inflammation pro-inflammatory cytokine Nuclear factor-kB air-pouch model

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Oxymatrine reduces neuroinflammation in rat brain A signaling pathway

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Neural Regeneration Research 2012年第30期7卷 2333-2339页

作者： Jiahui Mao Yae Hu Ailing Zhou Bing Zheng Yi Liu Yueming Du Jia Li Jinyang Lu Pengcheng Zhou Department of Pathophysiology Medical School of Nantong University Nantong 226001 Jiangsu Province China Department of Urology the First People's Hospital of Nantong Nantong 226001 Jiangsu Province China Undergraduate of Medical School of Nantong University Nantong 226001 Jiangsu Province China

Cerebral neuroinflammation models were established by injecting 10μg lipopolysaccharide into the hippocampus of male Sprague-Dawley rats. The rats were treated with an intraperitoneal injection of 120, 90, or 60 mg/kg oxymatrine daily for three days prior to the lipopolysaccharide injection. Twenty-four hours after model induction, the hippocampus was analyzed by real-time quantitative PCR, and the cerebral cortex was analyzed by enzyme-linked immunosorbent assay and western blot assay. The results of the enzyme-linked immunosorbent assay and the real-time quantitative PCR showed that the secretion and mRNA expression of the pro-inflammatory cytokines interleukin-113 and tumor necrosis factor-a were significantly decreased in the hippocampus and cerebral cortex of model rats treated with oxymatrine. Western blot assay and real-time quantitative PCR analysis indicated that toll-like receptor 4 mRNA and protein expression were significantly decreased in the groups receiving different doses of oxymatrine. Additionally, 120 and 90 mg/kg oxymatrine were shown to reduce protein levels of Nuclear factor-kB p65 in the nucleus and of phosphorylated Ikba in the cytoplasm of brain cells, as detected by western blot assay. Experimental findings indicate that oxymatrine may inhibit neuroinflammation in rat brain via downregulating the expression of molecules in the toll-like receptor 4/Nuclear factor-kB signaling Dathwav.

关键词： oxymatrine neuroinflammation toll-like receptor 4 Nuclear factor-kB signaling pathway inflammatory factors lipopolysaccharide hippocampus cerebral cortex neural regeneration

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The regulating role of mutant Ikbα in expression of TIMP-2 and MMP-9 in human glioblastoma multiform

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Chinese Medical Journal 2009年第2期122卷 205-211页

作者： HU Yu-hua YU Li-Jie SHAO En-de WU Jian-liang JI Jian-wen Department of Neurosurgery Second Hospital of Hebei Medical University Shijiazhuang Hebei 050000 China Department of Pathology Stomatological Hospital of Hebei Medical University Shijiazhuang Hebei 050000 China Department of Neurosurgery Langfang People's Hospital Langfang Hebei 065000 China

Background Our previous studies demonstrated that mutant Ikbα （IkbαM） inhibited the occurrence, growth and angiogenesis of human glioblastoma multiform （GBM）. However, the specific mechanism by which IkbaM regulates protein-degrading enzymes secreted from GBM to inhibit invasion and metastasis has remained unclear. The aim of the present study was to investigate the regulatory role and significance of IkbαM genes in the expression of tissue inhibitor of metalloproteinase （TIMP）-2 and matrix metalloproteinase （MMP）-9 in human GBM. Methods We established the following four GBM cell lines stably expressing IkbaM by plasmid construction, gene transfection and screening for IkbαM protein expression： mutant Ikba-transfected cells （G36A-M）, wild-type Ikba-transfected cells （G36A-W）, empty plasmid transfected cells （G36A-P） and untransfected cells （G36A）. The TIMP-2 and MMP-9 expression was detected by RT-PCR and Western blotting. Tumor cells were then implanted subcutaneously into nude mice to establish an animal model of ectopic tumor growth, and TIMP-2 and MMP-9 expression was determined by immunohistochemical methods. Results The results showed that there was a significant increase in TIMP-2 expression and a significant decrease in MMP-9 expression in the G36A-M group at both the RNA and protein levels compared with the G36A-W group, G36A-P group and G36A group. Similar results were observed in the immunohistochemical staining analysis of tumor tissues. In the G36A-M group, TIMP-2 expression was significantly higher while MMP-9 expression was significantly lower than in the other three groups. Conclusions Our findings indicate that IkbaM inhibits the activation of NF-kb. It significantly up-regulates TIMP-2 expression in human malignant glioma cells and down-regulates the expression of MMP-9. Thus, IkbαM maintains the integrity of the extracellular matrix and further inhibits the growth and metastasis of tumor tissues. Chin Med J 2009; 122（2）：205-211

关键词： Nuclear factor-kB mutant-type Ikbα metalloproteinases extracellular matrix glioma

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Effects of Andrographolide on the Activation of Mitogen Activated Protein Kinases and nuclear factor-κ B in Mouse Peritoneal Macrophage-derived Foam Cells

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Chinese Journal of Integrative Medicine 2012年第5期18卷 391-394页

作者：李福星李树生 Department of Emergency Tongji HospitalTongji Medical CollegeHuazhong University of Science and Technology Department of Emergency the Second Affiliated Hospital to Nanchang University

Objective： To observe the effect of andrographolide on the activation of mitogen-activated protein kinases （MAPKs） and expression of nuclear factor- kb （NF-kb） in macrophage foam cells. Methods： The mouse peritoneal macrophages were cultured in the media in the presence of oxidized low-density lipoprotein （ox-LDL）, ox-LDL＋andrographolide, or neither （control）. The phosphorylation of MAPK molecules （p38MAPK, JNK, ERK1/2） and the expressions of NK- kb p65 were examined by Western blot. Results： As compared with cells in the control group, the expressions of phospho-p38 and NF- kb p65 were increased in the cells cultured with either ox-LDL or ox-LDL＋andrographolide （P〈0.01）, but attenuated significantly in the presence of ox-LDL＋ andrographolide when compared with ox-LDL （P〈0.05）. The phospho-JNK increased in the presence of either ox-LDL or ox-LDL＋andrographolide when compared with control cells （P〈0.01）, but no significant difference existed between ox-LDL and ox-LDL＋andrographolide （P〉0.05）. The expression of phospho-ERK1/2 was increased in the presence of ox-LDL compared with the control cells （P〈0.01）, but no significant differences existed between the cells cultured in the presence of ox-LDL＋andrographolide and the control medium （P〉0.05）. Conclusions： Andrographolide could inhibit the activation of ERK1/2, p38MAPK and NK-kb induced by ox-LDL in macrophage foam cells, which might be one of its mechanisms in preventing atherosclerosis.

关键词： andrographolide mouse peritoneal macrophage foam cells mitogen activated protein kinasese Nuclear factor-kB atherosclerosis

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Naoxintong dose effects on inflammatory factor expression in the rat brain following focal cerebral ischemia

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Neural Regeneration Research 2008年第10期3卷 1111-1115页

作者： Xiangjian Zhang Li Xu Zuoran Chen Shuchao Hu Liying Zhang Haiyan Li Ruichun Liu Department of Neurology the Second Hospital of Hebei Medical University Shijiazhuang Department of Neurology Bejing Aerospace General Hospital Beijing 100076 China Department of Neurology Beijing Daxing Hospital of Capital University Beijing 102600 China Department of Neurology Beijing Shijingshan Hospital Beijing 100043 China Department of Neurology Beijing Shijitan Hospital Beijing 100038 China

BACKGROUND： Certain components of tetramethylpyrazine, a traditional Chinese medicine, exhibit protective effects against brain injury. OBJECTIVE： To investigate the effects of different Naoxintong doses on expression of nuclear factor-kappa B （ kb）, interleukin-6, tumor necrosis factor-α, and complement 3 in rats following focal cerebral ischemia. DESIGN, TIME AND SETTING： The randomized experiment was performed at the Laboratory of Neurology, Second Hospital of Hebei Medical University from June 2004 to June 2006. MATERIALS： A total of 150 adult, healthy, male, Sprague Dawley rats, weighing 280-320g, were selected. Naoxintong powder （mainly comprising szechwan lovage rhizome, milkvetch root, danshen root, and radix angelicae sinensis） was obtained from Buchang Pharmacy Co., Ltd. in Xianyang City of Shanxi Province of China, lot number 040608. METHODS： The rats were randomly assigned into sham operation, saline, high-dose Naoxintong, moderate-dose Naoxintong, and low-dose Naoxintong groups, with 30 rats in each group. Rat models of middle cerebral artery occlusion were established using the suture method, with the exception of the sham operation group. Rats in the high-dose, moderate-dose and low-dose Naoxintong groups received 4, 2, and 1 g/kg Naoxintong respectively, by gavage. Rats in the saline group were treated with 1 mL saline by gavage All rats were administered by gavage at 5 and 23 hours following surgery, and subsequently, once per day. MAIN OUTCOME MEASURES： At 6, 24, 48, 72 hours, and 7 days following model establishment, brain water content was measured. Histopathological changes in brain tissues were detected using hematoxylin-eosin staining. Expression of nuclear factor- kb, interleukin-6, tumor necrosis factor- α, and complement 3 was examined by immunohistochemistry. RESULTS： A total of 150 rats were included in the final analysis with no loss. Brain water content was significantly increased in the ischemic hemisphere of rats from the saline, as well as the high-dose, moderate-dose, and low-dos

关键词： brain ischemia complement 3 interleukin-6 Naoxintong Nuclear factor-kB rat tumor necrosis factor-α

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Mannan-binding lectin directly interacts with Toll-like receptor 4 and suppresses lipopolysaccharide-induced inflammatory cytokine secretion from THP-1 cells

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Cellular & Molecular Immunology 2011年第3期8卷 265-275页

作者： Mingyong Wang Yue Chen Yani Zhang Liyun Zhang Xiao Lu Zhengliang Chen Department of Immunology Southern Medical UniversityGuangzhou510515China Department of Medical Tests Xinxiang Medical UniversityXinxiang453003China

Mannan-binding lectin(MBL)plays a key role in the lectin pathway of complement activation and can influence cytokine expression.Toll-like receptor 4(TLR4)is expressed extensively and has been demonstrated to be involved in lipopolysaccharide(LPS)-induced signaling.We first sought to determine whether MBL exposure could modulate LPS-induced inflammatory cytokine secretion and Nuclear factor-kB(NF-kb)activity by using the monocytoid cell line THP-1.We then investigated the possible mechanisms underlying any observed regulatory effect.Using ELISA and reverse transcriptase polymerase chain reaction(RT-PCR)analysis,we found that at both the protein andmRNAlevels,treatment withMBLsuppresses LPS-induced tumor-necrosis factor(TNF)-a and IL-12 production in THP-1 cells.An electrophoretic mobility shift assay and western blot analysis revealed that MBL treatment can inhibit LPS-induced NF-kb DNA binding and translocation in THP-1 cells.While the binding of MBL to THP-1 cells was evident at physiological calcium concentrations,this binding occurred optimally in response to supraphysiological calcium concentrations.This binding can be partly inhibited by treatment with either a soluble form of recombinant TLR4 extracellular domain or anti-TLR4 monoclonal antibody(HTA125).Activation of THP-1 cells by LPS treatment resulted in increased MBL binding.We also observed that MBL could directly bind to the extracellular domain of TLR4 in a dose-dependent manner,and this interaction could attenuate the binding of LPS to cell surfaces.Taken together,these data suggest that MBL may affect cytokine expression through modulation of LPS-/TLR-signaling pathways.These findings suggest that MBL may play an important role in both immune regulation and the signaling pathways involved in cytokine networks.

关键词： cytokines mannan-binding lectin Nuclear factor-kB THP-1 cells Toll-like receptor 4

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The intrinsic PEDF is regulated by PPARγin permanent focal cerebral ischemia of rat

The intrinsic PEDF is regulated by PPARγin permanent focal ...

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2014中国医师协会中西医结合医师大会

作者：祝春华张祥建乔会敏王力娜张晓林河北医科大学第二医院神经内科

Background and object:Inflammatory damage plays a pivotal role in cerebral ischemia and may represent a target for treatment.Pigment epithelium-derived factor(PEDF) is proven to possess neuroprotective property.But there is little known about the intrinsic PEDF after cerebral ischemia.This study evaluated the time course expression of the intrinsic PEDF and its underlying regulation mechanisms after cerebral ischemia.Methods:Male Sprague-Dawley rats were subjected to permanent middle cerebral artery occlusion.Telmisartan(PPARy agonist) and GW9662(PPARy antagonist) were systemically administered to explore the effect on PPARy,PEDF,NF-kb and MMP-9 expression at 24 h after cerebral ischemia by western blot and qRT-PCR.The neurological deficits,brain water content and infarct volume were measured.Compared with normal group,the expressions of PEDF and PPARy decreased,and the expression of NF-kb and MMP-9 increased at early stage after ischemia(P kb and MMP-9 was down-regulated by telmisartan at 24 h(P < 0.05).The neurological deficits,brain water content and infarct volume were dramatically alleviated by telmisartan(P < 0.05).Telmisartan’s effects were reversed by GW9662 co-administration(P < 0.05).Conclusion;The expression of intrinsic PEDF was downregulated at the early stage of cerebral ischemia.The protective effects of intrinsic PEDF by activating PPARy pathway may be one of the strategic targets for cerebral ischemic therapies.

关键词： Peroxisome proliferator-activated receptor-gamma Pigment epithelium-derived factor Matrix metalloproteinases-9 Nuclear factor-kB Cerebral ischemia Telmisartan

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