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Steroids reduce local inflammatory mediator secretion and mucosal permeability in collagenous colitis patients

World Journal of Gastroenterology 2006年第43期12卷 7012-7018页

作者： Yesuf Taha Yngve Raab Marie Carlson Anders Larsson Mikael Lrdal Lars Lf Magnus Thrn Departments of Medical Sciences University Hospital Uppsala Sweden Department of Medicine KarolinskaInstitutet Karolinska University Hospital Huddinge Sweden Departments of Medical Sciences University Hospital Uppsala Sweden Departments of Clinical Chemistry University Hospital Uppsala Sweden Department of Medicine KarolinskaInstitutet Karolinska University Hospital Huddinge Sweden Center for Clinical Research Central Hospital Vsters Sweden Department of Surgery Karolinska Institutet South Stockholm General Hospital Stockholm Sweden

AIM：. To study the effect of oral steroids upon clinical response and rectal mucosa secretion of eosinophil cationic protein （ECP）, myeloperoxidase （NPO）, basic fibroblast growth factor （bFGF）, vascular endothelial growth factor （VEGF） and albumin in patients with collagenous colitis （CC）. METHODS： A segmental perfusion technique was used to collect perfusates from rectum of CC patients once before and twice （one and four weeks） after the start of steroid treatment. Clinical data was monitored and ECP, MPO, bFGF, VEGF and albumin concentrations were analyzed by immunochemical methods in perfusates and in serum. RESULTS： Steroids reduced the number of bowel movements by more than five times within one week and all patients reported improved subjective wellbeing at wk 1 and 4. At the same time, the median concentrations of ECP, bFGF, VEGF and albumin in rectal perfusates decreased significantly. MPO values were above the detection limit in only 3 patients before treatment and in none during treatment. VEGF, bFGF, ECP and albumin concentrations correlated with each other with the exception of ECP and albumin. A decrease of serum ECP and VEGF concentrations was also seen even if the overtime reduction was not significant.CONCLUSION： Oral steroid treatment in CC patients induced a simultaneous reduction of bowel movements and rectal release of ECP, bFGF, VEGF and albumin, suggesting that these polypeptides and increased mucosal permeability are important components of the pathophysiology in collagenous colitis.

关键词： Collagenous colitis inflammatory mediator Steroid treatment Eosinophil cationic protein Basicfibroblast growth factor Vascular endothelial growthfactor

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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

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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

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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 *** addition to respiratory symptoms,COVID-19 is usually accompanied by systemic inflammation and liver damage in moderate and severe *** 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 ***,we show the novel reciprocal regulation between NRF2 and inflammatory mediators associated with COVID-19-related liver ***,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

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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 mo

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

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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

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Antipyretic and anti-inflammatory activities of Thais luteostoma extracts and underlying mechanisms

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Chinese Journal of Natural Medicines 2015年第3期13卷 192-198页

作者： LIU Xin TANG Yu-Ping LIU Rui JIN Yi GUO Jian-Ming ZHAO Jin-Long DING Shao-Xiong LIN Xiang-Zhi LIN Ru-Rong DUAN Jin-Ao Jiangsu Collaborative Innovation Center of Chinese Medicinal Resources Industrialization and National and Local Collaborative Engineering Center of Chinese Medicinal Resources Industrialization and Formulae Innovative Nanjing University of Chinese Medicine College of Ocean and Environment Xiamen University Third Institute of Oceanography State Oceanic Administration

Thais luteostoma has been utilized as a crude drug whose shell and soft tissue have been widely used for the treatment of heat syndrome in China for thousands of years. The present study was designed to investigate the antipyretic and anti-inflammatory activities of T. luteostoma. T. luteostoma was divided into shell （TLSH） and soft tissue （TLST） samples in the present study. The rat model of yeast-induced fever was used to investigate their antipyretic effects; and the rat model of hind paw edema induced by carrageenan was utilized to study their anti-inflammatory activities, and at the same time, the concentration variations of the central neurotransmitter [prostaglandin E2 （PGE2） and cyclic adenosine monophosphate （cAMP）], inflammatory mediators [tumor necrosis factor （TNFα）, interleukin-1β （IL-1）, interleukin-2 （IL-2） and interleukin-6 （IL-6）] and ion （Na^＋ and Ca^2＋） were also tested. The results showed that TLSH and TLST extracts significantly inhibited yeast-induced pyrexia in rats （P 〈 0.05）, and exhibited more lasting effects as compared to aspirin, and TLSH had the better antipyretic activity than TLST, and that TLSH and TLST could significantly prevent against carrageenan induced paw edema in rats （P 〈 0.05）; and markedly reduced levels of PGE2, cAMP, TNFα, IL-1β, IL-2, IL-6, and Na^＋/Ca^2＋. In fever model, TLST could significantly reduce the levels of PGE2 （P 〈 0.01） in rats＇ homogenate and TNF a （P 〈 0.05）, IL-113 （P 〈 0.01） in the plasma than TLSH, whereas TLSH could reduce the content of IL-2 （P 〈 0.01） and IL-6 （P 〈 0.01） in plasma and increase the content of Ca2＋（P 〈 0.01） in plasma and homogenate more significantly than TLST. In conclusion, T. luteostoma extract has antipyretie and anti-inflammatory activities, which may be mediated through the suppression of production of PGE2, cAMP, Na^＋/Ca^2＋ , TNF a, IL-1β, IL-2, and IL-6.

关键词： Marine organism Thais luteostoma Antipyretic Anti-inflammatory inflammatory mediator

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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

PURPOSE: To 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 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-alpha and interleukin-1 alpha 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 th

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

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Understanding the mechanisms underlying obesity in remodeling the breast tumor immune microenvironment:from the perspective of inflammation

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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 *** 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-induced inflammation has become the focus of research ***,the development of cancer involves a complex interaction with numerous *** 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 *** 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 *** 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 *** 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

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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

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