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MicroRNA-451 from Human Umbilical Cord-Derived Mesenchymal Stem Cell Exosomes Inhibits Alveolar Macrophage Autophagy via Tuberous Sclerosis Complex 1/Mammalian Target of Rapamycin Pathway to Attenuate Burn-Induced Acute Lung Injury in Rats
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作者 Zhigang Jia Lin Li +5 位作者 Peng Zhao Guo Fei Shuangru Li Qinqin Song Guangpeng Liu Jisong Liu 《Biomedical and Environmental Sciences》 SCIE CAS CSCD 2024年第9期1030-1043,共14页
Objective Our previous studies established that microRNA(miR)-451 from human umbilical cord mesenchymal stem cell-derived exosomes(hUC-MSC-Exos)alleviates acute lung injury(ALI).This study aims to elucidate the mechan... Objective Our previous studies established that microRNA(miR)-451 from human umbilical cord mesenchymal stem cell-derived exosomes(hUC-MSC-Exos)alleviates acute lung injury(ALI).This study aims to elucidate the mechanisms by which miR-451 in hUC-MSC-Exos reduces ALI by modulating macrophage autophagy.Methods Exosomes were isolated from hUC-MSCs.Severe burn-induced ALI rat models were treated with hUC-MSC-Exos carrying the miR-451 inhibitor.Hematoxylin-eosin staining evaluated inflammatory injury.Enzyme-linked immunosorbnent assay measured lipopolysaccharide(LPS),tumor necrosis factor-α,and interleukin-1βlevels.qRT-PCR detected miR-451 and tuberous sclerosis complex 1(TSC1)expressions.The regulatory role of miR-451 on TSC1 was determined using a dual-luciferase reporter system.Western blotting determined TSC1 and proteins related to the mammalian target of rapamycin(mTOR)pathway and autophagy.Immunofluorescence analysis was conducted to examine exosomes phagocytosis in alveolar macrophages and autophagy level.Results hUC-MSC-Exos with miR-451 inhibitor reduced burn-induced ALI and promoted macrophage autophagy.MiR-451 could be transferred from hUC-MSCs to alveolar macrophages via exosomes and directly targeted TSC1.Inhibiting miR-451 in hUC-MSC-Exos elevated TSC1 expression and inactivated the mTOR pathway in alveolar macrophages.Silencing TSC1 activated mTOR signaling and inhibited autophagy,while TSC1 knockdown reversed the autophagy from the miR-451 inhibitor-induced.Conclusion miR-451 from hUC-MSC exosomes improves ALI by suppressing alveolar macrophage autophagy through modulation of the TSC1/mTOR pathway,providing a potential therapeutic strategy for ALI. 展开更多
关键词 acute lung injury Human umbilical cord mesenchymal stem cell-derived exosomes MicroRNA-451 Tuberous sclerosis complex 1 Mammalian target of rapamycin pathway AUTOPHAGY
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Mogroside IIE,an in vivo metabolite of sweet agent,alleviates acute lung injury via Pla2g2a-EGFR inhibition
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作者 Weichao Lü Guoqing Ren +2 位作者 Kuniyoshi Shimizu Renshi Li Chaofeng Zhang 《Food Science and Human Wellness》 SCIE CSCD 2024年第1期299-312,共14页
In the face of increasingly serious environmental pollution,the health of human lung tissues is also facing serious threats.Mogroside IIE(M2E)is the main metabolite of sweetening agents mogrosides from the anti-tussiv... In the face of increasingly serious environmental pollution,the health of human lung tissues is also facing serious threats.Mogroside IIE(M2E)is the main metabolite of sweetening agents mogrosides from the anti-tussive Chinese herbal Siraitia grosvenori.The study elucidated the anti-inflammatory action and molecular mechanism of M2E against acute lung injury(ALI).A lipopolysaccharide(LPS)-induced ALI model was established in mice and MH-S cells were employed to explore the protective mechanism of M2E through the western blotting,co-immunoprecipitation,and quantitative real time-PCR analysis.The results indicated that M2E alleviated LPS-induced lung injury through restraining the activation of secreted phospholipase A2 type IIA(Pla2g2a)-epidermal growth factor receptor(EGFR).The interaction of Pla2g2a and EGFR was identified by co-immunoprecipitation.In addition,M2E protected ALI induced with LPS against inflammatory and damage which were significantly dependent upon the downregulation of AKT and m TOR via the inhibition of Pla2g2a-EGFR.Pla2g2a may represent a potential target for M2E in the improvement of LPS-induced lung injury,which may represent a promising strategy to treat ALI. 展开更多
关键词 Mogroside IIE acute lung injury Secreted phospholipase A2 type IIA(Pla2g2a) Epidermal growth factor receptor(EGFR)
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Impact of interleukin 6 levels on acute lung injury risk and disease severity in critically ill sepsis patients
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作者 Ya Liu Li Chen 《World Journal of Clinical Cases》 SCIE 2024年第23期5374-5381,共8页
BACKGROUND Sepsis is a life-threatening condition characterized by a dysregulation of the host response to infection that can lead to acute lung injury(ALI)and multiple organ dysfunction syndrome(MODS).Interleukin 6(I... BACKGROUND Sepsis is a life-threatening condition characterized by a dysregulation of the host response to infection that can lead to acute lung injury(ALI)and multiple organ dysfunction syndrome(MODS).Interleukin 6(IL-6)is a pro-inflammatory cytokine that plays a crucial role in the pathogenesis of sepsis and its complications.AIM To investigate the relationship among plasma IL-6 levels,risk of ALI,and disease severity in critically ill patients with sepsis.METHODS This prospective and observational study was conducted in the intensive care unit of a tertiary care hospital between January 2021 and December 2022.A total of 83 septic patients were enrolled.Plasma IL-6 levels were measured upon admission using an enzyme-linked immunosorbent assay.The development of ALI and MODS was monitored during hospitalization.Disease severity was evaluated by Acute Physiology and Chronic Health Evaluation II(APACHE II)and Sequential Organ Failure Assessment(SOFA)scores.RESULTS Among the 83 patients with sepsis,38(45.8%)developed ALI and 29(34.9%)developed MODS.Plasma IL-6 levels were significantly higher in patients who developed ALI than in those without ALI(median:125.6 pg/mL vs 48.3 pg/mL;P<0.001).Similarly,patients with MODS had higher IL-6 levels than those without MODS(median:142.9 pg/mL vs 58.7 pg/mL;P<0.001).Plasma IL-6 levels were strongly and positively correlated with APACHE II(r=0.72;P<0.001)and SOFA scores(r=0.68;P<0.001).CONCLUSIONElevated plasma IL-6 levels in critically ill patients with sepsis were associated with an increased risk of ALI andMODS.Higher IL-6 levels were correlated with greater disease severity,as reflected by higher APACHE II andSOFA scores.These findings suggest that IL-6 may serve as a biomarker for predicting the development of ALI anddisease severity in patients with sepsis. 展开更多
关键词 SEPSIS acute lung injury Multiple organ dysfunction syndrome INTERLEUKIN-6 BIOMARKER Disease severity
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Research Progress on the Pathogenesis of Acute Lung Injury(ALI)
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作者 Jincun LI Wenyu MA Gang LI 《Medicinal Plant》 2024年第4期122-128,共7页
In this review,the databases searched were PubMed and Web of Science.It is believed that the main causes of acute lung injury(ALI)and acute respiratory distress syndrome(ARDS)are inflammatory response disorders,excess... In this review,the databases searched were PubMed and Web of Science.It is believed that the main causes of acute lung injury(ALI)and acute respiratory distress syndrome(ARDS)are inflammatory response disorders,excessive oxidative stress,cell death,endoplasmic reticulum stress,coagulation dysfunction,and weakened aquaporin function. 展开更多
关键词 acute lung injury(ALI) Pathogenesis Inflammatory responses Oxidative stress Cell death Endoplasmic reticulum stress COAGULOPATHY Downregulation of aquaporin
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Mechanisms and Research Progress of Traditional Chinese Medicine Regulating NF-κB in the Treatment of Acute Lung Injury/Acute Respiratory Distress Syndrome
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作者 Wanzhao Zuo Fanian Tian +3 位作者 Jia Ke Cheng Jiang Yi Yang Cong He 《Chinese Medicine and Natural Products》 CAS 2024年第3期93-105,共13页
Acute lung injury(ALI)has multiple causes and can easily progress to acute respiratory distress syndrome(ARDS)if not properly treated.Nuclear factorκB(NF-κB)is a key pathway in the treatment of ALI/ARDS.By exploring... Acute lung injury(ALI)has multiple causes and can easily progress to acute respiratory distress syndrome(ARDS)if not properly treated.Nuclear factorκB(NF-κB)is a key pathway in the treatment of ALI/ARDS.By exploring the relevance of NF-κB and the pathogenesis of this disease,it was found that this disease was mainly associated with inflammation,dysfunction of the endothelial barrier,oxidative stress,impaired clearance of alveolar fluid,and coagulation disorders.Traditional Chinese medicine(TCM)has the characteristics of multitargeting,multipathway effects,and high safety,which can directly or indirectly affect the treatment of ALI/ARDS.This article summarizes the mechanism and treatment strategies of TCM in recent years through intervention in the NF-κB-related signaling pathways for treating ALI/ARDS.It provides an overview from the perspectives of Chinese herbal monomers,TCM couplet medicines,TCM injections,Chinese herbal compounds,and Chinese herbal preparations,offering insights into the prevention and treatment of ALI/ARDS with TCM. 展开更多
关键词 acute lung injury acute respiratory distress syndrome traditional Chinese medicine NF-ΚB
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Modulating the crosstalk between macrophage and Th17: potential mechanism of natural products on acute lung injury
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作者 Xi-Xing Fang Han-Zhou Li +7 位作者 Ning Wang Wen-Ju He Yu-Lin Wu Li-Ying Guo Li-Wei Xing Wei-Bo Wen Qian-Qian Wan Huan-Tian Cui 《Biomedical Engineering Communications》 2024年第3期31-37,共7页
Sepsis is a life-threatening multiple organ dysfunction syndrome caused by the imbalance of the immune response to infection,featuring complex and variable conditions,and is one of the leading causes of mortality in I... Sepsis is a life-threatening multiple organ dysfunction syndrome caused by the imbalance of the immune response to infection,featuring complex and variable conditions,and is one of the leading causes of mortality in ICU patients.Lung injury is a common organ damage observed in sepsis patients.Macrophages and Th17 cells,as crucial components of innate and adaptive immunity,play pivotal roles in the development of sepsis-induced acute lung injury(ALI).This review summarizes the alterations and mechanisms of macrophages and Th17 cells in sepsis-induced ALI.By focusing on the“cross-talk”between macrophages and Th17 cells,this review aims to provide a solid theoretical foundation for further exploring the therapeutic targets of traditional Chinese medicine formulas in the treatment of sepsis complicated with ALI,thereby offering insights and guidance for the clinical application of traditional Chinese medicine in managing sepsis-associated ALI. 展开更多
关键词 sepsis-induced acute lung injury MACROPHAGES Th17 cells traditional Chinese medicine
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Acute lung injury and ARDS in acute pancreatitis: Mechanisms and potential intervention 被引量:66
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作者 Roland Andersson 《World Journal of Gastroenterology》 SCIE CAS CSCD 2010年第17期2094-2099,共6页
Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) in acute pancreatitis still represents a substantial problem,with a mortality rate in the range of 30%-40%.The present review evaluates underlying... Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) in acute pancreatitis still represents a substantial problem,with a mortality rate in the range of 30%-40%.The present review evaluates underlying pathophysiological mechanisms in both ALI and ARDS and potential clinical implications.Several mediators and pathophysiological pathways are involved during the different phases of ALI and ARDS.The initial exudative phase is characterized by diffuse alveolar damage,microvascular injury and influx of inflammatory cells.This phase is followed by a fibro-proliferative phase with lung repair,type Ⅱ pneumocyte hypoplasia and proliferation of fibroblasts.Proteases derived from polymorphonuclear neutrophils,various pro-inflammatory mediators,and phospholipases are all involved,among others.Contributing factors that promote pancreatitis-associated ALI may be found in the gut and mesenteric lymphatics.There is a lack of complete understanding of the underlying mechanisms,and by improving our knowledge,novel tools for prevention and intervention may be developed,thus contributing to improved outcome. 展开更多
关键词 acute lung injury acute respiratory distress syndrome acute pancreatitis ETIOLOGY PATHOPHYSIOLOGY
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Review:Acute lung injury/acute respiratory distress syndrome (ALI/ARDS): the mechanism,present strategies and future perspectives of therapies 被引量:53
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作者 LUH Shi-ping CHIANG Chi-huei 《Journal of Zhejiang University-Science B(Biomedicine & Biotechnology)》 SCIE CAS CSCD 2007年第1期60-69,共10页
Acute lung injury/acute respiratory distress syndrome (ALI/ARDS), which manifests as non-cardiogcnic pulmonary edema, respiratory distress and hypoxemia, could be resulted from various processes that directly or ind... Acute lung injury/acute respiratory distress syndrome (ALI/ARDS), which manifests as non-cardiogcnic pulmonary edema, respiratory distress and hypoxemia, could be resulted from various processes that directly or indirectly injure the lung. Extensive investigations in experimental models and humans with ALI/ARDS have revealed many molecular mechanisms that offer therapeutic opportunities for cell or gene therapy. Herein the present strategies and future perspectives of the treatment for ALI/ARDS, include the ventilatory, pharmacological, as well as cell therapies. 展开更多
关键词 acute lung injury acute respiratory distress syndrome VENTILATOR Cell therapy
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Therapeutic effects of Caspase-1 inhibitors on acute lung injury in experimental severe acute pancreatitis 被引量:26
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作者 Xiao-Hua Zhang Ren-Min Zhu Wen-An Xu Hai-Jun Wan Heng Lu 《World Journal of Gastroenterology》 SCIE CAS CSCD 2007年第4期623-627,共5页
AIM: To assess the therapeutic effect of Caspase-1 inhibitors (ICE-I) on acute lung injury (ALI) in experimental severe acute pancreatitis (SAP). METHODS: Forty-two SD rats were randomly divided into 3 groups... AIM: To assess the therapeutic effect of Caspase-1 inhibitors (ICE-I) on acute lung injury (ALI) in experimental severe acute pancreatitis (SAP). METHODS: Forty-two SD rats were randomly divided into 3 groups: healthy controls (HC, n = 6); SAP-S group (n = 18); SAP-ICE-i group (n = 18). SAP was induced by retrograde infusion of 5% sodium taurocholate into the bile-pancreatic duct. HC rats underwent the same surgical procedures and duct cannulation without sodium taurocholate infusion, in SAP-S group, rats received the first intraperitoneal injection of isotonic saline 2 h after induction of acute pancreatitis and a repeated injection after 12 h. In SAP-ICE-I group, the rats were firstly given ICE inhibitors intraperitoneally 2 h after induction of pancreatitis. As in SAP-S group, the injection was repeated at 12 h. Serum 1L-1β was measured by EUSA. Intrapulmonary expression of Caspase-1, IL-1β and IL-18 mRNA were detected by semi-quantitative RT-PCR. The wet/dry weight ratios and histopathological changes of the lungs were also evaluated. RESULTS: Serum IL-1β levels in SAP-S group were 276.77 ± 44.92 pg/mL at 6 h, 308.99 ± 34.95 pg/mL at 12 h, and 311.60 ± 46.51 pg/mL at 18 h, which were increased significantly (P 〈 0.01, vs HC). in SAP- ICE-I group, those values were decreased significantly (P 〈 0.01, vs SAP-S). intrapulmonary expression of Caspase-1, IL-1β and IL-18 mRNA were observed in the HC group, while they were increased significantly in the SAP-S group (P 〈 0.01, vs HC). The expression of IL-lβ and IL-18 mRNA were decreased significantly in the SAP- ICE-I group (P 〈 0.01, vs SAP-S), whereas Caspase-1 mRNA expression had no significant difference (P 〉 0.05). The wet/dry weight ratios of the lungs in the SAP-S group were increased significantly (P 〈 0.05 at 6 h, P 〈 0.01 at 12 h and 18 h, vs HC) and they were decreased significantly in the SAP-ICE-I group (P 〈 0.05, vs SAP-S).Caspase-1 inhibitors ameliorated the severity of ALl in SAP.CONCLUSION: Caspase-1 activation, and overproduction of IL-1β and IL-18 play an important role in the course of ALI, and Caspase-1 inhibition is effective for the treatment of ALI in experimental SAP. 展开更多
关键词 Severe acute pancreatitis CASPASE-1 Interleukin-lβ INTERLEUKIN-18 acute lung injury
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Dexmedetomidine Alleviates Pulmonary Edema by Upregulating AQP1 and AQP5 Expression in Rats with Acute Lung Injury Induced by Lipopolysaccharide 被引量:30
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作者 姜远旭 戴中亮 +3 位作者 张雪萍 赵伟 黄强 高利昆 《Journal of Huazhong University of Science and Technology(Medical Sciences)》 SCIE CAS 2015年第5期684-688,共5页
This study aims to elucidate the mechanisms by which dexmedetomidine alleviates pulmonary edema in rats with acute lung injury induced by lipopolysaccharide (LPS). Male Wistar rats were randomly divided into five gr... This study aims to elucidate the mechanisms by which dexmedetomidine alleviates pulmonary edema in rats with acute lung injury induced by lipopolysaccharide (LPS). Male Wistar rats were randomly divided into five groups: normal saline control (NS) group, receiving intravenous 0.9% normal saline (5 mL/kg); LPS group, receiving intravenous LPS (10 mg/kg); small-dose dexmedetomidine (S) group, treated with a small dose of dexmedetomidine (0.5 μg·kg^-1·h^-1); medium-dose dexmedetomidine (M) group, treated with a medium dose of dexmedetomidine (2.5 μg·kg^-1·h^-1); high-dose dexmedetomidine (H) group, treated with a high dose of dexmedetomidine (5μg·kg^-1·h^-1). The rats were sacrificed 6 h after intravenous injection of LPS or NS, and the hmgs were removed for evaluating histological characteristics and determining the lung wet/dry weight ratio (W/D). The levels of tumor necrosis factor-alpha (TNF-α) and interleukin-1β (IL-1β) in the lung tissues were assessed by enzyme-linked immunosorbent assay (ELISA). The mRNA and protein expression levels of aquaporin-1 (AQP1) and aquaporin-5 (AQP5) were detected by RT-PCR, immunohistochemistry, and Western blot- ting. The lung tissues from the LPS groups were significantly damaged, which were less pronounced in the H group but not in the small-dose dexmedetomidine group or medium-dose dexmedetomidine group. The W/D and the concentrations of TNF-α and IL-1β in the pulmonary tissues were increased in the LPS group as compared with those in NS group, which were reduced in the H group but not in S group or M group (P〈0.01). The expression of AQP1 and AQP5 was lower in the LPS group than in the NS group, and significantly increased in the H group but not in the S group or M group (P〈0.01). Our findings suggest that dexmedetomidine may alleviate pulmonary edema by increasing the expression of AQP-1 and AQP-5. 展开更多
关键词 DEXMEDETOMIDINE acute lung injury lung edema AQUAPORIN-1 AQUAPORIN-5
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Circulating miRNAs as biomarkers for severe acute pancreatitis associated with acute lung injury 被引量:22
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作者 Xiao-Guang Lu Xin Kang +3 位作者 Li-Bin Zhan Li-Min Kang Zhi-Wei Fan Li-Zhi Bai 《World Journal of Gastroenterology》 SCIE CAS 2017年第41期7440-7449,共10页
AIM To identify circulating micro(mi)RNAs as biological markers for prediction of severe acute pancreatitis(SAP) with acute lung injury(ALI).METHODS Twenty-four serum samples were respectively collected and classified... AIM To identify circulating micro(mi)RNAs as biological markers for prediction of severe acute pancreatitis(SAP) with acute lung injury(ALI).METHODS Twenty-four serum samples were respectively collected and classified as SAP associated with ALI and SAP without ALI, and the mi RNA expression profiles were determined by microarray analysis. These mi RNAs were validated by quantitative reverse transcriptionpolymerase chain reaction, and their putative targets were predicted by the online software Target Scan, mi Randa and Pic Tar database. Gene ontology(GO) and Kyoto encyclopedia of genes and genomes(commonly known as KEGG) were used to predict their possible functions and pathways involved.RESULTS We investigated 287 mi RNAs based on microarray data analysis. Twelve mi RNAs were differentially expressed in the patients with SAP with ALI and those with SAP without ALI. Hsa-mi R-1260 b, 762, 22-3 p, 23 b and 23 a were differently up-regulated and hsa-mi R-550 a*, 324-5 p, 484, 331-3 p, 140-3 p, 342-3 p and 150 were differently down-regulated in patients with SAP with ALI compared to those with SAP without ALI. In addition, 85 putative target genes of the significantly dysregulated mi RNAs were found by Target Scan, mi Randa and Pic Tar. Finally, GO and pathway network analysis showed that they were mainly enriched in signal transduction, metabolic processes, cytoplasm and cell membranes.CONCLUSION This is the first study to identify 12 circulating mi RNAs in patients with SAP with ALI, which may be biomarkers for prediction of ALI after SAP. 展开更多
关键词 MIRNAS Severe acute pancreatitis acute lung injury BIOMARKER Microarray analysis
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Pathogenesis of acute lung injury in rats with severe acute pancreatitis 被引量:18
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作者 Xue-Min Liu, Jun Xu and Zi-Fa Wang Department of Hepatobiliary Surgery, First Hospital, Xi’an Jiaotong University, Xi’an 710061 , China 《Hepatobiliary & Pancreatic Diseases International》 SCIE CAS 2005年第4期614-617,共4页
BACKGROUND: Acute lung injury (ALI) is the most common and severe complication of severe acute pancreatitis (SAP). The elucidation of the mechanism of ALI contributes to the diagnosis and treatment of the illness. In ... BACKGROUND: Acute lung injury (ALI) is the most common and severe complication of severe acute pancreatitis (SAP). The elucidation of the mechanism of ALI contributes to the diagnosis and treatment of the illness. In this study, we studied the pathogenesis of ALI in rats with severe acute pancreatitis. METHODS: The rats were sacrificed at 1, 3, 5, 6, 9 and 12 hours after the establishment of the model of SAP. Pancreas and lung tissues were obtained for pathological study, and examination of microvascular permeability and myeloperoxidase (MPO) examination. The gene expressions of tumor necrosis factor-α (TNF-α) and intercellular adhesion molecule-1 (ICAM-1) in the pancreas and lung tissues were detected by reverse transcriptase-polymerase chain reaction (RT-PCR). RESULTS: After the establishment of the SAP model, the degree of pancreatic and lung injury increased gradually along with the gradual increase of MPO activity and micro-vascular permeability. Gene expressions of TNF-α and ICAM-1 in the pancreas rose at 1 hour and peaked at 7 hours. In contrast, their gene expression in the lungs rose slightly at 1 hour and peaked at 9-12 hours. CONCLUSION: An obvious time window existed between SAP and lung injury, which is beneficial to the early prevention of the development of ALI. 展开更多
关键词 PATHOGENESIS severe acute pancreatitis acute lung injury
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Perioperative"remote"acute lung injury:recent update 被引量:8
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作者 Zhaosheng Jin Ka Chun Suen Daqing Ma 《The Journal of Biomedical Research》 CAS CSCD 2017年第3期197-212,共16页
Perioperative acute lung injury(ALI) is a syndrome characterised by hypoxia and chest radiograph changes.It is a serious post-operative complication,associated with considerable mortality and morbidity.In addition t... Perioperative acute lung injury(ALI) is a syndrome characterised by hypoxia and chest radiograph changes.It is a serious post-operative complication,associated with considerable mortality and morbidity.In addition to mechanical ventilation,remote organ insult could also trigger systemic responses which induce ALI.Currently,there are limited treatment options available beyond conservative respiratory support.However,increasing understanding of the pathophysiology of ALI and the biochemical pathways involved will aid the development of novel treatments and help to improve patient outcome as well as to reduce cost to the health service.In this review we will discuss the epidemiology of peri-operative ALI;the cellular and molecular mechanisms involved on the pathological process;the clinical considerations in preventing and managing perioperative ALI and the potential future treatment options. 展开更多
关键词 acute lung injury intraoperative care/adverse effects postoperative complications inflammation anesthetics general fluid therapy
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Effects of Yue-Bi-Tang on water metabolism in severe acute pancreatitis rats with acute lung-kidney injury 被引量:8
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作者 Jing Hu Yu-Mei Zhang +6 位作者 Yi-Fan Miao Lv Zhu Xiao-Lin Yi Huan Chen Xi-Jing Yang Mei-Hua Wan Wen-Fu Tang 《World Journal of Gastroenterology》 SCIE CAS 2020年第43期6810-6821,共12页
BACKGROUND The complications acute lung injury and acute kidney injury caused by severe inflammation are the main reasons of high mortality of severe acute pancreatitis(SAP).These two complications can both lead to wa... BACKGROUND The complications acute lung injury and acute kidney injury caused by severe inflammation are the main reasons of high mortality of severe acute pancreatitis(SAP).These two complications can both lead to water metabolism and acid-base balance disorders,which could act as additional critical factors affecting the disease trend.Aquaporins(AQPs),which can regulate the transmembrane water transport,have been proved to participate in the pathophysiological process of SAP and the associated complications,such as acute lung injury and acute kidney injury.Thus,exploring herbs that can effectively regulate the expression of AQP in SAP could benefit the prognosis of this disease.AIM To determine whether Yue-Bi-Tang(YBT)can regulate the water metabolism in rats with severe acute pancreatitis via regulating the expression of aquaporins.METHODS Sprague-Dawley rats were randomly divided into three groups,sham operation group(SOG),model group(MG),and treatment group(TG).SAP was induced with 3.5%sodium taurocholate in the MG and TG.Rats in the TG were administered with YBT while SOG and MG rats were given the same volume of saline.Blood and tissue samples were harvested to detect serum inflammatory cytokines,histopathological changes,malondialdehyde and superoxide dismutase in the lung,and protein and mRNA expression of kidney injury molecule-1,α-smooth muscle actin,and vimentin in the kidney,and AQP1 and 4 in the lung,pancreas,and kidney.RESULTS The serum interleukin-10,tumor necrosis factorα,and creatinine levels were higher in the MG than in the SOG.Tumor necrosis factorαlevel in the TG was lower than that in the MG.Malondialdehyde level in lung tissues was higher than in the SOG.The pathological scores and edema scores of the pancreas,lung,and kidney tissues in the MG were all higher than those in the SOG and TG.The protein expression of AQP4 in lung tissues and AQP1 in kidney tissues in the MG were higher than those in the SOG and TG.The expression of vimentin was significantly higher in the MG than in the SOG.The expression of AQP1 mRNA in the lung and kidney,and AQP4 mRNA in the kidney was up-regulated in the MG compared to the SOG.CONCLUSION YBT might regulate water metabolism to reduce lung and kidney edema of SAP rats via decreasing AQP expression,and alleviate the tissue inflammatory injury. 展开更多
关键词 Yue-Bi-Tang AQUAPORINS Sever acute pancreatitis acute lung injury acute kidney injury Water metabolism
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Acute lung injury and acute respiratory distress syndrome: experimental and clinical investigations 被引量:7
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作者 Hsing I Chen 《Journal of Geriatric Cardiology》 SCIE CAS CSCD 2011年第1期44-54,共11页
Acute lung injury (ALl) or acute respiratory distress syndrome (ARDS) can be associated with various disorders. Recent investigation has involved clinical studies in collaboration with clinical investigators and p... Acute lung injury (ALl) or acute respiratory distress syndrome (ARDS) can be associated with various disorders. Recent investigation has involved clinical studies in collaboration with clinical investigators and pathologists on the pathogenetic mechanisms of ALl or ARDS caused by various disorders. This literature review includes a brief historical retrospective of ALI/ARDS, the neurogenic pulmonary edema due to head injury, the long-term experimental studies and clinical investigations from our laboratory, the detrimental role of NO, the risk factors, and the possible pathogenetic mechanisms as well as therapeutic regimen for ALI/ARDS. 展开更多
关键词 acute lung injury acute respiratory distress syndrome neurogenic pulmonary edema nitric oxide free radicals CYTOKINES
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Alleviation of acute pancreatitis-associated lung injury by inhibiting the p38 mitogen-activated protein kinase pathway in pulmonary microvascular endothelial cells 被引量:6
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作者 Xiao-Xin Zhang Hao-Yang Wang +8 位作者 Xue-Fei Yang Zi-Qi Lin Na Shi Chan-Juan Chen Lin-Bo Yao Xin-Min Yang Jia Guo Qing Xia Ping Xue 《World Journal of Gastroenterology》 SCIE CAS 2021年第18期2141-2159,共19页
BACKGROUND Previous reports have suggested that the p38 mitogen-activated protein kinase signaling pathway is involved in the development of severe acute pancreatitis(SAP)-related acute lung injury(ALI).Inhibition of ... BACKGROUND Previous reports have suggested that the p38 mitogen-activated protein kinase signaling pathway is involved in the development of severe acute pancreatitis(SAP)-related acute lung injury(ALI).Inhibition of p38 by SB203580 blocked the inflammatory responses in SAP-ALI.However,the precise mechanism associated with p38 is unclear,particularly in pulmonary microvascular endothelial cell(PMVEC)injury.AIM To determine its role in the tumor necrosis factor-alpha(TNF-α)-induced inflammation and apoptosis of PMVECs in vitro.We then conducted in vivo experiments to confirm the effect of SB203580-mediated p38 inhibition on SAP-ALI.METHODS In vitro,PMVEC were transfected with mitogen-activated protein kinase kinase 6(Glu),which constitutively activates p38,and then stimulated with TNF-α.Flow cytometry and western blotting were performed to detect the cell apoptosis and inflammatory cytokine levels,respectively.In vivo,SAP-ALI was induced by 5%sodium taurocholate and three different doses of SB203580(2.5,5.0 or 10.0 mg/kg)were intraperitoneally injected prior to SAP induction.SAP-ALI was assessed by performing pulmonary histopathology assays,measuring myeloperoxidase activity,conducting arterial blood gas analyses and measuring TNF-α,interleukin(IL)-1βand IL-6 levels.Lung microvascular permeability was measured by determining bronchoalveolar lavage fluid protein concentration,Evans blue pulmonary cells was confirmed by performing a terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling analysis and examining the Bcl2,Bax,Bim and cle-caspase3 levels.The proteins levels of P-p38,NFκB,IκB,P-signal transducer and activator of transcription-3,nuclear factor erythroid 2-related factor 2,HO-1 and Myd88 were detected in the lungs to further evaluate the potential mechanism underlying the protective effect of SB203580.RESULTS In vitro,mitogen-activated protein kinase(Glu)transfection resulted in higher apoptotic rates and cytokine(IL-1βand IL-6)levels in TNF-α-treated PMVECs.In vivo,SB2035080 attenuated lung histopathological injury,decreased inflammatory activity(TNF-α,IL-1β,IL-6 and myeloperoxidase)and preserved pulmonary function.Furthermore,SB203580 significantly reversed changes in the bronchoalveolar lavage fluid protein concentration,Evans blue accumulation,terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling-positive cell numbers,apoptosis-related proteins(cle-caspase3,Bim and Bax)and endothelial microstructure.Moreover,SB203580 significantly reduced the pulmonary P-p38,NFκB,P-signal transducer and activator of transcription-3 and Myd88 levels but increased the IκB and HO-1 levels.CONCLUSION p38 inhibition may protect against SAP-ALI by alleviating inflammation and the apoptotic death of PMVECs. 展开更多
关键词 acute pancreatitis acute lung injury Pulmonary microvascular endothelial cells P38 SB203580 Apoptosis
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Calycosin attenuates severe acute pancreatitis-associated acute lung injury by curtailing high mobility group box 1-induced inflammation 被引量:5
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作者 Chang-Ju Zhu Wan-Guang Yang +8 位作者 De-Jian Li Yao-Dong Song San-Yang Chen Qiao-Fang Wang Yan-Na Liu Yan Zhang Bo Cheng Zhong-Wei Wu Zong-Chao Cui 《World Journal of Gastroenterology》 SCIE CAS 2021年第44期7669-7686,共18页
BACKGROUND Acute lung injury(ALI)is a common and life-threatening complication of severe acute pancreatitis(SAP).There are currently limited effective treatment options for SAP and associated ALI.Calycosin(Cal),a bioa... BACKGROUND Acute lung injury(ALI)is a common and life-threatening complication of severe acute pancreatitis(SAP).There are currently limited effective treatment options for SAP and associated ALI.Calycosin(Cal),a bioactive constituent extracted from the medicinal herb Radix Astragali exhibits potent anti-inflammatory properties,but its effect on SAP and associated ALI has yet to be determined.AIM To identify the roles of Cal in SAP-ALI and the underlying mechanism.METHODS SAP was induced via two intraperitoneal injections of L-arg(4 g/kg)and Cal(25 or 50 mg/kg)were injected 1 h prior to the first L-arg challenge.Mice were sacrificed 72 h after the induction of SAP and associated ALI was examined histologically and biochemically.An in vitro model of lipopolysaccharide(LPS)-induced ALI was established using A549 cells.Immunofluorescence analysis and western blot were evaluated in cells.Molecular docking analyses were conducted to examine the interaction of Cal with HMGB1.RESULTS Cal treatment substantially reduced the serum amylase levels and alleviated histopathological injury associated with SAP and ALI.Neutrophil infiltration and lung tissue levels of neutrophil mediator myeloperoxidase were reduced in line with protective effects of Cal against ALI in SAP.Cal treatment also attenuated the serum levels and mRNA expression of pro-inflammatory cytokines tumor necrosis factor-α,interleukin-6,IL-1β,HMGB1 and chemokine(CXC motif)ligand 1 in lung tissue.Immunofluorescence and western blot analyses showed that Cal treatment markedly suppressed the expression of HMGB1 and phosphorylated nuclear factor-kappa B(NF-κB)p65 in lung tissues and an in vitro model of LPSinduced ALI in A549 cells suggesting a role for HGMB1 in the pathogenesis of ALI.Furthermore,molecular docking analysis provided evidence for the direct interaction of Cal with HGMB1.CONCLUSION Cal protects mice against L-arg-induced SAP and associated ALI by attenuating local and systemic neutrophil infiltration and inflammatory response via inhibition of HGMB1 and the NF-κB signaling pathway. 展开更多
关键词 Severe acute pancreatitis acute lung injury CALYCOSIN Mouse model Highmobility group box 1 Nuclear factor-kappa B
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Drug repurposing of histone deacetylase inhibitors that alleviate neutrophilic inflammation in acute lung injury and idiopathic pulmonary fibrosis via inhibiting leukotriene a4 hydrolase and blocking LTB4 biosynthesis 被引量:4
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作者 Wei-qiang LU Jing-yuan WANG +4 位作者 Xue YAO Ping OUYANG Ning-ning DONG Dang WU Jin HUANG 《中国药理学与毒理学杂志》 CAS CSCD 北大核心 2017年第10期972-972,共1页
OBJECTIVE Leukotriene B4(LTB4)biosynthesis and subsequently neutrophilic inflammation may provide a potential strategy for the treatment of acute lung injury(ALI)or idiopathic pulmonary fibrosis(IPF).To provide a pote... OBJECTIVE Leukotriene B4(LTB4)biosynthesis and subsequently neutrophilic inflammation may provide a potential strategy for the treatment of acute lung injury(ALI)or idiopathic pulmonary fibrosis(IPF).To provide a potential strategy for the treatment of ALI or IPF,we identified potent inhibitors of Leukotriene A4 hydrolase(LTA4H),a key enzyme in the biosynthesis of LTB4.METHODS In this study,we identified two known histone deacetylase(HDAC)inhibitors,suberanilohydroxamic acid(SAHA)and its analogue 4-(dimethylamino)-N-[7-(hydroxyamino)-7-oxoheptyl]benzamide(M344),as effective inhibitors of LTA4H using enzymatic assay,thermofluor assay,and X-ray crystallographic investigation.We next tested the effect of SAHA and M344 on endogenous LTB4 biosynthesis in neutrophils by ELISA and neutrophil migration by transwell migration assay.A murine experimental model of ALI was induced by lipopolysaccharide(LPS)inhalation.Histopathological analysis of lung tissue using H&E staining revealed the serious pulmonary damage caused by LPS treatment and the effect of the SAHA.We next examined m RNA and protein levels of pro-inflammatory cytokines in lung tissue and bronchoalveolar lavage fluid using q RT-PCR and ELISA to further investigate the underlying mechanisms of anti-inflammatory activities by SAHA.We also investigated the effects of SAHA and M344 on a murine experimental model of bleomycin(BLM)-induced IPF model.RESULTS The results of enzymatic assay and X-ray crystallography showed that both SAHA and M344 bind to LTA4H,significantly decrease LTB4 levels in neutrophil,and markedly diminish early neutrophilic inflammation in mouse models of ALI and IPF under a clinical safety dose.CONCLUSION Collectively,SAHA and M344 would provide promising agents with well-known clinical safety for potential treatment in patients with ALI and IPF via pharmacologically inhibiting LAT4H and blocking LTB4 biosynthesis. 展开更多
关键词 acute lung injury idiopathic pulmonary fibrosis histone deacetylase inhibitors alleviate neutrophilic inflammation leukotriene A4 hydrolase leukotriene B4
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Protective Effect of Curcumin on Endotoxin-induced Acute Lung Injury in Rats 被引量:4
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作者 连庆泉 李兴旺 +3 位作者 尚游 姚尚龙 马利 金胜威 《Journal of Huazhong University of Science and Technology(Medical Sciences)》 SCIE CAS 2006年第6期678-681,共4页
To investigate the protective effect of curcumin on endotoxin-induced acute lung injury in rats, and explore the underlying mechanisms, 24 male Wistar rats were randomly divided into 4 experimental groups: sham-vehic... To investigate the protective effect of curcumin on endotoxin-induced acute lung injury in rats, and explore the underlying mechanisms, 24 male Wistar rats were randomly divided into 4 experimental groups: sham-vehicle (S), sham-curcumin (C), lipopolysaccharide (LPS)-vehicle (L), and curcumin-lipopolysaccharide (C-L) groups. The wet/dry (W/D) weight ratio of the lung and bronchoalveolar lavage (BAL) fluid protein content were used as measures of lung injury. Neutrophil recruitment and activation were evaluated by BAL fluid cellularity and myeloperoxidase (MPO) activity in cell-free BAL and lung tissue. The levels of cytokine-induced neutrophil chemoattractant-1 (CINC-1) in lung tissues were measured by ELISA. were observed by using the HE staining. Our results the wet/dry weight ratio and protein content in BALE The histopathological changes of lung tissues showed that lung injury parameters, including were significantly higher in the L group than in the S group (P〈0.01). In the L group, higher numbers of neutrophils and greater MPO activity in cell-free BAL and lung homogenates were observed when compared with the S group (P〈0.01). There was a marked increase in CINC-1 levels in lung tissues in response to LPS challenge (P〈0.01, L group vs S group). Curcumin pretreatment significantly attenuated LPS-induced changes in these indices. LPS caused extensive morphological lung damage, which was also lessened after curcumin pretreatment. All the above-mentioned parameters in the C group were not significantly different from those of the S group. It is concluded that curcumin pretreatment attenuates LPS-induced lung injury in rats. This beneficial effect of curcumin may involves, in part, inhibition of neutrophilic recruitment and activity, possibly through inhibition of lung CINC-1 expression. 展开更多
关键词 acute lung injury LIPOPOLYSACCHARIDE NEUTROPHILS CINC-1
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Expression of phosphatidylinositol-3 kinase and effects of inhibitor Wortmannin on expression of tumor necrosis factor-α in severe acute pancreatitis associated with acute lung injury 被引量:19
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作者 Ming Wei Yan-jie Gong +3 位作者 Ling Tu Jia Li Ying-hong Liang Yi-hua Zhang 《World Journal of Emergency Medicine》 CAS 2015年第4期299-304,共6页
BACKGROUND: Acute lung injury(ALI) is a common and serious complication of severe acute pancreatitis(SAP). The study aimed to investigate the protective effect and mechanism of phosphatidylinositol-3 kinase(PI3K) inhi... BACKGROUND: Acute lung injury(ALI) is a common and serious complication of severe acute pancreatitis(SAP). The study aimed to investigate the protective effect and mechanism of phosphatidylinositol-3 kinase(PI3K) inhibitor Wortmannin in SAP associated with ALI.METHODS: Ninety rats were randomly divided into three groups: sham operation(SO) group(n=30), SAP group(n=30), and SAP+Wortmannin(SAP+W) group(n=30). SAP model was induced by retrograde injection of 4% sodium taurocholate into the biliopancreatic duct of rats. The rate of lung water content, myeloperoxidase(MPO), matrix metalloproteinase 9(MMP-9), protein kinase B(PKB), abdphosphorylation of protein kinase B(P-PKB) activity in the lung tissue were evaluated.RESULTS: In the SAP group, the p-PKB expression in the lung tissue began to rise at 3 hours after modeling, and peaked at 12 hours(P<0.05); the rate of lung water content, MPO and TNF-α activity were also gradually increased, and the degree of lung lesion gradually increased(P<0.05). In the SAP+Wortmannin group, the p-PKB expression in the lung tissue began to rise at 3 hours after modeling, and peaked at 12 hours; it was higher than that in the SO group(P<0.05), but significantly lower than that in the SAP group(P<0.05). The rest indicators in the SAP+Wortmannin group were also significantly decreased as compared with the SAP group(P<0.05).CONCLUSIONS: The expression of phosphatidylinositol-3 kinase/protein kinase B was elevated in severe pancreatitis rats with lung injury. This suggested that PI3 K signal transduction pathway is involved in the control and release of proinfl ammatory cytokines TNF-α, which may play an important role in the pathogenesis of severe acute pancreatitis associated with lung injury. This finding indicated that Wortmannin can block the PI3 K signal transduction pathway, and inhibit the release of infl ammatory factor TNF-α. 展开更多
关键词 WORTMANNIN Phosphatidylinositol-3 kinase/protein kinase B Severe acute pancreatitis acute lung injury
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