检索结果-南通市图书馆

emodin promotes the recovery of rheumatoid arthritis by regulating the crosstalk between macrophage subsets and synovial fibroblast subsets

引用

Animal Models and Experimental Medicine 2025年第1期8卷 44-56页

作者： Lianying Cheng Xiaofeng Rong Department of Integrated Traditional Chinese and Western Medicine The First Affiliated Hospital of Chongqing Medical UniversityChongqingChina

Background : To study the relationships among emodin, synovial fibroblasts (FLSs), and macrophages (STMs) to provide guidance for the use of emodin in rheumatoid arthritis (RA) treatment. Methods : RA clinical samples from patients with different pathological processes were collected, and the correlations between the subsets of FLSs and STMs and pathological processes were analyzed via flow cytometry. In vitro experimental methods such as enzyme linked immunosorbent assay (ELISA), Western blotting, Transwell assays, CCK- 8 assays and cell coculture were used to assess cell proliferation, migration and secretion of inflammatory factors. A collagen- induced arthritis mouse model was constructed to investigate the therapeutic potential of emodin in RA by flow cytometry, micro- CT and staining. Results : Unique subsets of FLSs and STMs, namely, FAPα ^(+)THY1 − FLSs, FAPα ^(+)THY1 ^(+)FLSs, and MerTK ^(pos) TREM2 ^(high) STMs, were identified in synovial tissues from RA patients. The number of MerTK ^(pos) TREM2 ^(high) STMs was negatively correlated with the degree of damage in RA, while the number of FAPα ^(+)THY1 − FLSs was positively correlated with damage. On the one hand, emodin promoted the aggregation of MerTKposTREM2high STMs. Moreover, MerTK pos TREM2 high STM- mediated secretion of exosomes was promoted, which can inhibit the secretion of pro- inflammatory factors by FAPα ^(+)THY1 ^(+)FLSs and promote the secretion of anti- inflammatory factors by FAPα ^(+)THY1 ^(+)FLSs, thereby inhibiting FAPα ^(+)THY1 − FLS proliferation and migration, improving the local immune microenvironment, and inhibiting RA damage. Conclusion : emodin was shown to regulate the aggregation of STM subsets and exosome secretion, affecting the secretion, proliferation and migration of inflammatory factors in FLS subsets, and ultimately achieving good therapeutic efficacy in RA patients, suggesting that it has important clinical value.

关键词： emodin fibroblast synoviocytes macrophages rheumatoid arthritis

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

emodin attenuates severe acute pancreatitis-associated acute lung injury by suppressing pancreatic exosome-mediated alveolar macrophage activation

引用

Acta Pharmaceutica Sinica B 2022年第10期12卷 3986-4003页

作者： Qian Hu Jiaqi Yao Xiajia Wu Juan Li Guixiang Li Wenfu Tang Jingping Liu Meihua Wan Department of Integrated Traditional Chinese and Western Medicine National Clinical Research Center for GeriatricsWest China HospitalSichuan UniversityChengdu 610041China NHC Key Laboratory of Transplant Engineering and Immunology Frontiers Science Center for Disease-Related Molecular NetworkWest China HospitalSichuan UniversityChengdu 610041China

Severe acute pancreatitis-associated acute lung injury(SAP-ALI) is a serious disease associated with high mortality. emodin has been applied to alleviate SAP-ALI;however, the mechanism remains unclear. We report that the therapeutic role of emodin in attenuating SAP-ALI is partly dependent on an exosomal mechanism. SAP rats had increased levels of plasma exosomes with altered protein contents compared to the sham rats. These infused plasma exosomes tended to accumulate in the lungs and promoted the hyper-activation of alveolar macrophages and inflammatory damage. Conversely,emodin treatment decreased the plasma/pancreatic exosome levels in the SAP rats. emodin-primed exosomes showed less pro-inflammatory effects in alveolar macrophages and lung tissues than SAP exosomes. In detail, emodin-primed exosomes suppressed the NF-κB pathway to reduce the activation of alveolar macrophage and ameliorate lung inflammation by regulating PPARγ pathway, while these effects were amplified/abolished by PPARγ agonist/antagonist. Blockage of pancreatic acinar cell exosome biogenesis also exhibited suppression of alveolar macrophage activation and reduction of lung inflammation. This study suggests a vital role of exosomes in participating inflammation-associated organ-injury,and indicates emodin can attenuate SAP-ALI by reducing the pancreatic exosome-mediated alveolar macrophage activation.

关键词： Severe acute pancreatitis Acute lung injury emodin Exosome Macrophages Lisocitrate dehydrogenase 1 Peroxisome proliferatoractivated receptorγ Nuclear factor kB

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

emodin Ameliorates High Glucose-Induced Podocyte Apoptosis via Regulating AMPK/mTOR-Mediated Autophagy Signaling Pathway

引用

Chinese Journal of Integrative Medicine 2023年第9期29卷 801-808页

作者： LIU Hong CHEN Wei-dong HU Yang-lin YANG Wen-qiang HU Tao-tao WANG Huan-lan ZHANG Yan-min Department of Nephrology Wuhan No.1 HospitalWuhan430022China Department of Central Laboratory Wuhan No.1 HospitalWuhan430022China

Objective To investigate the effect of emodin on high glucose(HG)-induced podocyte apoptosis and whether the potential anti-apoptotic mechanism of emodin is related to induction of adenosine-monophosphate-activated protein kinase(AMPK)/mammalian target of rapamycin(mTOR)-mediated autophagy in podocytes(MPC5 cells)in *** MPC5 cells were treated with different concentrations of HG(2.5,5,10,20,40,80 and 160 mmol/L),emodin(2,4,8µmol/L),or HG(40 mmol/L)and emodin(4µmol/L)with or without rapamycin(Rap,100 nmol/L)and compound C(10µmol/L).The viability and apoptosis of MPC5 cells were detected using cell counting kit-8(CCK-8)assay and flow cytometry analysis,*** expression levels of cleaved caspase-3,autophagy marker light chain 3(LC3)Ⅰ/Ⅱ,and AMPK/mTOR signaling pathway-related proteins were determined by Western *** changes of morphology and RFP-LC3 fluorescence were observed under *** HG at 20,40,80 and 160 mmol/L dose-dependently induced cell apoptosis in MPC5 cells,whereas emodin(4µmol/L)significantly ameliorated HG-induced cell apoptosis and caspase-3 cleavage(Pemodin(4µmol/L)significantly increased LC3-Ⅱ protein expression levels and induced RFP-LC3-containing punctate structures in MPC5 cells(Pemodin were mimicked by rapamycin(100 nmol/L).Moreover,emodin increased the phosphorylation of AMPK and suppressed the phosphorylation of *** AMPK inhibitor compound C(10µmol/L)reversed emodin-induced autophagy *** emodin ameliorated HG-induced apoptosis of MPC5 cells in vitro that involved induction of autophagy through the AMPK/mTOR signaling pathway,which might provide a potential therapeutic option for diabetic nephropathy.

关键词： emodin diabetic nephropathy autophagy podocyte apoptosis adenosine-monophosphate-activated protein kinase/mammalian target of rapamycin signaling pathways

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

emodin Inhibits Lipopolysaccharide-Induced Inflammation by Activating Autophagy in RAW 264.7 Cells

引用

Chinese Journal of Integrative Medicine 2021年第5期27卷 345-352页

作者： TU Yan-jie TAN Bo JIANG Lei WU Zhong-hua YU Hong-ji LI Xiao-qian YANG Ai-dong Research Centre on Application of Classical Prescriptions Basic Medical CollegeShanghai University of Traditional Chinese MedicineShanghai 201203China Department of Febrile Disease Basic Medical CollegeShanghai University of Traditional Chinese MedicineShanghai 201203China Clinical Pharmacokinetic Laboratory Shuguang Hospital Affiliated to Shanghai University of Traditional Chinese MedicineShanghai 201203China

Objective:To investigate the effects of emodin on inflammation and autophagy in lipopolysaccharide(LPS)-induced RAW 264.7 macrophages and reveal its underlying ***:3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2 H-tetrazolium(MTS)assay was conducted to find the appropriate dose for ***264.7 cells pretreated with different concentrations(0–50μmol/L)of emodin or vehicle for 2 h prior to exposure to LPS for 16 *** morphology was examined and propidium iodide staining was used to examine cell *** of inflammation-related proteins[nuclear factor-kappa B(NF-κB)and I-kappa B(IκB)α]and autophagy-related proteins[light chain(LC)3,P62/sequestosome 1,mammalian target of rapamycin(m TOR),and p-m TOR]were examined using Western blot *** of inflammation-related cytokines including tumor necrosis factor(TNF)-α,interleukin(IL)-1βand IL-6 were detected by enzyme-linked immunosorbent *** was examined with LC3 B fluorescence intensity and *** effect of emodin on autophagy was conducted with an autophagy inhibitor,3-methyladenine(3-MA).Results:The expression of NF-κB in LPS-induced cells was significantly increased(Pemodin at different doses(12.5,25,and 50μmol/L,Pemodin decreased the expressions of NF-κB,P62 and p-m TOR(Pemodin,such as the increment of LC3 BⅡ/ratio and the decrement of P62 expression,were suppressed by autophagy inhibitor ***:emodin could inhibit inflammation of m

关键词： emodin lipopolysaccharide inflammation autophagy

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

emodin enhances alveolar epithelial barrier function in rats with experimental acute pancreatitis

引用

World Journal of Gastroenterology 2010年第24期16卷 2994-3001页

作者： Xia, Xian-Ming Wang, Fang-Yu Wang, Zhen-Kai Wan, Hai-Jun Xu, Wen-An Lu, Heng Jinling Hosp Dept Gastroenterol & Hepatol Nanjing 210002 Jiangsu Prov Peoples R China

AIM: To investigate the effect of emodin on expression of claudin4, claudin5 and occludin, as well as the alveolar epithelial barrier in rats with pancreatitis induced by sodium taurocholate. METHODS: Experimental pancreatitis was induced by retrograde injection of 5% sodium taurocholate into the biliopancreatic duct. emodin was injected via the external jugular vein 3 h after induction of acute pancreatitis. Rats from sham operation group and acute pancreatitis group were injected with normal saline (an equivalent volume as emodin) at the same time point. Samples of lung and serum were obtained 6 h after drug administration. Pulmonary morphology was examined with HE staining. Pulmonary edema was estimated by measuring water content in lung tissue samples. Tumor necrosis factorα (TNFα) and interleukin6 (IL6) level were measured by enzymelinked immunospecific assay. Serum amylase and pulmonary myeloperoxidase (MPO) activity were detected by spectrophotometry. Alveolar epithelial barrier was assessed by pulmonary dye extravasation. Expression of claudin4, claudin5 and occludin in lung tissue samples was examined by immunohistology, quantitative realtime reverse transcription polymerase chain reaction and Western blotting analysis, ***: Pancreatitis-associated lung injury was char-acterized by pulmonary edema, leukocyte infiltration, alveolar collapse, and elevated serum amylase level. The pulmonary damage, pulmonary pathological scores, serum amylase and MPO activity, TNF-α and IL-6 levels, and wet/dry ratio were decreased in rats after treatment with emodin. Immunostaining of claudin-4, claudin-5 and occludin was detected in lung tissue samples from rats in sham operation group, which was distributed in alveolar epithelium, vascular endothelium, and bron-chial epithelium, respectively. The mRNA and protein expression levels of claudin-4, claudin-5 and occludin in lung tissue samples were markedly decreased, the expression level of claudin-4, claudin-

关键词： Acute pancreatitis emodin Lung injury Claudin Occludin Epithelial barrier

来源：

维普期刊数据库评论

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

emodin alleviates intestinal mucosal injury in rats with severe acute pancreatitis via the caspase-1 inhibition

引用

Hepatobiliary & Pancreatic Diseases International 2017年第4期16卷 431-436页

作者： Jian-Wen Ning Yan Zhang Mo-Sang Yu Meng-Li Gu Jia Xu Ali Usman Feng Ji Division of Emergency First Affiliated HospitalZhejiang University School of MedicineHangzhou 310003China Division of Gastroenterology First Affiliated HospitalZhejiang University School of MedicineHangzhou 310003China Division of Gastroenterology Yixing People’s HospitalYixing 214200China

BACKGROUND: emodin, a traditional Chinese medicine, has a therapeutic effect on severe acute pancreatitis (SAP), whereas the underlying mechanism is still unclear. Studies showed that the intestinal mucosa impairment, and subsequent release of endotoxin and proinflammatory cytokines such as IL-1 beta, which further leads to the dysfunction of multiple organs, is the potentially lethal mechanism of SAP. Caspase-1, an IL-1 beta converting enzyme, plays an important role in this cytokine cascade process. Investigation of the effect of emodin on regulating the caspase-1 expression and the release proinflammatory cytokines will help to reveal mechanism of emodin in treating SAP. METHODS: Eighty Sprague-Dawley rats were randomly divided into four groups (n=20 each group): SAP, sham-operated (SO), emodin-treated (EM) and caspase-1 inhibitor-treated (ICE-I) groups. SAP was induced by retrograde infusion of 3.5% sodium taurocholate into the pancreatic duct. emodin and caspase-1 inhibitor were given 30 minutes before and 12 hours after SAP induction. Serum levels of IL-1 beta, IL-18 and endotoxin, histopathological alteration of pancreas tissues, intestinal mucosa, and the intestinal caspase-1 mRNA and protein expressions were assessed 24 hours after SAP induction. RESULTS: Rats in the SAP group had higher serum levels of IL-1 beta and IL-18 (P<0.05), pancreatic and gut pathological scores (P<0.05), and caspase-1 mRNA and protein expressions (P<0.05) compared with the SO group. Compared with the SAP group, rats in the EM and ICE-I groups had lower IL-1 beta and IL-18 levels (P<0.05), lower pancreatic and gut pathological scores (P<0.05), and decreased expression of intestine caspase-1 mRNA (P<0.05). Ultrastructural analysis by transmission electron microscopy found that rats in the SAP group had vaguer epithelial junctions, more disappeared intercellular joints, and more damaged intracellular organelles compared with those in the SO group or the EM and ICE-I groups. CONCLUSIO

关键词： severe acute pancreatitis intestinal mucosa emodin caspase-1 inhibitor

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

Preparation and Osteogenic Efficacy of emodin-loaded Hydroxyapatite Electrospun Fibers

引用

Journal of Bionic Engineering 2023年第3期20卷 1060-1071页

作者： Yiwen Pan Mu He Shaoqing Chen Yanyan Meng Cheli Wang Xinye Ni School of Pharmacy Changzhou UniversityChangzhou213000China Department of Radiotherapy Changzhou Second People’s HospitalNanjing Medical UniversityChangzhou213000China Laboratory of Medical Physics Center Nanjing Medical UniversityNanjing210000China Changzhou Key Laboratory of Medical Physics Changzhou213000China

Biological scaffolds have been the focus of bone tissue engineering research in recent years. In this paper, emodin (EM), macromolecular compound polycaprolactone (PCL), and hydroxyapatite (HA) were used as raw materials to prepare EM/PCL/HA fibers containing different EM ratios by electrospinning, and the properties and osteogenic efficacy of EM/PCL/HA were studied. Scanning electron microscopy, transmission electron microscopy, and atomic force microscopy were used to characterize the structures of HA and the electrospun fibers. Results showed that HA has high crystallinity and loose porous structure, and the electrospun fibers have a smooth and flat surface. In vitro release results showed that EM was slowly released from EM/PCL/HA within 216 h. Cell proliferation assay in mouse embryonic osteoblast precursor cells (MC3T3-E1) exhibited that 5% EM/PCL/HA had the best effect on promoting cell proliferation. Alkaline phosphatase (ALP) and mineralized nodules staining results also showed that 5% EM/PCL/HA had the best effect on promoting osteogenic differentiation. qRT-PCR results showed that the mRNA expression level of osteoblast differentiation markers, namely, bone morphogenetic protein (BMP)-2, BMP-9, and osteocalcin were significantly upregulated by 5% EM/PCL/HA treatment. These results indicate that EM/PCL/HA is a potential osteogenic material, which can provide a reference for the development of bone injury repair materials.

关键词： emodin Hydroxyapatite Electrospinning Bone regeneration

来源：

维普期刊数据库评论

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

emodin alleviates cardiac fibrosis by suppressing activation of cardiac fibroblasts via upregulating metastasis associated protein 3

引用

Acta Pharmaceutica Sinica B 2019年第4期9卷 724-733页

作者： Dan Xiao Yue Zhang Rui Wang Yujie Fu Tong Zhou Hongtao Diao Zhixia Wang Yuan Lin Zhange Li Lin Wen Xujuan Kang Philipp Kopylov Dmitri Shchekochikhin Yong Zhang Baofeng Yang Department of Pharmacology(State-Province Key Laboratories of Biomedicine-Pharmaceutics of China Key Laboratory of Cardiovascular ResearchMinistry of Education)Harbin Medical UniversityHarbin 150081China Department of Pharmacy The First Affiliated Hospital of Harbin Medical UniversityHarbin 150081China Department of Preventive and Emergency Cardiology Sechenov First Moscow State Medical UniversityMoscow 119991Russian Federation Institute of Metabolic Disease Heilongjiang Academy of Medical ScienceHarbin 150086China Department of Pharmacology and Therapeutics Melbourne School of Biomedical SciencesFaculty of MedicineDentistry and Health SciencesThe University of MelbourneMelbourne 3010Australia

Excess activation of cardiac fibroblasts inevitably induces cardiac fibrosis. emodin has been used as a natural medicine against several chronic diseases. The objective of this study is to determine the effects of emodin on cardiac fibrosis and the underlying molecular mechanisms. Intragastric administration of emodin markedly decreased left ventricular wall thickness in a mouse model of pathological cardiac hypertrophy with excess fibrosis induced by transaortic constriction(TAC) and suppressed activation of cardiac fibroblasts induced by angiotensin II(AngII). emodin upregulated expression of metastasis associated protein 3(MTA3) and restored the MTA3 expression in the setting of cardiac fibrosis. Moreover, overexpression of MTA3 promoted cardiac fibrosis;in contrast, silence of MTA3 abrogated the inhibitory effect of emodin on fibroblast activation. Our findings unraveled the potential of emodin to alleviate cardiac fibrosis via upregulating MTA3 and highlight the regulatory role of MTA3 in the development of cardiac fibrosis.

关键词： emodin Cardiac fibrosis MTA3 Angiotensin Ⅱ Cardiac fibroblast Mouse

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

emodin attenuates inflammation and demyelination in experimental autoimmune encephalomyelitis

引用

Neural Regeneration Research 2023年第7期18卷 1535-1541页

作者： Yue-Ran Cui Zhong-Qi Bu Hai-Yang Yu Li-Li Yan Juan Feng Department of Neurology Shengjing Hospital of China Medical UniversityShenyangLiaoning ProvinceChina

emodin,a substance extracted from herbs such as rhubarb,has a protective effect on the central nervous ***,the potential therapeutic effect of emodin in the context of multiple sclerosis remains *** this study,a rat model of experimental autoimmune encephalomyelitis was established by immune induction to simulate multiple sclerosis,and the rats were intraperitoneally injected with emodin(20 mg/kg/d)from the day of immune induction until they were *** this model,the nucleotide-binding domain-like receptor family pyrin domain containing 3(NLRP3)inflammasome and the microglia exacerbated neuroinflammation,playing an important role in the development of multiple *** addition,silent information regulator of transcription 1(SIRT1)/peroxisome proliferator-activated receptor-alpha coactivator(PGC-1α)was found to inhibit activation of the NLRP3 inflammasome,and SIRT1 activation reduced disease severity in experimental autoimmune ***,treatment with emodin decreased body weight loss and neurobehavioral deficits,alleviated inflammatory cell infiltration and demyelination,reduced the expression of inflammatory cytokines,inhibited microglial aggregation and activation,decreased the levels of NLRP3 signaling pathway molecules,and increased the expression of SIRT1 and PGC-1α.These findings suggest that emodin improves the symptoms of experimental autoimmune encephalomyelitis,possibly through regulating the SIRT1/PGC-1α/NLRP3 signaling pathway and inhibiting microglial *** findings provide experimental evidence for treatment of multiple sclerosis with emodin,enlarging the scope of clinical application for emodin.

关键词： demyelination emodin experimental autoimmune encephalomyelitis microglia multiple sclerosis neuroinflammation NLRP3 inflammasome PGC-1α pyroptosis SIRT1

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

emodin and baicalein inhibit sodium taurocholate-induced vacuole formation in pancreatic acinar cells

引用

World Journal of Gastroenterology 2018年第1期24卷 35-45页

作者： jun li rui zhou bei-bei bie na huang ying guo hai-yan chen meng-jiao shi jun yang jian zhang zong-fang li National and Local Joint Engineering Research Center of Biodiagnostics and Biotherapy the Second Affiliated Hospital of Xi’an Jiaotong UniversityXi’an 710004Shaanxi ProvinceChina

AIM To investigate the effects of combined use of emodin and baicalein(CEB) at the cellular and organism levelsin severe acute pancreatitis(SAP) and explore the underlying *** SAP was induced by retrograde infusion of 5% sodium taurocholate into the pancreatic duct in 48 male SD rats. Pancreatic histopathology score, serum amylase activity, and levels of tumour necrosis factor alpha(TNf-α), interleukin 6(IL-6), and IL-10 were determined to assess the effects of CEB at 12 h after the surgery. The rat pancreatic acinar cells were isolated from healthy male SD rats using collagenase. The cell viability, cell ultrastructure, intracellular free Ca2+ concentration, and inositol(1,4,5)-trisphosphate receptor(IP3 R) expression were investigated to assess the mechanism of *** Pancreatic histopathology score(2.07 ± 1.20 vs 6.84 ± 1.13, P 0.05).CONCLUSION These results at the cellular and organism levels reflect a preliminary mechanism of CEB in SAP and indicate that CEB is a suitable approach for SAP treatment.

关键词： inositol(1,4,5)-trisphosphate receptor Severe acute pancreatitis Calcium overload emodin Baicalein Pancreatic acinar cell

来源：

维普期刊数据库评论

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

欢迎您,

建议与咨询留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

时间限定

文献类型

馆藏选择

核心期刊

语言

文献类型

帮助

文字说明：

检索规则说明：

检索范例：

分类表

所选分类

限定检索结果

文献类型

馆藏范围

日期分布

学科分类号

主题

机构

作者

语言

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

请选择保存的检索档案：

请选择收藏分类：

通借通还

欢迎您,

建议与咨询 留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

时间限定

文献类型

馆藏选择

核心期刊

语言

文献类型

帮助

文字说明：

检索规则说明：

检索范例：

分类表

所选分类

限定检索结果

文献类型

馆藏范围

日期分布

学科分类号

主题

机构

作者

语言

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

请选择保存的检索档案： 新增检索档案 确定 取消

请选择收藏分类： 新增自定义分类 确定 取消

通借通还

建议与咨询留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

请选择保存的检索档案：

请选择收藏分类：