LIVIVO - The Search Portal for Life Sciences

zur deutschen Oberfläche wechseln
Advanced search

Search results

Result 1 - 6 of total 6

Search options

  1. Article ; Online: Activation of AMPK improves lipopolysaccharide-induced dysfunction of the blood-brain barrier in mice.

    Yu, Hai-Ya / Cai, Yu-Bing / Liu, Zhan

    publication RETRACTED

    Brain injury

    2015  Volume 29, Issue 6, Page(s) 777–784

    Abstract: Primary objective: Lipopolysaccharide (LPS) is known to alter the integrity of the blood-brain barrier (BBB) in sepsis, although the underlying mechanism remains unknown. The aim of this study was to elucidate the molecular mechanisms underlying ... ...

    Abstract Primary objective: Lipopolysaccharide (LPS) is known to alter the integrity of the blood-brain barrier (BBB) in sepsis, although the underlying mechanism remains unknown. The aim of this study was to elucidate the molecular mechanisms underlying disruption of the BBB in LPS-induced sepsis.
    Research design: Both in vitro and in vivo experiments were designed to test the role of AMP-activated protein kinase (AMPK) in LPS-induced BBB dysfunction.
    Methods and procedures: Human brain microvascular endothelial cells (HBMECs) were cultured. The protein expressions were detected by western blot. BBB integrity was determined by Evans Blue.
    Main outcomes and results: LPS (1 μg ml(-1)) dramatically increased the permeability of the BBB and the ROS productions, as well as reducing the expression levels of occludin and claudin-5 in cultured HBMECs. Inhibition of NAD(P)H oxidase by apocynin or up-regulation of AMPK reversed the LPS-induced abnormities in HBMECs. In LPS-induced sepsis in mice, it was found that LPS dramatically increased NAD(P)H oxidase protein expressions and ROS productions in the brain and disrupted BBB function assayed by Evans blue staining, which were abolished by AICAR treatment.
    Conclusions: It is concluded that AMPK activation improves the functions of the BBB impaired by LPS through suppression of NAD(P)H oxidase-derived ROS in mice.
    MeSH term(s) AMP-Activated Protein Kinases/metabolism ; Animals ; Blood-Brain Barrier/drug effects ; Blood-Brain Barrier/metabolism ; Brain/blood supply ; Brain/metabolism ; Cell Membrane Permeability/drug effects ; Cells, Cultured ; Endothelial Cells/drug effects ; Endothelial Cells/enzymology ; Humans ; Lipopolysaccharides/pharmacology ; Male ; Mice ; NADPH Oxidases/metabolism ; Reactive Oxygen Species/metabolism ; Sepsis/chemically induced ; Sepsis/metabolism ; Sepsis/pathology ; Tight Junction Proteins
    Chemical Substances Lipopolysaccharides ; Reactive Oxygen Species ; Tight Junction Proteins ; NADPH Oxidases (EC 1.6.3.-) ; AMP-Activated Protein Kinases (EC 2.7.11.31)
    Language English
    Publishing date 2015-03-20
    Publishing country England
    Document type Comparative Study ; Journal Article ; Research Support, Non-U.S. Gov't ; Retracted Publication
    ZDB-ID 639115-1
    ISSN 1362-301X ; 0269-9052
    ISSN (online) 1362-301X
    ISSN 0269-9052
    DOI 10.3109/02699052.2015.1004746
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

    In stock of ZB MED Cologne/Königswinter

    Zs.A 2242: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

  2. Article ; Online: Berberine promotes ischemia-induced angiogenesis in mice heart via upregulation of microRNA-29b.

    Zhu, Mo-Li / Yin, Ya-Ling / Ping, Song / Yu, Hai-Ya / Wan, Guang-Rui / Jian, Xu / Li, Peng

    Clinical and experimental hypertension (New York, N.Y. : 1993)

    2017  Volume 39, Issue 7, Page(s) 672–679

    Abstract: Background: Berberine has several preventive effects on cardiovascular diseases. Increased expression of miR-29b has been reported to attenuate cardiac remodeling after myocardial infarction (MI). We hypothesized that berberine via an miR-29b-dependent ... ...

    Abstract Background: Berberine has several preventive effects on cardiovascular diseases. Increased expression of miR-29b has been reported to attenuate cardiac remodeling after myocardial infarction (MI). We hypothesized that berberine via an miR-29b-dependent mechanism promotes angiogenesis and improves heart functions in mice after MI.
    Methods: The MI model was established in mice by ligation of left anterior descending coronary artery. The expression of miR-29b was examined by RT-qPCR. Angiogenesis was assessed by immunohistochemistry.
    Results: Berberine increased miR-29b expression and promoted cell proliferations and migrations in cultured endothelial cells, which were abolished by miR-29b antagomir or AMP-activated protein kinase inhibitor compound C. In mice following MI, administration of berberine significantly increased miR-29b expressional level, promoted angiogenesis, reduced infarct size, and improved heart functions after 14 postoperative days. Importantly, these in vivo effects of berberine were ablated by antagonism of miR-29b.
    Conclusion: Berberine via upregulation of miR-29b promotes ischemia-induced angiogenesis and improves heart functions.
    Language English
    Publishing date 2017
    Publishing country England
    Document type Journal Article
    ZDB-ID 604757-9
    ISSN 1525-6006 ; 0730-0077
    ISSN (online) 1525-6006
    ISSN 0730-0077
    DOI 10.1080/10641963.2017.1313853
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

    In stock of ZB MED Cologne/Königswinter

    Zs.A 1429: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

  3. Article ; Online: Up-regulation of paired-related homeobox 2 promotes cardiac fibrosis in mice following myocardial infarction by targeting of Wnt5a.

    Bai, Wen-Wu / Tang, Zhen-Yu / Shan, Ti-Chao / Jing, Xue-Jiao / Li, Peng / Qin, Wei-Dong / Song, Ping / Wang, Bo / Xu, Jian / Liu, Zhan / Yu, Hai-Ya / Ma, Zhi-Min / Wang, Shuang-Xi / Liu, Chao / Guo, Tao

    Journal of cellular and molecular medicine

    2019  Volume 24, Issue 3, Page(s) 2319–2329

    Abstract: Cardiac fibrosis is a key factor to determine the prognosis in patient with myocardial infarction (MI). The aim of this study is to investigate whether the transcriptional factor paired-related homeobox 2 (Prrx2) regulates Wnt5a gene expression and the ... ...

    Abstract Cardiac fibrosis is a key factor to determine the prognosis in patient with myocardial infarction (MI). The aim of this study is to investigate whether the transcriptional factor paired-related homeobox 2 (Prrx2) regulates Wnt5a gene expression and the role in myocardial fibrosis following MI. The MI surgery was performed by ligation of left anterior descending coronary artery. Cardiac remodelling was assessed by measuring interstitial fibrosis performed with Masson staining. Cell differentiation was examined by analysis the expression of alpha-smooth muscle actin (α-SMA). Both Prrx2 and Wnt5a gene expressions were up-regulated in mice following MI, accompanied with increased mRNA and protein levels of α-SMA, collagen I and collagen III, compared to mice with sham surgery. Adenovirus-mediated gene knock down of Prrx2 increased survival rate, alleviated cardiac fibrosis, decreased infarction sizes and improved cardiac functions in mice with MI. Importantly, inhibition of Prrx2 suppressed ischaemia-induced Wnt5a gene expression and Wnt5a signalling. In cultured cardiac fibroblasts, TGF-β increased gene expressions of Prrx2 and Wnt5a, and induced cell differentiations, which were abolished by gene silence of either Prrx2 or Wnt5a. Further, overexpression of Prrx2 or Wnt5a mirrored the effects of TGF-β on cell differentiations of cardiac fibroblasts. Gene silence of Wnt5a also ablated cell differentiations induced by Prrx2 overexpression in cardiac fibroblasts. Mechanically, Prrx2 was able to bind with Wnt5a gene promoter to up-regulate Wnt5a gene expression. In conclusions, targeting Prrx2-Wnt5a signalling should be considered to improve cardiac remodelling in patients with ischaemic heart diseases.
    MeSH term(s) Animals ; Cell Differentiation/genetics ; Collagen Type I/genetics ; Collagen Type III/genetics ; Fibroblasts/pathology ; Fibrosis/genetics ; Gene Expression Regulation/genetics ; Heart/physiology ; Homeodomain Proteins/genetics ; Male ; Mice ; Myocardial Infarction/genetics ; Myocardial Infarction/pathology ; Myocardium/pathology ; Myofibroblasts/pathology ; Promoter Regions, Genetic/genetics ; Signal Transduction/genetics ; Transforming Growth Factor beta1/genetics ; Up-Regulation/genetics ; Wnt-5a Protein/genetics
    Chemical Substances Collagen Type I ; Collagen Type III ; Homeodomain Proteins ; Prrx2 protein, mouse ; Transforming Growth Factor beta1 ; Wnt-5a Protein ; Wnt5a protein, mouse
    Language English
    Publishing date 2019-12-27
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2074559-X
    ISSN 1582-4934 ; 1582-4934 ; 1582-1838
    ISSN (online) 1582-4934
    ISSN 1582-4934 ; 1582-1838
    DOI 10.1111/jcmm.14914
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

    In stock of ZB MED Cologne/Königswinter

    Zs.A 5752: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

  4. Article ; Online: Traditional Chinese medicine Ka-Sai-Ping suppresses the growths of gastric cancers via induction of autophagy.

    Zhu, Mo-Li / Lu, Jun-Xiu / Pan, Guo-Pin / Ping, Song / Zhao, Fan-Rong / Qi, Heng-Tian / Yu, Hai-Ya / Jian, Xu / Wan, Guang-Rui / Li, Peng

    Oncotarget

    2017  Volume 8, Issue 56, Page(s) 95075–95082

    Abstract: Traditional Chinese medication is increasingly used to treat a wide range of human chronic diseases like cardiovascular diseases and cancers. This study was designed to explore whether ka-sai-ping (KSP), a novel traditional Chinese medicine developed by ... ...

    Abstract Traditional Chinese medication is increasingly used to treat a wide range of human chronic diseases like cardiovascular diseases and cancers. This study was designed to explore whether ka-sai-ping (KSP), a novel traditional Chinese medicine developed by us, prevents gastric cancer growths and to investigate the underlying mechanism. The xenograft model of mouse gastric cancer was established by injecting MFCs into nude mouse subcutaneously. Cell autophagy was assessed by MDC staining. Lysosome and mitochondria were detected by Lyso-Tracker Red and Mito-Traker Green staining. Incubation of cultured mouse gastric cancer cell line MFCs with KSP for 48 hours, concentration-dependently reduced cell survivals and activated autophagy, which were accompanied with damaged lysosomes and mitochondria.
    Language English
    Publishing date 2017-11-10
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2560162-3
    ISSN 1949-2553 ; 1949-2553
    ISSN (online) 1949-2553
    ISSN 1949-2553
    DOI 10.18632/oncotarget.18041
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

  5. Article ; Online: Traditional Chinese medicine xin-mai-jia recouples endothelial nitric oxide synthase to prevent atherosclerosis in vivo.

    Yin, Ya-Ling / Zhu, Mo-Li / Wan, Jia / Zhang, Chong / Pan, Guo-Pin / Lu, Jun-Xiu / Ping, Song / Chen, Yuan / Zhao, Fan-Rong / Yu, Hai-Ya / Guo, Tao / Jian, Xu / Liu, Li-Ying / Zhang, Jia-Ning / Wan, Guang-Rui / Wang, Shuang-Xi / Li, Peng

    Scientific reports

    2017  Volume 7, Page(s) 43508

    Abstract: Endothelial dysfunction, which is caused by endothelial nitric oxide synthase (eNOS) uncoupling, is an initial step in atherosclerosis. This study was designed to explore whether Chinese medicine xin-mai-jia (XMJ) recouples eNOS to exert anti- ... ...

    Abstract Endothelial dysfunction, which is caused by endothelial nitric oxide synthase (eNOS) uncoupling, is an initial step in atherosclerosis. This study was designed to explore whether Chinese medicine xin-mai-jia (XMJ) recouples eNOS to exert anti-atherosclerotic effects. Pretreatment of XMJ (25, 50, 100 μg/ml) for 30 minutes concentration-dependently activated eNOS, improved cell viabilities, increased NO generations, and reduced ROS productions in human umbilical vein endothelial cells incubated with H
    MeSH term(s) Animals ; Atherosclerosis/drug therapy ; Atherosclerosis/etiology ; Atherosclerosis/metabolism ; Atherosclerosis/pathology ; Biomarkers ; Cell Survival/drug effects ; Cytokines/metabolism ; Diet, High-Fat ; Disease Models, Animal ; Drugs, Chinese Herbal/pharmacology ; Endothelium, Vascular/drug effects ; Endothelium, Vascular/metabolism ; Endothelium, Vascular/pathology ; Gene Expression Profiling ; Human Umbilical Vein Endothelial Cells ; Humans ; Hydrogen Peroxide/pharmacology ; Male ; Medicine, Chinese Traditional ; Nitric Oxide/biosynthesis ; Nitric Oxide Synthase Type III/metabolism ; Oxidative Stress/drug effects ; Phosphorylation ; Plaque, Atherosclerotic/metabolism ; Plaque, Atherosclerotic/pathology ; Rats ; Reactive Oxygen Species/metabolism ; Signal Transduction/drug effects ; Transcriptome
    Chemical Substances Biomarkers ; Cytokines ; Drugs, Chinese Herbal ; Reactive Oxygen Species ; Nitric Oxide (31C4KY9ESH) ; Hydrogen Peroxide (BBX060AN9V) ; Nitric Oxide Synthase Type III (EC 1.14.13.39)
    Language English
    Publishing date 2017-03-02
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2615211-3
    ISSN 2045-2322 ; 2045-2322
    ISSN (online) 2045-2322
    ISSN 2045-2322
    DOI 10.1038/srep43508
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

  6. Article ; Online: Pravastatin activates activator protein 2 alpha to augment the angiotensin II-induced abdominal aortic aneurysms.

    Ma, Hui / Liang, Wen-Jing / Shan, Mei-Rong / Wang, Xue-Qing / Zhou, Sheng-Nan / Chen, Yuan / Guo, Tao / Li, Peng / Yu, Hai-Ya / Liu, Chao / Yin, Ya-Ling / Wang, Yu-Lin / Dong, Bo / Pang, Xin-Yan / Wang, Shuang-Xi

    Oncotarget

    2017  Volume 8, Issue 9, Page(s) 14294–14305

    Abstract: We have previously reported that activation of AMP-activated kinase alpha 2 (AMPKα2) by nicotine or angiotensin II (AngII) instigates formation of abdominal aortic aneurysms (AAA) in Apoe-/- mice. Statins, used to treat hyperlipidemia widely, activate ... ...

    Abstract We have previously reported that activation of AMP-activated kinase alpha 2 (AMPKα2) by nicotine or angiotensin II (AngII) instigates formation of abdominal aortic aneurysms (AAA) in Apoe-/- mice. Statins, used to treat hyperlipidemia widely, activate AMPK in vascular cells. We sought to examine the effects of pravastatin on AAA formation and uncover the molecular mechanism. The AAA model was induced by AngII and evaluated by incidence, elastin degradation, and maximal abdominal aortic diameter in Apoe-/- mice. The phosphorylated levels of AMPKα2 and activator protein 2 alpha (AP-2α) were examined in cultured vascular smooth muscle cells (VSMCs) or in mice. We observed that pravastatin (50 mg/kg/day, 8 weeks) remarkably increased the AngII-induced AAA incidence in mice. In VSMCs, pravastatin increased the levels of pAMPK, pAP-2α, and MMP2 in both basal and AngII-stressed conditions, which were abolished by tempol and compound C. Pravastatin-upregulated MMP2 was abrogated by AMPKα2 or AP-2α siRNA. Lentivirus-mediated gene silence of AMPKα2 or AP-2α abolished pravastatin-worsened AAA formations in AngII-infused Apoe-/- mice. Clinical investigations demonstrated that both AMPKα2 and AP-2α phosphorylations were increased in AAA patients or human subjects taking pravastatin. In conclusion, pravastatin promotes AAA formation through AMPKα2-dependent AP-2α activations.
    MeSH term(s) AMP-Activated Protein Kinases/metabolism ; Angiotensin II/adverse effects ; Animals ; Anticholesteremic Agents/pharmacology ; Aortic Aneurysm, Abdominal/etiology ; Aortic Aneurysm, Abdominal/metabolism ; Aortic Aneurysm, Abdominal/pathology ; Apolipoproteins E/physiology ; Blotting, Western ; Cells, Cultured ; Disease Models, Animal ; Gene Expression Regulation/drug effects ; Humans ; Male ; Mice ; Mice, Knockout ; Myocytes, Smooth Muscle/drug effects ; Myocytes, Smooth Muscle/metabolism ; Myocytes, Smooth Muscle/pathology ; Phosphorylation ; Pravastatin/adverse effects ; Signal Transduction ; Transcription Factor AP-2/metabolism
    Chemical Substances Anticholesteremic Agents ; Apolipoproteins E ; Transcription Factor AP-2 ; Angiotensin II (11128-99-7) ; AMPK alpha2 subunit, mouse (EC 2.7.11.1) ; AMP-Activated Protein Kinases (EC 2.7.11.31) ; Pravastatin (KXO2KT9N0G)
    Language English
    Publishing date 2017-02-28
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2560162-3
    ISSN 1949-2553 ; 1949-2553
    ISSN (online) 1949-2553
    ISSN 1949-2553
    DOI 10.18632/oncotarget.15104
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

To top