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Cancer Biology & Medicine 2023年第4期20卷 268-286页

作者： Hengjun Zhang Mozhi Wang Yingying Xu Department of Breast Surgery The First Hospital of China Medical UniversityShenyang 110001China

Obesity is a well-known modifiable risk factor for breast cancer and is considered a poor prognostic factor in pre-and post-menopausal women.While the systemic effects of obesity have been extensively studied,less is known about the mechanisms underlying obesityassociated cancer risk and the local consequences of obesity.Thus,obesity-induced inflammation has become the focus of research interest.Biologically,the development of cancer involves a complex interaction with numerous components.As the tumor immune microenvironment changes due to obesity-triggered inflammation,an increase in infiltration occurs for proinflammatory cytokines and adipokines,as well as adipocytes,immune cells,and tumor cells in the expanded adipose tissue.Complicated cellular-molecular crosstalk networks change critical pathways,mediate metabolic and immune function reprogramming,and have a significant role in tumor metastasis,proliferation,resistance,angiogenesis,and tumorigenesis.This review summarizes recent research findings on how inflammatory mediators in the in situ tumor microenvironment regulate the occurrence and development of breast cancer in the context of obesity.We analyzed the heterogeneity and potential mechanisms of the breast cancer immune microenvironment from the perspective of inflammation to provide a reference for the clinical transformation of precision targeted cancer therapy.

关键词： Breast cancer obesity inflammatory mediator tumor microenvironment metabolism

Aerosolized STAT1 Antisense Oligodeoxynucleotides Decrease the Concentrations of inflammatory mediators in Bronchoalveolar Lavage Fluid in Bleomycin-Induced Rat Pulmonary Fibrosis

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Cellular & Molecular Immunology 2008年第3期5卷 219-224页

作者： Ming Zeng Bin Liao Chen Zhu Wenjun Wang Xiaoqin Zhan Xianming Fan The Department of Respiratory Medicine Affiliated Hospital of Luzhou Medical College Luzhou 646000 China The Department of Cardiothoracic Surgery Affiliated Hospital of LuzhouMedical College Luzhou 646000 China Department of Respiratory Medicine Affiliated Hospital of Luzhou Medical College Luzhou 646000 China.

It has been demonstrated that alveolar macrophages （AMs） play a key role in the pathogenesis of pulmonary fibrosis by releasing a variety of cytokines and inflammatory mediators. In addition, abnormal signal transducer and activator of transcription-1 （STAT1） activation in AMs may play a pivotal role in the process of alveolitis and pulmonary fibrosis. In this study, we transfected STAT1 antisense oligodeoxynucleotide （ASON） into rats by aerosolization, and then investigated the effect of STAT1 ASON on inflammatory mediators such as TGF-β, PDGF and TNF-α in bronchoalveolar lavage fluid （BALF） from rats with bleomycln （BLM）-induced rat pulmonary fibrosis. Our results showed that STAT1 ASON by aerosolization could enter into lung tissues and AMs. STAT1 ASON could inhibit mRNA and protein expressions of STAT1 and ICAM-1 in AMs of rat with pulmonary fibrosis, and had no toxic side effect on liver and kidney. Aerosolized STAT1 ASON could ameliorate the alveolitis through inhibiting the secretion of inflammatory mediators in BLM-induced rat pulmonary fibrosis. These results suggest that aerosolized STAT1 ASON might be considered as a promising new strategy in the treatment of pulmonary fibrosis.

关键词： pulmonary fibrosis STAT1 ASON aerosolization inflammatory mediator

Cationic antimicrobial protein of Mr 37 kDa:a multifunctional inflammatory protein

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Chinese Medical Journal 2001年第1期114卷 9-13页

作者： H.Anne Pereira Department of Pathology University of Oklahoma Health Sciences CenterOklahoma 73190USA

investigate the role of cationic antimicrobial protein of Mr 37?kDa (CAP37) a neutrophil derived inflammatory mediator on endothelial cell function Data sources Endothelial cells used in this study were obtained from human lung microvessels and rat aorta The latter was a kind gift of Dr Paula Grammas The mono mac 6 cell line used in this study was the generous gift of Dr H W Loms Ziegler Heitbrock Study selection and data extraction Endothelial cell proteins kinase C activity was determined by measuring calcium and phospholipid dependent phosphorylation of histone Endothelial cell migration was determined using Costar TM Transwell apparatus Cell surface expression of adhesion molecules, ICAM 1 and PECAM 1 was determined using flow cytometry RT PCR was used to amplify the CAP37 from endothelial cells treated with LPS Results We demonstrated that CAP37 which was originally identified as having potent antimicrobial activity and chemotactic activity for monocytes was capable of modulating endothelial cell functions CAP37 activated endothelial cell protein kinase C in a dose and time dependent fashion Importantly CAP37 increased the adhesive properties of the endothelium for monocytes CAP37 upregulated the well known adhesion molecules, ICAM 1 and PECAM 1 in a dose and time dependent manner In addition, CAP37 promoted endothelial cell migration Further investigations indicated that CAP37 was induced in endothelial cells in response to pro inflammatory cytokines such as tumor necrosis factor α and interleukin 1α as well as inflammatory mediators such as lipopolysaccharide Unstimulated endothelial cells did not constitutively express CAP37 The cDNA sequence of endothelial CAP37 was determined and found to be highly homologous to the sequence obtained for neutrophil derived CAP37 Conclusions Our studies strongly suggest that CAP37 plays a pivotal role in monocyte endothelial interactions and the transmigration of monocytes from the vasculature into extravascular

关键词： cationic antimicrobial protein Mr 37 kDa inflammatory mediator function

Fingolimod alters inflammatory mediators and vascular permeability in intracerebral hemorrhage

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Neuroscience Bulletin 2015年第6期31卷 755-762页

作者： Yu-Jing Li Guo-Qiang Chang Yuanchu Liu Ye Gong Chunsheng Yang Kristofer Wood Fu-Dong Shi Ying Fu Yaping Yan Department of Neurology Tianjin Neurological InstituteTianjin Medical University General Hospital Key Laboratory of the Ministry of Education for Medicinal Resources and Natural Pharmaceutical Chemistry National Engineering Laboratory for Resource Development of Endangered Crude Drugs in Northwest ChinaCollege of Life SciencesShaanxi Normal University Department of Neurology Barrow Neurological InstituteSt. Joseph's Hospital and Medical Center

Intracerebral hemorrhage （ICH） leads to high rates of death and disability. The pronounced inflammatory reactions that rapidly follow ICH contribute to disease progression. Our recent clinical trial demonstrated that oral administration of an immune modulator fingolimod restrained secondary injury derived from initial hematoma, but the mechanisms remain unknown. In this study, we aim to investigate the effects of fingolimod on inflammatory mediators and vascular permeability in the clinical trial of oral fingolimod for intracerebral hemorrhage （ICH）. The results showed that fingolimod decreased the numbers of circulating CD4~ T, CD8~ T, CD19~ B, NK, and NKT cells and they recovered quickly after the drug＇ was stopped. The plasma ICAM level was decreased and IL-10 was increased by fingolimod. Interestingly, fingolimod protected vascular permeability as indicated by a decreased plasma level of MMP9 and the reduced rT1%. In conclusion, modulation of systemic inflammation by fingolimod demonstrates that it is an effective therapeutic agent for ICH. Fingolimod may prevent perihematomal edema enlargement by protecting vascular permeability.

关键词： fingolimod inflammatory mediator vascular permeability intracerebral hemorrhage

Interplay between nuclear factor erythroid 2-related factor 2 and inflammatory mediators in COVID-19-related liver injury

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World Journal of Gastroenterology 2021年第22期27卷 2944-2962页

作者： Dan-Dan Zhu Xue-Mei Tan Li-Qing Lu Si-Jia Yu Ru-Li Jian Xin-Fang Liang Yi-Xuan Liao Wei Fan LucíiaBarbier-Torres Austin Yang He-Ping Yang Ting Liu Department of Gastroenterology Xiangya HospitalCentral South UniversityChangsha 410008Hunan ProvinceChina Key Laboratory of Cancer proteomics of Chinese Ministry of Health Xiangya HospitalCentral South UniversityChangsha 410008Hunan ProvinceChina Department of Medicine Division of Digestive and Liver DiseasesCedars-Sinai Medical CenterLos AngelesCA 90048United States Department of Biology East Los Angeles CollegeLos AngelesCA 91008United States

Coronavirus disease 2019(COVID-19)caused by severe acute respiratory syndrome coronavirus 2 is a global pandemic and poses a major threat to human health worldwide.In addition to respiratory symptoms,COVID-19 is usually accompanied by systemic inflammation and liver damage in moderate and severe cases.Nuclear factor erythroid 2-related factor 2(NRF2)is a transcription factor that regulates the expression of antioxidant proteins,participating in COVID-19-mediated inflammation and liver injury.Here,we show the novel reciprocal regulation between NRF2 and inflammatory mediators associated with COVID-19-related liver injury.Additionally,we describe some mechanisms and treatment strategies.

关键词： COVID-19-related liver injury Nuclear factor erythroid 2-related factor 2 inflammatory mediator Oxidative stress Therapeutic targets

Effects of realgar on stress proteins, inflammatory mediators, and complement in brain tissue and serum of rats with inflammatory brain injury

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Neural Regeneration Research 2008年第8期3卷 885-889页

作者： Yishan Tang Ningsheng Wang Yinqing Zhang Shaomei Ye Weiping Ou Institute of Clinical Pharmacology Guangzhou University of Traditional Chinese Medicine Guangzhou 510405 Guangdong Province China

BACKGROUND：The Chinese herbal compound realgar exerts detoxification effects as an adjuvant. It is suggested that realgar exerts detoxification via the following pathways： in the pathological state, realgar corrects the oxidative stress state by increasing stress levels, activating some endogenous protective factors and antagonizing the excessive release of inflammatory factors, as well as inhibiting complement activation. OBJECTIVE： To observe the changes in stress proteins, inflammatory mediators, and complement in the brain tissue and serum of rats with inflammatory brain injury, which have been treated with the Chinese herbal compound Angong Niuhuang, and to compare the efficacy of Angong Niuhuang with that of realgar, to verify the mechanism of action of realgar. DESIGN, TIME AND SETTING： Randomized, controlled, cytological experiment, performed in the Institute of Clinical Pharmacology, Guangzhou University of Traditional Chinese Medicine in March 2006. MATERIALS： Thirty-six healthy, male, Sprague Dawley rats received 250 U/kg Bordetella pertussis via the common carotid artery within 15 seconds to induce inflammatory brain injury. Reagents and kits were as follows： Realgar and Angong Niuhuang powder （Foshan Second Pharmaceutical Factory, China）, Bordetella pertussis diagnostic antigen （National Institute for the Control of Pharmaceutical and Biological Products, China）, heat shock protein 70 （HSP70） enzyme-labeled immunosorbent assay （ELISA） kit （Stressgen, USA）, tumor necrosis factor-α （TNF-α） ELISA kit （Biosource, USA）, nitric oxide synthase （NOS） kit, Coomassie brilliant blue protein kit （Nanjing Jiancheng Bioengineering Co.,Ltd., China）, and complements C3 and C4 （Shanghai Kehua Dongling Diagnositic Products Co.,Ltd., China）. METHODS： Thirty-six rats were randomly and evenly divided into the following six groups： normal control, model, high-, middle-, and low-dose realgar-treated, and Angong Niuhuang-treated groups. At one hour prior to establishing the model, rats in the high-, middle-, and low-dose re

关键词： realgar Angong Niuhuang powder stress protein inflammatory mediator complement inflammatory brain injury

The Effects of Aerosolized STAT1 Antisense Oligodeoxynucleotides on Rat Pulmonary Fibrosis

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Cellular & Molecular Immunology 2009年第1期6卷 51-59页

作者： Wenjun Wang Bin Liao Ming Zeng Chen Zhu Xianming Fan The Department of Respiratory Medicine Affiliated Hospital of Luzhou Medical College Luzhou 646000 China The Department of Cardiothoracic Surgery Affiliated Hospital of Luzhou Medical College Luzhou 646000 China

Previous study showed that aerosolized signal transducer and activator of transcription-1 （STAT1） antisense oligodeoxynucleotide （ASON） inhibited the expression of STAT1 and ICAM-1 mRNA and protein in alveolar macrophages （AMs） and decreased the concentrations of TGF-β, PDGF and TNF-α in bronchioalveolar lavage fluid （BALF） in bleomycin （BLM）-induced rat pulmonary fibrosis. Administration of STAT1 ASON ameliorated alveolitis in rat pulmonary fibrosis. However, further investigations are needed to determine whether there is an effect from administration of STAT1 ASON on fibrosis. This study investigated the effect of aerosolized STAT1 ASON on the expressions of inflammatory mediators, hydroxyproline and type Ⅰ and type Ⅲcollagen mRNA in BLM-induced rat pulmonary fibrosis. The results showed that STAT1 ASON applied by aerosolization could ameliorate alveolitis and fibrosis, inhibit the expressions of inflammatory mediators, decrease the content of hydroxyproline, and suppress the expressions of type Ⅰand type Ⅲcollagen mRNA in lung tissue in BLM-induced rat pulmonary fibrosis. These results suggest that aerosolized STAT1 ASON might be considered as a promising new strategy in the treatment of pulmonary fibrosis. Cellular ＆ Molecular Immunology.

关键词： pulmonary fibrosis STAT1 ASON inflammatory mediator type Ⅰ and type Ⅲcollagen mRNA

EFFECTS OF FILTER MEMBRANES ADSORBING inflammatory mediatorS IN HEMOFILTRATI ON

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Journal of Pharmaceutical Analysis 2004年第2期16卷 164-166,187页

作者：蒋红利薛武军尹爱萍李大庆鞠峰炽孔澍 Hemodialysis Center First Hospital of Xi'an Jiaotong University Xi'an 710061 China Department of Biomedical Engineering XianJiaotong UniversityXian710053China

Objective In this study, an in vitro hemofiltration model was set up to investigate adsorptive saturati on time of different membrane under different blood flow rate (Q B)and filt rate rate(Q F). Methods Anticoagulated cattle blood (2000 mL per bag) was stimulated with 1μg·mL -1 endotoxin to induce i nflammatory mediators before hemofiltration (HF) using AN69, PS and PMMA filters in vitro. Adsorptive saturation time of membrane was observed using data br idge in different Q B and different Q F. TNF was measured by radioimmu noassays. Results Before the resistance level reached the peak value in the same group, resistance level increased significantly (P05). It was suggested tha t the resistance level reached plateau at 150,120,90,120, and150 minutes in Q F of 100 mL·minute -1, 200 mL·minute -1, 300 mL·minute -1 , respectively and in Q F of 1L·hour -1, 2L·hour -1, 4L·hour -1, respectively. And with the Q B and Q F increasing, resistanc e level increased significantly (P<0.01) among different groups at the same time point in A, B, C, D and E group. Conclusion Membrane resis tance level online measured by Data Bridge can instantly reflect the degree of m embrane adsorption. Adsorptive saturation time of filter membrane in different f iltration flow rate and blood flow rate are different.

关键词： hemofiltration inflammatory mediator adsorption filter membrane

EFFECT OF HIGH TIDAL VOLUME VENTILATION AND LIPOPOLYSACCHARIDE ON MITOGEN-ACTIVATED PROTEIN KINASE IN RAT LUNG TISSUE

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Chinese Medical Journal 2006年第1期119卷 53-56页

作者： QIU Hai-bo LU Xiao-min ZHOU Shao-xia YANG Yi GUO Feng-mei Department of Critical Care Medicine Zhong-da Hospital and School of Clinical Medicine Southeast University Nanjing 210009 China

Mechanical ventilation, a crucial therapy to acute respiratory distress syndrome （ARDS）,could exacerbate lung injury, and even result in ventilator-induced lung injury （VILI） if misused in some condition1. Over-activating inflammatory cells and expanding inflammatory responses, which are induced by infection, are fundamental reasons for ARDS. Among them,

关键词： mechanical ventilation high tidal volume lipopolysaccharide mitogen-activated protein kinase inflammatory mediator

Sepsis and immune response

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World Journal of Emergency Medicine 2011年第2期2卷 88-92页

作者： Xing-hai Chen Yong-jie Yin Jing-xiao Zhang Department of Emergency Medicine Second Hospital of Jilin University Changchun 130041 China

BACKGROUND:Sepsis and secondary multiple organ failure in critically ill patients are the major cause of death, but the pathogenesis of sepsis is not clear, especially the dysfunction of the immune system. In this paper, we review the response and regulation of the immune system and the functions of a variety of inflammatory mediators in sepsis.;METHODS:Studies were identified by searching MEDLINE and PubMed for articles using the keywords "sepsis", "immune response", and "inflammatory mediator" up to October 2010. Additional papers were identified by a manual search of the references from the key articles.;RESULTS:THIS SYSTEMATIC REVIEW WAS CONDUCTED OF: 1) the immune response; 2) immune regulation; 3) inflammatory mediators; 4) high-mobility group box 1 protein; 5) the complement system; and 6) the autonomic nervous system. There are no therapeutic approaches available for sepsis that target inflammatory response; the mortality of sepsis has not been significantly reduced.;CONCLUSIONS:Sepsis is complex and dynamic, and it has a group of heterogeneous syndromes. Since different patients with sepsis have different etiology, susceptibility, and responses, treatment should be prescribed individually.

关键词： Immune response inflammatory mediator Sepsis