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Effects of ketamine on proinflammatory cytokines and nuclear factor kappab in polymicrobial sepsis rats

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World Journal of Gastroenterology 2006年第45期12卷 7350-7354页

作者： Xue-Min Song Jian-Guo Li Yan-Lin Wang Qing Zhou Zhao-Hui Du bao-Hui Jia Jian-Juan Ke Department of Anesthesiology Zhongnan Hospital of Wuhan University Wuhan 430071 Hubei Province China

AIM： To explore the effects of ketamine on hemodynamics, plasma proinflammatory cytokine （TNF-α and IL-6） levels and nuclear factor kappa b （NF-κb） activation during polymicrobial sepsis. METHODS： Male Sprague-Dawlay rats were subjected to cecal ligation and puncture （CLP） or sham operation. The rats were randomly assigned into four equal groups： sham CLP group, CLP group, ketamine （KT）Ⅰ group and KTⅡgroup. Thirty minutes before CLP, ketamine （5 mg/kg per hour and 10 mglkg per hour, respectively） was infused continuously through the left femoral vein cannula in KT Ⅰ group or KTⅡgroup. Sham CLP group and CLP group received 0.9% saline only （5 mL/kg per hour）. The right femoral artery was cannulated to monitor mean arterial pressure （MAP） and heart rates （HR）,and draw blood samples. The proinflammatory cytokine （TNF-α and IL-6） levels of plasma were measured using enzyme-linked immunosorbent assays （ELISA）. The hepatic NF-κb activation was determined by Western blot and HPIAS 2000 image analysis system. Twenty hours after CLP, the rats were killed by right femoral artery phlebotomization. RESULTS： CLP produced progressive hypotension, and a first increase followed by a decrease in HR. The hypotension was prevented, and the HR was slightly steady in ketamine treated rats. TNF-α levels of plasma reached a peak value at 2 h after CLP. Ketamine （KT Ⅰ group or KTⅡgroup） caused a significant decrease compared with CLP group at 2, 5 and 9 h time points after CLP （14.3 ± 1.9 vs 4.3 ± 0.9, 9.7 ± 1.4 vs 4.3 ± 0.9; 9.3 ± 1.5 vs 4.3 ± 0.9, 8.7 ± 1.4 vs 4.3 ±0.9; 6.0 ± 1.5 vs 5.0 ± 1.7, 5.3 ± 0.8 vs 5.0 ± 1.7; P 〈 0.01, respectively）. The IL-6 levels of plasma firstly ascended and then descended in CLP group, and reached a peak value at 9 h after CLP. Ketamine （KT I group or KTH group） caused a significant decrease compared with CLP group at 5, 9 or 20 h after CLP （135.0 ± 52.6 vs 60.0 ± 16.3, 112.5 ± 52.6 vs 60.0 ± 16.3; 410.0 ± 68.7 vs 62.5 ± 12.5, 250.0 ± 28.0 vs 62.5 ± 12.

关键词： Ketamine Sepsis Hemodynamics Tumor necrosis factor α Interleukin 6 nuclear factor kappa b

15-deoxy-△12,14-prostaglandin J2 ameliorates endotoxin-induced acute lung injury in rats

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Chinese Medical Journal 2014年第5期127卷 815-820页

作者： Geng Zhilong Zhu Wankun Wang Huiwen Chen Ye Liang Juan Liu Dong Department of Critical Care Medicine General Hospital of Lanzhou Military Region Lanzhou Gansu 730050 China

background A proinflammatory milieu emerging in the lung due to neutrophil accumulation and activation is a key in the pathogenesis of acute lung injury （ALI）.15-deoxy-△12,14-prostaglandin J2 （15d-PGJ2）,one of the terminal products of the cyclooxygenase-2 pathway,is known to be the endogenous ligand of peroxisome proliferator-activated receptor y （PPAR-y） with multiple physiological *** evidence indicates that 15d-PGJ2 has anti-inflammatory,antiproliferative,cytoprotective and pro-resolving *** investigated whether 15d-PGJ2 has a protective effect against endotoxin-induced acute lung injury in *** Twenty-four male Wistar rats were randomly assigned into four groups （n=6 per group）：sham＋vehicle group,sham＋15d-PGJ2 group,LPS＋vehicle group,and LPS＋15d-PGJ2 *** rats were given either lipopolysaccharide （LPS,6 mg/kg intravenously） or saline,and pretreated with 15d-PGJ2 （0.3 mg/kg intravenously） or its vehicle （dimethyl sulphoxide） 30 minutes before *** alterations,wet/dry weight （W/D） ratio and myeloperoxidase （MPO） activity as well as tumor necrosis factor （TNF）-α and cytokine-induced neutrophil chemoattractant-1 （CINC-1） levels were determined in lung tissues four hours after LPS *** analysis for intercellular adhesion molecule-1 （ICAM-1） expression and Western blotting analysis for nuclear factor （NF）-κb p65 translocation and Iκbα protein levels were also *** 15d-PGJ2 pretreatment significantly attenuated LPS-induced lung injury,and reduced the increased W/D ratio,MPO activity,TNF-α,CINC-1 levels,and ICAM-1 expression in the lung.15d-PGJ2 also suppressed the nuclear NF-Κb p65 translocation and increased cytosolic IKbα *** 15d-PGJ2 protects against endotoxin-induced acute lung injury,most likely through the reduction of proinflammatory protein levels during endotoxemia subsequent to the inhibition of NF-Κb activation.

关键词： acute lung injury endotoxin 15-deoxy-△12, 14-prostaglandin J2 nuclear factor kappa b

DOK3 promotes proliferation and inhibits apoptosis of prostate cancer via the NF-κb signaling pathway

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Chinese Medical Journal 2023年第4期136卷 423-432页

作者： Kun Jin Shi Qiu bo Chen Zilong Zhang Chichen Zhang Xianghong Zhou Lu Yang Jianzhong Ai Qiang Wei Department of Urology and National Clinical Research Center for Geriatrics West China HospitalSichuan UniversityChengduSichuan 610041China Center of biomedical big Data West China HospitalSichuan UniversityChengduSichuan 610041China Department of Urology and Institute of Urology West China HospitalSichuan UniversityChengduSichuan 610041China

background: DOK3 (Downstream of kinase 3) is involved primarily with immune cell infiltration. Recent research reported the role of DOK3 in tumor progression, with opposite effects in lung cancer and gliomas;however, its role in prostate cancer (PCa) remains elusive. This study aimed to explore the role of DOK3 in PCa and to determine the mechanisms involved. Methods: To investigate the functions and mechanisms of DOK3 in PCa, we performed bioinformatic and biofunctional analyses. Samples from patients with PCa were collected from West China Hospital, and 46 were selected for the final correlation analysis. A lentivirus-based short hairpin ribonucleic acid (shRNA) carrier was established for silencing DOK3. A series of experiments involving the cell counting kit-8, bromodeoxyuridine, and flow cytometry assays were performed to identify cell proliferation and apoptosis. Changes in biomarkers from the nuclear factor kappa b (NF-κb) signaling pathway were detected to verify the relationship between DOK3 and the NF-κb pathway. A subcutaneous xenograft mouse model was performed to examine phenotypes after knocking down DOK3 in vivo . Rescue experiments with DOK3 knockdown and NF-κb pathway activation were designed to verify regulating effects. Results: DOK3 was up-regulated in PCa cell lines and tissues. In addition, a high level of DOK3 was predictive of higher pathological stages and worse prognoses. Similar results were observed with PCa patient samples. After silencing DOK3 in PCa cell lines 22RV1 and PC3, cell proliferation was significantly inhibited while apoptosis was promoted. Gene set enrichment analysis revealed that DOK3 function was enriched in the NF-κb pathway. Mechanism experiments determined that knockdown of DOK3 suppressed activation of the NF-κb pathway, increased the expressions of b-cell lymphoma-2 like 11 (bIM) and b-cell lymphoma-2 associated X (bAX), and decreased the expression of phosphorylated-P65 and X-linked inhibitor of apoptosis (XIAP). In

关键词： Prostate cancer Downstream of kinase 3 Prognosis nuclear factor kappa b

Role of Notch-1 signaling pathway in PC12 cell apoptosis induced by amyloid beta-peptide(25–35)

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Neural Regeneration Research 2014年第13期9卷 1297-1302页

作者： Huimin Liang Yaozhou Zhang Xiaoyan Shi Tianxiang Wei Jiyu Lou Second Affiliated Hospital of Zhengzhou University Huaihe Hospital of Henan University Department of biotechnology Xinyang Agricultural College Pharmaceutical College of Henan University

Recent studies have demonstrated that Notch-1 expression is increased in the hippocampus of Alzheimer＇s disease patients. We speculate that Notch-1 signaling may be involved in PC12 cell apoptosis induced by amyloid beta-peptide （25-35）（Aβ25-35）. In the present study, PC12 cells were cultured with different doses （0, 0.1, 1.0, 10 and 100 nmol/L） of N-[N-（3,5-Difluorophenacetyl）-L-alanyl]-S-phenylglycine t-butyl ester, a Notch-1 signaling pathway inhibitor, for 30 minutes. Then cultured cells were induced with Aβ25-3s for 48 hours. Pretreatment of PC12 cells with high doses of N-[N-（3,5-Difluorophenacetyl）-L-alanyl]-S-phenylglycine t-butyl ester （〉 10 nmol/L） prolonged the survival of PC12 cells after Aβ25-35 induction, decreased the expression of apoptosis-related proteins caspase-3, -8, -9, increased the activity of oxidative stress-related superoxide dismutase and catalase, inhibited the production of active oxygen, and reduced nuclear factor kappa b expression. This study indicates that the Notch-1 signaling pathway plays a pivotal role in Aβ25-35-induced PC12 apoptosis.

关键词： nerve regeneration Alzheimer's disease amyloid beta-peptide (25-35) Notch-l PC12cells apoptosis oxidative stress nuclear factor kappa b neural regeneration

Ketamine inhibits c-Jun protein expression in mouse hippocampus following cerebral ischemia/reperfusion injury

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Neural Regeneration Research 2012年第11期7卷 833-836页

作者： Feng Xiao Liangzhi xiong Qingxiu Wang Long Zhou Qingshan Zhou Department of Anesthesiology Affiliated Taihe Hospital of Yunyang Medical College Shiyan 442000 Hubei Province China Department of Anesthesiology Shanghai East Hospital Affiliated to Tongji University Shanghai 200120 China Department of Anesthesiology People＇s Hospital Affiliated to Wuhan University Medical College Wuhan 430070 Hubei Province China

A model of cerebral ischemia and reperfusion was established in *** were treated with ketamine via intraperitoneal injection immediately following ischemia or ischemia/*** did not remarkably change infarct volume in mice immediately following ischemia,but injection immediately following ischemia/reperfusion significantly decreased infarct *** injection immediately after ischemia or ischemia/reperfusion inhibited c-Jun protein expression in mouse hippocampus,but nuclear factor kappa b expression was *** addition,the Longa scale score for neural impairment was not reduced in mice following cerebral ischemia/*** results indicate that ketamine can protect mice against cerebral ischemia and reperfusion injury by modulating c-Jun protein expression in mouse hippocampus.

关键词： ketamine ischemia/reperfusion c-Jun nuclear factor kappa b infarct volume

Activation of nuclear factor κb and induction of inducible nitric oxide synthase by lipid-associated membrane proteins isolated from Mycoplasma penetrans

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Chinese Medical Journal 2004年第7期117卷 997-1001页

作者：曾焱华吴移谋张文波余敏君朱翠明谭立志 Department of Microbiology

background This study was designed to investigate the potential pathogenicity of Mycoplasma penetrans (M. penetrans) and its molecular mechanisms responsible for the induction of iNOS gene expression in mouse macrophages stimulated by lipid-associated membrane proteins (LAMPs) prepared from M. *** Mouse macrophages were stimulated with M. penetrans LAMPs to assay the production of nitric oxide (NO). The expression of inducible nitric oxide synthase (iNOS) was detected by RT-PCR and Western blotting. The activity of nuclear factor κb (NF-κb) and the effects of pyrrolidine dithiocarbamate (PDTC), an inhibitor of NF-κb, on the production of nitric oxide and the expression of iNOS were also assessed in mouse macrophages treated with M. penetrans LAMPs by indirect immunofluorescence and Western *** M. penetrans LAMPs stimulated mouse macrophages to produce nitric oxide in a dose- and time-dependent manner. The mRNA and protein levels of iNOS were also upregulated in response to LAMP stimulation and inhibited by PDTC treatment. M. penetrans LAMPs were found to trigger NF-κb activation, a possible mechanism for the induction of iNOS *** This study demonstrated that M. penetrans may be an important etiological factor of certain diseases due to the ability of M. penetrans LAMPs to stimulate the expression of iNOS, which is probably mediated through the activation of NF-κb.

关键词： mycoplasma penetrans nuclear factor kappa b nitric oxide synthase membrane proteins

3D-QSAR and action mechanism of potential dual inhibitors towards AP-1 and NF-κb

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Journal of Chemistry and Chemical Engineering 2009年第1期3卷 1-12页

作者： QIAN Li LIAO Si-yan MIAO Ti-fang SHEN Yong ZHENG Kang-cheng School of Chemistry and Chemical Engineering Sun Yat-Sen University Guangzhou 510275 China

Three-dimensional quantitative structure-activity relationship （3D-QSAR） and docking studies of a series of novel dioxopyrrolinyl-amino-pyrimidine derivatives, which are potential dual inhibitors mediating a transcriptional activation towards protein-1 （AP-1） and nuclear factor kappa b （NF-κb）, have been carried out. The QS, AR models established by comparative molecular field analysis （CoMFA） and comparative molecular similarity index analysis （CoMSIA） show a good predictive ability with cross-validated coefficients q2 of 0.644 and 0.636, respectively. The docking result shows that there are quite lower average values of the flexible and rigid energy scores on the selected binding sites, meanwhile, it further shows that the binding sites just fall on the joint regions between AP-1 （and NF-κb） and DNA. The reason that these analogues have inhibition function towards AP-I and NF-κb is that their existence on these joint regions can effectively prevent free AP-I and NF-κb from binding to DNA. These results can offer a valuable theoretical reference to the pharmaceutical molecular design as well as the action mechanism analysis.

关键词： pyrimidine derivative 3D-QSAR docking analysis activator protein-1 nuclear factor kappa b

Protection of carbon monoxide-releasing molecule against lung injury induced by limb ischemia-reperfusion

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Chinese Journal of Traumatology 2009年第2期12卷 71-76页

作者：周君琳李钢海涌关立黄新莉孙鹏 Department of Orthopedics Beijing ChaoyangHospital Capital Medical University Beijing 100020 China Peking North Hospital of Ministry of Ordance Industryof China Beijing 100089 China Department of Pathophysiology Hebei MedicalUniversity Shijiazhuang 050017China

Objective： To observe the role and mechanism of CO- releasing molecule （CORM）-2 in lung injury induced by ischemia-reperfusion （IR） of hind limbs in rats. Methods： Arat model of lung injury induced by IR of hind limbs was established. A total of 40 Sprague Dawley （SD） rats were randomly divided into 5 groups （n = 8）： sham, sham ＋ CORM-2, IR, IR ＋ CORM-2 and IR ＋ dimethyl sulfoxide （DMSO）. Rats in the IR group received hind limb ischemia for 2 hours and reperfusion for 2 hours, rats in the sham group underwent sham surgery without infrarenal aorta occlusion, rats in the IR＋CORM-2 group and in the sham ＋ CORM-2 group were given CORM-2 （10 μmol/kg intravenous bolus） 5 minutes before reperfusion or at the corresponding time points, while rats in the IR ＋ DMSO group was treated with the same dose of vehicle （DMSO） at the same time. The lung tissue structure, polymorphonuclear neutrophil （PMN） count, wet-to-dry weight ratio （W/D）, malondialdehyde （MDA） content, myeloperoxidase （MPO） activity, intercellular adhesion molecule- 1 （ICAM- 1）expression, I κbα degradation and nuclear factor （NF）-κb activity in the lungs were assessed. Results： As compared with the sham group, lung PMNs number, W/D, MDA content, MPO activity, ICAM-1 expression and NF- κb activity significantly increased in the IR group, but the level of I κbα decresed （P〈0.01）. Compared with the IR group, lung PMNs number, W/D, MDA content, MPO activity and ICAM- 1 expression significantly decreased in the IR＋COMR-2 group （P〈0.01）, while the level of Iκbα increased. Conclusions： These data demonstrate that CORM-2 attenuates limb IR-induced lung injury through inhibiting ICAM-1 protein expression, NF-κb pathway and the leu- kocytes sequestration in the lungs following limb IR in rats, suggesting that CORM-2 may be used as a therapeutic agent against lung injury induced by limb IR.

关键词： Carbon monoxide Lung Reperfusioninjury nuclear factor kappa b

Experimental study on the invasiveness inhibition of bladder cancer cells by nuclear factor-κb decoy——circular dumbbell oligodeoxynucleotides

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The Chinese-German Journal of Clinical Oncology 2006年第6期5卷 438-441页

作者： bo Wen Siwei Zhou Weimin Yang Guohao Li Zhen Liu Huifang Liang Department of Urology Tongji Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan 430030 China Department of Immunology Tongji Medical College Huazhong University of Science and Technology Wuhan 430030 China

Objective:To determine whether NF-κb is constitutively activated in human bladder cancer cell and,if so,to deter-mine the invasiveness inhibition of bladder cancer cells by nuclear factor-κb decoy—circular dumbbell oligodeoxynucleotides(CD-ODN).Methods:NF-κbp65 activation was determined by immunohistochemical analysis of formalin-fixed,paraffin-embed-ded specimens from 38 cases of bladder transitional cell carcinoma *** quantified nuclear staining of RelA as a marker of NF-κbp65 ***-ODN were transfected into human bladder cancer cell line bIU87 by *** reporter were applied to detecting NF-κb DNA binding *** expression levels of uPA were detected by RT-PCR and the cells’ invasion ability by transwell cell culture ***:P65 excessive activation existed in tumor cell(Pb in bIU87 cell line was suppressed remarkably,the expression level of uPA was decreased and the cells’ invasiveness was weakened as ***:Excessively activated NF-κb is related to tumor progression pos-sibly due to its transcriptional regulation of invasion-related factors such as ***-ODN can efficiently suppress DNA binding activity of NF-κb to reduce the invasive potency of tumor.

关键词： decoy strategy nuclear factor kappa b bladder cancer