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Article ; Online: DPP4 deficiency preserved cardiac function in abdominal aortic banding rats.

Ku, Hui-Chun / Su, Ming-Jai

PloS one

2014 Volume 9, Issue 1, Page(s) e85634

Abstract: Dipeptidyl peptidase-4 (DPP4) enzyme inhibition has been reported to increase plasma glucagon-like peptide-1 (GLP-1) level for controlling postprandial glucose concentration. A prominent GLP-1 level in DPP4-deficient rats contributed to the resistance of ...

Abstract	Dipeptidyl peptidase-4 (DPP4) enzyme inhibition has been reported to increase plasma glucagon-like peptide-1 (GLP-1) level for controlling postprandial glucose concentration. A prominent GLP-1 level in DPP4-deficient rats contributed to the resistance of endotoxemia and myocardial infarction. DPP4 deficiency also increased the capability against H₂O₂-induced stress in cardiomyocyte. However, long term effect of loss DPP4 activity on cardiac performance remained unclear. We used abdominal aortic banding (AAB) to induce pressure overload in wild-type and DPP4-deficient rats, and investigated the progression of heart failure. Cardiac histology and function were determined. Blood sample was collected for the plasma biochemical marker measurement. Heart weight to body weight ratio increased 1.2-fold after 6 weeks of AAB surgery. Cardiac function was compensated against pressure overload after 6 weeks of AAB surgery, but progressed to deterioration after 10 weeks of AAB surgery. AAB induced cardiac dysfunction was alleviated in DPP4-deficient rats. DPP4 activity increased significantly in wild-type rats after 10 weeks of AAB surgery, but remained unchanged in DPP4-deficient rats. In contrast, GLP-1 concentration was elevated by AAB after 6 weeks of surgery in DPP4-deficient rats, and remained high after 10 weeks of surgery. Ang II level markedly increased after 6 weeks of AAB surgery, but were less in DPP4-deficient rats. Massive collagen deposits in wild-type rat hearts appeared after 10 weeks of AAB surgery, which were alleviated in DPP4-deficient rats. Long term deficiency of DPP4 activity improved cardiac performance against pressure overload in rat, which may be attributed to a great quantity of GLP-1 accumulation during AAB.
MeSH term(s)	Angiotensin II/blood ; Animals ; Aorta, Abdominal/pathology ; Aorta, Abdominal/physiopathology ; Aorta, Abdominal/surgery ; Cardiomegaly/pathology ; Cardiomegaly/physiopathology ; Collagen/metabolism ; Dipeptidyl Peptidase 4/deficiency ; Dipeptidyl Peptidase 4/metabolism ; Glucagon-Like Peptide 1/blood ; Heart Function Tests ; Hemodynamics ; Male ; Pressure ; Rats ; Rats, Inbred F344 ; Signal Transduction ; Up-Regulation
Chemical Substances	Angiotensin II (11128-99-7) ; Glucagon-Like Peptide 1 (89750-14-1) ; Collagen (9007-34-5) ; Dipeptidyl Peptidase 4 (EC 3.4.14.5)
Language	English
Publishing date	2014-01-09
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0085634
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Article ; Online: A novel isoquinoline derivative exhibits anti-inflammatory properties and improves the outcomes of endotoxemia.

Lee, Shih-Yi / Hsin, Ling-Wei / Su, Ming-Jai / ChangChien, Ching-Chia / Ku, Hui-Chun

Pharmacological reports : PR

2019 Volume 71, Issue 6, Page(s) 1281–1288

Abstract: Background: Sepsis initiates an inflammatory response that causes widespread injury, and candidates for related myocardial depressant factors include cytokines and nitric oxide (NO). Nuclear factor kappa-B (NF-κB) stimulated by toll-like receptor 4 ... ...

Abstract	Background: Sepsis initiates an inflammatory response that causes widespread injury, and candidates for related myocardial depressant factors include cytokines and nitric oxide (NO). Nuclear factor kappa-B (NF-κB) stimulated by toll-like receptor 4 activation in sepsis mediates the transcription of multiple proinflammatory genes. These inflammatory mediators can cause myocardial dysfunction, which may deteriorate sepsis outcomes. To address this risk, we investigated the potential beneficial effects of a novel isoquinolines derivative, CYY054c, in LPS-induced inflammatory response leading to endotoxemia. Methods: The effects of CYY054c on cytokine and inflammatory-related protein production were evaluated in lipopolysaccharide (LPS)-stimulated macrophages. To determine whether CYY054c alleviates inflammatory storm-induced myocardial dysfunction in vivo, LPS was injected in rats, and cardiac function was measured by a pressure-volume loop. Results: CYY054c inhibited LPS-induced NF-κB expression in macrophages and reduced the release of tumor necrosis factor-alpha (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6), as well as the expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2). In the animal studies, CYY054c alleviated LPS-upregulated plasma TNF-α, IL-1β, IL-6, and NO concentrations, as well as cardiac monocyte chemotactic protein-1, iNOS, and COX-2 expression in rats, contributing to the improvement of cardiac function during endotoxemia. Conclusions: The reduction of NF-κB-mediated inflammatory mediators and the maintenance of hemodynamic performance by CYY054c improved the outcomes during endotoxemia. CYY054c may be a potential therapeutic agent for sepsis.
MeSH term(s)	Animals ; Anti-Inflammatory Agents/pharmacology ; Cell Line ; Cyclooxygenase 2/metabolism ; Cytokines/metabolism ; Endotoxemia/drug therapy ; Endotoxemia/metabolism ; Inflammation/drug therapy ; Inflammation/metabolism ; Inflammation Mediators/metabolism ; Interleukin-6/metabolism ; Isoquinolines/pharmacology ; Lipopolysaccharides ; Macrophages/drug effects ; Male ; Mice ; Nitric Oxide/metabolism ; Nitric Oxide Synthase Type II/metabolism ; RAW 264.7 Cells ; Rats ; Rats, Sprague-Dawley ; Signal Transduction/drug effects ; Tumor Necrosis Factor-alpha/metabolism
Chemical Substances	Anti-Inflammatory Agents ; Cytokines ; Inflammation Mediators ; Interleukin-6 ; Isoquinolines ; Lipopolysaccharides ; Tumor Necrosis Factor-alpha ; Nitric Oxide (31C4KY9ESH) ; Nitric Oxide Synthase Type II (EC 1.14.13.39) ; Cyclooxygenase 2 (EC 1.14.99.1) ; isoquinoline (JGX76Y85M6)
Language	English
Publishing date	2019-07-01
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2186248-5
ISSN	2299-5684 ; 1734-1140
ISSN (online)	2299-5684
ISSN	1734-1140
DOI	10.1016/j.pharep.2019.06.015
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Zs.A 861: Show issues

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Article ; Online: 5-hydroxytryptamine has an endothelium-derived hyperpolarizing factor-like effect on coronary flow in isolated rat hearts.

Chien, Ching-Chia Chang / Su, Ming-Jai

Journal of biomedical science

2015 Volume 22, Page(s) 42

Abstract: Background: 5-hydroxytryptamine (5-HT)-induced coronary artery responses have both vasoconstriction and vasorelaxation components. The vasoconstrictive effects of 5-HT have been well studied while the mechanism(s) of how 5-HT causes relaxation of ... ...

Abstract	Background: 5-hydroxytryptamine (5-HT)-induced coronary artery responses have both vasoconstriction and vasorelaxation components. The vasoconstrictive effects of 5-HT have been well studied while the mechanism(s) of how 5-HT causes relaxation of coronary arteries has been less investigated. In isolated rat hearts, 5-HT-induced coronary flow increases are partially resistant to the nitric oxide synthase inhibitor Nω-Nitro-L-arginine methyl ester (L-NAME) and are blocked by 5-HT7 receptor antagonists. In the present study, we investigated the role of 5-HT7 receptor in 5-HT-induced coronary flow increases in isolated rat hearts in the absence of L-NAME, and we also evaluated the involvement of endothelium-derived hyperpolarizing factor (EDHF) in 5-HT-induced coronary flow increases in L-NAME-treated hearts with the inhibitors of arachidonic acid metabolism and the blockers of Ca(2+)-activated K(+) channels. Results: In isolated rat hearts, 5-HT and the 5-HT7 receptor agonist 5-carboxamidotryptamine induced coronary flow increases, and both of these effects were blocked by the selective 5-HT7 receptor antagonist SB269970; in SB269970-treated hearts, 5-HT induced coronary flow decreases, which effect was blocked by the 5-HT2A receptor blocker R96544. In L-NAME-treated hearts, 5-HT-induced coronary flow increases were blocked by the phospholipase A2 inhibitor quinacrine and the cytochrome P450 inhibitor SKF525A, but were not inhibited by the cyclooxygenase inhibitor indomethacin. As to the effects of the Ca(2+)-activated K(+) channel blockers, 5-HT-induced coronary flow increases in L-NAME-treated hearts were inhibited by TRAM-34 (intermediate-conductance Ca(2+)-activated K(+) channel blocker) and UCL1684 (small-conductance Ca(2+)-activated K(+) channel blocker), but effects of the large-conductance Ca(2+)-activated K(+) channel blockers on 5-HT-induced coronary flow increases were various: penitrem A and paxilline did not significantly affect 5-HT-induced coronary flow responses while tetraethylammonium suppressed the coronary flow increases elicited by 5-HT. Conclusion: In the present study, we found that 5-HT-induced coronary flow increases are mediated by the activation of 5-HT7 receptor in rat hearts in the absence of L-NAME. Metabolites of cytochrome P450s, small-conductance Ca(2+)-activated K(+) channel, and intermediate-conductance Ca(2+)-activated K(+) channel are involved in 5-HT-induced coronary flow increases in L-NAME-treated hearts, which resemble the mechanisms of EDHF-induced vasorelaxation. The role of large-conductance Ca(2+)-activated K(+) channel in 5-HT-induced coronary flow increases in L-NAME-treated hearts needs further investigation.
MeSH term(s)	Animals ; Biological Factors/metabolism ; Calcium/metabolism ; Coronary Circulation/drug effects ; Coronary Vessels/drug effects ; Heart/drug effects ; Humans ; NG-Nitroarginine Methyl Ester/administration & dosage ; Organ Culture Techniques ; Potassium Channels, Calcium-Activated/antagonists & inhibitors ; Potassium Channels, Calcium-Activated/metabolism ; Pyrazoles/metabolism ; Rats ; Receptors, Serotonin/metabolism ; Serotonin/administration & dosage ; Vasoconstriction/drug effects ; Vasodilation/drug effects
Chemical Substances	Biological Factors ; Potassium Channels, Calcium-Activated ; Pyrazoles ; Receptors, Serotonin ; TRAM 34 ; endothelium-dependent hyperpolarization factor ; serotonin 7 receptor ; Serotonin (333DO1RDJY) ; Calcium (SY7Q814VUP) ; NG-Nitroarginine Methyl Ester (V55S2QJN2X)
Language	English
Publishing date	2015-06-16
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1193378-1
ISSN	1423-0127 ; 1021-7770
ISSN (online)	1423-0127
ISSN	1021-7770
DOI	10.1186/s12929-015-0149-8
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Zs.A 4037: Show issues

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Article ; Online: KS370G, a caffeamide derivative, attenuates unilateral ureteral obstruction-induced renal fibrosis by the reduction of inflammation and oxidative stress in mice.

Chuang, Sung-Ting / Kuo, Yueh-Hsiung / Su, Ming-Jai

European journal of pharmacology

2015 Volume 750, Page(s) 1–7

Abstract: Unilateral ureteral obstruction (UUO) is an established animal model used to study renal nephropathy. Caffeic acid phenethyl ester, a natural phenolic compound, possesses antifibrotic, anti-inflammation and anti-oxidative stress effects; however, rapid ... ...

Abstract	Unilateral ureteral obstruction (UUO) is an established animal model used to study renal nephropathy. Caffeic acid phenethyl ester, a natural phenolic compound, possesses antifibrotic, anti-inflammation and anti-oxidative stress effects; however, rapid decomposition by esterases substantially decreases its bioavailability. The goal of this study was to investigate the beneficial effects of KS370G, a synthetic caffeamide derivative, on UUO-induced renal injury. Following the UUO, KS370G (10mg/kg) was administered by oral gavage once a day. Renal injury was analyzed at 14 days post-operation. Our results show that KS370G significantly attenuated collagen deposition in the obstructed kidney and inhibited UUO-induced renal fibrosis markers expression, including fibronectin, type I collagen, vimentin, and α-smooth muscle actin (α-SMA). KS370G significantly lowered the expression of renal inflammatory chemokines/adhesion molecules and monocyte cells marker (MCP-1, VCAM-1, ICAM-1 and CD11b). KS370G also reduced renal malondialdehyde levels and reversed the expression of renal antioxidant enzymes (SOD and catalase) after UUO. Furthermore, KS370G significantly inhibited UUO-induced elevated plasma AngII and TGF-β1 levels, TGF-β1 protein expression and Smad3 phosphorylation. These findings demonstrate that KS370G reduces renal obstructive nephropathy by possibly inhibiting AngII, TGF-β and Smad3 signaling pathways.
MeSH term(s)	Angiotensin II/metabolism ; Animals ; Biomarkers/metabolism ; Caffeic Acids/pharmacology ; Catalase/metabolism ; Cell Adhesion Molecules/metabolism ; Chemokines/metabolism ; Collagen Type I/metabolism ; Cytoprotection/drug effects ; Fibronectins/metabolism ; Fibrosis ; Gene Expression Regulation/drug effects ; Inflammation/metabolism ; Kidney/drug effects ; Kidney/pathology ; Lipid Peroxidation/drug effects ; Male ; Mice ; Oxidative Stress/drug effects ; Smad3 Protein/metabolism ; Superoxide Dismutase/metabolism ; Transforming Growth Factor beta1/metabolism ; Ureteral Obstruction/metabolism ; Ureteral Obstruction/pathology
Chemical Substances	Biomarkers ; Caffeic Acids ; Cell Adhesion Molecules ; Chemokines ; Collagen Type I ; Fibronectins ; KS370G ; Smad3 Protein ; Transforming Growth Factor beta1 ; Angiotensin II (11128-99-7) ; Catalase (EC 1.11.1.6) ; Superoxide Dismutase (EC 1.15.1.1)
Language	English
Publishing date	2015-03-05
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80121-5
ISSN	1879-0712 ; 0014-2999
ISSN (online)	1879-0712
ISSN	0014-2999
DOI	10.1016/j.ejphar.2015.01.020
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Article: Soluble Dipeptidyl Peptidase-4 Induces Fibroblast Activation Through Proteinase-Activated Receptor-2.

Lee, Shih-Yi / Wu, Shao-Tung / Liang, Yao-Jen / Su, Ming-Jai / Huang, Cheng-Wei / Jao, Yu-Hsuan / Ku, Hui-Chun

Frontiers in pharmacology

2020 Volume 11, Page(s) 552818

Abstract: Fibroblasts are the chief secretory cells of the extracellular matrix (ECM) responsible for basal deposition and degradation of the ECM under normal conditions. During stress, fibroblasts undergo continuous activation, which is defined as the ... ...

Abstract	Fibroblasts are the chief secretory cells of the extracellular matrix (ECM) responsible for basal deposition and degradation of the ECM under normal conditions. During stress, fibroblasts undergo continuous activation, which is defined as the differentiation of fibroblasts into myofibroblasts, a cell type with an elevated capacity for secreting ECM proteins. Dipeptidyl peptidase-4 (DPP4) is a ubiquitously expressed transmembrane glycoprotein and exerts effects that are both dependent and independent of its enzymatic activity. DPP4 has been demonstrated to define fibroblast populations in human skin biopsies of systemic sclerosis. Shedding of DPP4 from different tissues into the circulation appears to be involved in the pathogenesis of the diseases. The mechanism underlying soluble DPP4-induced dermal fibrosis has not been clearly determined. The effects of DPP4 on murine 3T3 fibroblasts and human dermal fibroblasts were evaluated by measuring the expression of fibrotic proteins, such as α-SMA and collagen. Soluble DPP4 stimulated the activation of fibroblasts in a dose-dependent manner by activating nuclear factor-kappa B (NF-κB) and suppressor of mothers against decapentaplegic (SMAD) signaling. Blocking proteinase-activated receptor-2 (PAR2) abrogated the DPP4-induced activation of NF-κB and SMAD and expression of fibrosis-associated proteins in fibroblasts. Linagliptin, a clinically available DPP4 inhibitor, was observed to abrogate the soluble DPP4-induced expression of fibrotic proteins. This study demonstrated the mechanism underlying soluble DPP4, which activated NF-κB and SMAD signaling through PAR2, leading to fibroblast activation. Our data extend the current view of soluble DPP4. Elevated levels of circulating soluble DPP4 may contribute to one of the mediators that induce dermal fibrosis in patients.
Language	English
Publishing date	2020-09-30
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2587355-6
ISSN	1663-9812
ISSN	1663-9812
DOI	10.3389/fphar.2020.552818
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Article ; Online: Antifibrotic effects of KS370G, a caffeamide derivative, in renal ischemia-reperfusion injured mice and renal tubular epithelial cells.

Chuang, Sung-Ting / Kuo, Yueh-Hsiung / Su, Ming-Jai

Scientific reports

2014 Volume 4, Page(s) 5814

Abstract: Accumulating evidence suggests that renal tubulointerstitial fibrosis is a main cause of end-stage renal disease. Clinically, there are no beneficial treatments that can effectively reverse the progressive loss of renal functions. Caffeic acid phenethyl ... ...

Abstract	Accumulating evidence suggests that renal tubulointerstitial fibrosis is a main cause of end-stage renal disease. Clinically, there are no beneficial treatments that can effectively reverse the progressive loss of renal functions. Caffeic acid phenethyl ester is a natural phenolic antifibrotic agent, but rapid decomposition by an esterase leads to its low bioavailability. In this study, we evaluated the effects of KS370G, a caffeic acid phenylethyl amide, on murine renal fibrosis induced by unilateral renal ischemia-reperfusion injury (IRI) and in TGF-β₁ stimulated renal tubular epithelial cells (NRK52E and HK-2). In the animal model, renal fibrosis was evaluated at 14 days post-operation. Immediately following the operation, KS370G (10 mg/kg) was administered by oral gavage once a day. Our results show that KS370G markedly attenuates collagen deposition and inhibits an IRI-induced increase of fibronectin, vimentin, α-SMA and TGF-β₁ expression and plasma TGF-β₁ levels in the mouse kidney. Furthermore, KS370G reverses TGF-β1-induced downregulation of E-cadherin and upregulation of α-SMA and also decreases the expression of fibronectin, collagen I and PAI-1 and inhibits TGF-β₁-induced phosphorylation of Smad2/3. These findings show the beneficial effects of KS370G on renal fibrosis in vivo and in vitro with the possible mechanism being the inhibition of the Smad2/3 signaling pathway.
MeSH term(s)	Animals ; Caffeic Acids/pharmacology ; Caffeic Acids/therapeutic use ; Cdh1 Proteins/metabolism ; Cell Line ; Collagen/metabolism ; Epithelial Cells/drug effects ; Epithelial Cells/physiology ; Epithelial-Mesenchymal Transition ; Fibronectins/metabolism ; Fibrosis ; Humans ; Ischemia/drug therapy ; Ischemia/pathology ; Kidney Diseases/drug therapy ; Kidney Diseases/metabolism ; Kidney Tubules/blood supply ; Kidney Tubules/metabolism ; Kidney Tubules/pathology ; Male ; Mice, Inbred ICR ; Phosphorylation ; Protein Processing, Post-Translational/drug effects ; Reperfusion Injury/drug therapy ; Reperfusion Injury/metabolism ; Serpin E2/metabolism ; Smad2 Protein/metabolism ; Smad3 Protein/metabolism ; Transforming Growth Factor beta1/metabolism ; Vimentin/metabolism
Chemical Substances	Caffeic Acids ; Cdh1 Proteins ; Fibronectins ; Fzr1 protein, mouse ; KS370G ; Serpin E2 ; Serpine2 protein, mouse ; Smad2 Protein ; Smad2 protein, mouse ; Smad3 Protein ; Smad3 protein, mouse ; Tgfb1 protein, mouse ; Transforming Growth Factor beta1 ; Vimentin ; Collagen (9007-34-5)
Language	English
Publishing date	2014-07-24
Publishing country	England
Document type	Journal Article ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/srep05814
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Article ; Online: Activation of serotonin 5-HT₇ receptor induces coronary flow increase in isolated rat heart.

Chang Chien, Ching-Chia / Hsin, Ling-Wei / Su, Ming-Jai

European journal of pharmacology

2015 Volume 748, Page(s) 68–75

Abstract: Serotonin (5-Hydroxytryptamine, 5-HT) can elicit both vasoconstrictive and relaxant responses on rat coronary artery. The constrictive response has been well discussed, but the mechanism of relaxant response is less studied. In the present study, we ... ...

Abstract	Serotonin (5-Hydroxytryptamine, 5-HT) can elicit both vasoconstrictive and relaxant responses on rat coronary artery. The constrictive response has been well discussed, but the mechanism of relaxant response is less studied. In the present study, we found serotonin (0.3 and 1 μM) increased coronary flow on isolated rat hearts, and treatment of nitric oxide synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME) 300 μM reduced but not totally blocked this coronary flow increasing effect. In L-NAME 10 μM treated heart, treatment of selective serotonin 5-HT₇ receptor antagonist SB269970 0.1 μM blocked serotonin induced coronary flow increasing response, and in the presence of 1 μM SB269970, serotonin turned into reducing coronary flow. Treatment of TCW295 (8-(2,4-Dimethoxyphenyl)-6-methoxy-2-phenethyl-1,2,3,4-tetrahydroisoquinolin-7-ol hydrochloride), a novel serotonin 5-HT₂A/₇ receptor antagonist, inhibited both serotonin induced coronary flow increasing and decreasing effects. In conclusion, we found serotonin increases coronary flow of isolated rat heart by activating serotonin 5-HT₇ receptor activation, and this effect can be, at least partially, resistant to L-NAME.
MeSH term(s)	Adenosine/pharmacology ; Animals ; Coronary Circulation/drug effects ; Dose-Response Relationship, Drug ; In Vitro Techniques ; Isoquinolines/chemistry ; Isoquinolines/pharmacology ; Male ; NG-Nitroarginine Methyl Ester/pharmacology ; Phenols/pharmacology ; Rats ; Rats, Sprague-Dawley ; Receptors, Serotonin/metabolism ; Serotonin/pharmacology ; Serotonin Antagonists/pharmacology ; Sulfonamides/pharmacology
Chemical Substances	Isoquinolines ; Phenols ; Receptors, Serotonin ; SB 269970 ; Serotonin Antagonists ; Sulfonamides ; serotonin 7 receptor ; Serotonin (333DO1RDJY) ; isoquinoline (JGX76Y85M6) ; Adenosine (K72T3FS567) ; NG-Nitroarginine Methyl Ester (V55S2QJN2X)
Language	English
Publishing date	2015-02-05
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80121-5
ISSN	1879-0712 ; 0014-2999
ISSN (online)	1879-0712
ISSN	0014-2999
DOI	10.1016/j.ejphar.2014.08.027
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Zs.A 522: Show issues

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Article ; Online: DPP4 deficiency exerts protective effect against H2O2 induced oxidative stress in isolated cardiomyocytes.

Ku, Hui-Chun / Chen, Wen-Pin / Su, Ming-Jai

PloS one

2013 Volume 8, Issue 1, Page(s) e54518

Abstract: Apart from the antihyperglycemic effects, DPP4 inhibitors and GLP-1 molecules are involved in the preservation of cardiac functions. We have demonstrated that DPP4-deficient rats possess resistance to endotoxemia and ischemia/reperfusion stress. However, ...

Abstract	Apart from the antihyperglycemic effects, DPP4 inhibitors and GLP-1 molecules are involved in the preservation of cardiac functions. We have demonstrated that DPP4-deficient rats possess resistance to endotoxemia and ischemia/reperfusion stress. However, whether the decrease of DPP4 activity simply augmented the GLP-1 signaling or that such decrease resulted in a change of cellular function remain unclear. Accordingly, we investigated the responses of H(2)O(2)-induced oxidative stress in adult wild-type and DPP4-deficient rats isolated cardiomyocytes. The coadministration of GLP-1 or DPP4 inhibitor was also performed to define the mechanisms. Cell viability, ROS concentration, catalase activity, glucose uptake, prosurvival, proapoptotic signaling, and contractile function were examined after cells exposed to H(2)O(2). DPP4-deficient cardiomyocytes were found to be resistant to H(2)O(2)-induced cell death via activating AKT signaling, enhancing glucose uptake, preserving catalase activity, diminishing ROS level and proapoptotic signaling. GLP-1 concentration-dependently improved cell viability in wild-type cardiomyocyte against ROS stress, and the ceiling response concentration (200 nM) was chosen for studies. GLP-1 was shown to decrease H(2)O(2)-induced cell death by its receptor-dependent AKT pathway in wild-type cardiomyocytes, but failed to cause further activation of AKT in DPP4-deficient cardiomyocytes. Acute treatment of DPP4 inhibitor only augmented the protective effect of low dose GLP-1, but failed to alter fuel utilization or ameliorate cell viability in wild-type cardiomyocytes after H(2)O(2) exposure. The improvement of cell viability after H(2)O(2) exposure was correlated with the alleviation of cellular contractile dysfunction in both DPP4-deficient and GLP-1 treated wild-type cardiomyocytes. These findings demonstrated that GLP-1 receptor-dependent pathway is important and exert protective effect in wild-type cardiomyocyte. Long term loss of DPP4 activity increased the capability against ROS stress, which was more than GLP-1 dependent pathway.
MeSH term(s)	Animals ; Dipeptidyl Peptidase 4/genetics ; Dipeptidyl Peptidase 4/metabolism ; Enzyme Activation ; Enzyme-Linked Immunosorbent Assay ; Hydrogen Peroxide/pharmacology ; Myocytes, Cardiac/drug effects ; Myocytes, Cardiac/metabolism ; Oxidative Stress/drug effects ; Rats ; Rats, Inbred F344 ; Reactive Oxygen Species/metabolism
Chemical Substances	Reactive Oxygen Species ; Hydrogen Peroxide (BBX060AN9V) ; Dipeptidyl Peptidase 4 (EC 3.4.14.5)
Language	English
Publishing date	2013-01-24
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0054518
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Article: Reduction of blood pressure elevation by losartan in spontaneously hypertensive rats through suppression of LARG expression in vascular smooth muscle cells.

Chiu, Wei-Chiao / Chiang, Jiun-Yang / Juang, Jyh-Ming / Wu, Cho-Kai / Tsai, Chia-Ti / Tseng, Yung-Zu / Su, Ming-Jai / Chiang, Fu-Tien

Journal of the Formosan Medical Association = Taiwan yi zhi

2019 Volume 119, Issue 1 Pt 1, Page(s) 164–172

Abstract: Background/purpose: This study sought to elucidate the mechanism by which losartan inhibits blood pressure (BP) elevation in spontaneously hypertensive rats (SHRs).: Methods: Four-week-old Wistar-Kyoto (WKY) rats and SHRs were either treated with ... ...

Abstract	Background/purpose: This study sought to elucidate the mechanism by which losartan inhibits blood pressure (BP) elevation in spontaneously hypertensive rats (SHRs). Methods: Four-week-old Wistar-Kyoto (WKY) rats and SHRs were either treated with losartan (20 mg/kg/day) for 8 weeks or served as untreated controls. BP was measured by the tail-cuff method. At 12 weeks, isometric contraction of the aortic rings of the rats was evaluated with a force transducer and recorder. The mRNA and protein levels of the target Rho guanine nucleotide exchange factors (RhoGEFs), and the extent of myosin phosphatase target subunit 1 (MYPT-1) phosphorylation in the aorta, were determined using quantitative real-time polymerase chain reaction (qPCR) assay and Western blot analysis. Results: The BP of the four-week-old SHRs did not differ from that of the age-matched WKY rats, whereas the BP of the twelve-week-old control group SHRs was higher than that of the control group WKY rats. Losartan treatment, however, inhibited BP elevation in both rat strains, doing so to a greater extent in the treatment group SHRs. The contractile force in response to angiotensin II of the aortic rings from the SHRs treated with losartan was significantly lower than that of the aortic rings from the non-treated SHRs. The protein expression of leukemia-associated RhoGEF (LARG) was significantly higher in the non-treated SHRs compared to the non-treated WKY rats. Conclusion: The study results showed that the reduction of BP elevation by losartan in SHRs occurs through the suppression of LARG expression and MYPT-1 phosphorylation in vascular smooth muscle cells.
MeSH term(s)	Animals ; Antihypertensive Agents/pharmacology ; Blood Pressure/drug effects ; Gene Expression Regulation/drug effects ; Hypertension/drug therapy ; Hypertension/metabolism ; Losartan/pharmacology ; Male ; Muscle, Smooth, Vascular/drug effects ; Muscle, Smooth, Vascular/metabolism ; Phosphorylation ; Protein Phosphatase 1/drug effects ; Protein Phosphatase 1/metabolism ; Rats ; Rats, Inbred SHR ; Rats, Inbred WKY ; Rho Guanine Nucleotide Exchange Factors/drug effects ; Rho Guanine Nucleotide Exchange Factors/metabolism
Chemical Substances	Antihypertensive Agents ; Arhgef12 protein, rat ; Rho Guanine Nucleotide Exchange Factors ; Ppp1r12a protein, rat (EC 3.1.3.16) ; Protein Phosphatase 1 (EC 3.1.3.16) ; Losartan (JMS50MPO89)
Language	English
Publishing date	2019-04-05
Publishing country	Singapore
Document type	Journal Article
ZDB-ID	2096659-3
ISSN	1876-0821 ; 0929-6646
ISSN (online)	1876-0821
ISSN	0929-6646
DOI	10.1016/j.jfma.2019.03.015
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Article ; Online: Comparison of the cardiac effects between quinazoline-based alpha1-adrenoceptor antagonists on occlusion-reperfusion injury.

Lee, An-Sheng / Su, Ming-Jai

Journal of biomedical science

2008 Volume 15, Issue 2, Page(s) 239–249

Abstract: Quinazoline-based compounds such as prazosin and its congeners including doxazosin, bunazosin, and terazosin are widely used as antihypertensive agents. However, there were many clinical observations showing that using these agents may result in higher ... ...

Abstract	Quinazoline-based compounds such as prazosin and its congeners including doxazosin, bunazosin, and terazosin are widely used as antihypertensive agents. However, there were many clinical observations showing that using these agents may result in higher risk of cardiovascular accidents in recent years. In this study, we compared the effects of four alpha-adrenoceptor antagonists: prazosin, doxazosin, bunazosin, and terazosin on occlusion-reperfusion injury. Langendorff-perfused rat hearts were pretreated with these four antagonists, and then the left main coronary artery was occluded. After 30 min occlusion, the hearts were reperfused for 2 h and the infarct sizes were measured. Two of the compounds studied, prazosin and doxazosin, apparently increased infarct size, CK-MB, and LDH activities after 2 h reperfusion. In contrast, bunazosin decreased infarct size and those biochemical indicators of cellular damage compared to control hearts. Although infarct size after reperfusion was differently changed by these four alpha-adrenoceptor antagonists, TUNEL-positive nuclei and caspase-3 protein expressions of all the groups were not significantly different. We supposed that the different effects of these four agents on infarct size came from the difference in necrosis rather than apoptosis.
MeSH term(s)	Adrenergic alpha-Antagonists/pharmacology ; Animals ; Apoptosis/drug effects ; Caspase 3/metabolism ; Male ; Myocardial Infarction/drug therapy ; Myocardial Infarction/metabolism ; Myocardial Infarction/pathology ; Myocardial Reperfusion Injury/drug therapy ; Myocardial Reperfusion Injury/metabolism ; Myocardial Reperfusion Injury/pathology ; Necrosis ; Rats ; Rats, Wistar
Chemical Substances	Adrenergic alpha-Antagonists ; Casp3 protein, rat (EC 3.4.22.-) ; Caspase 3 (EC 3.4.22.-)
Language	English
Publishing date	2008-03
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1193378-1
ISSN	1423-0127 ; 1021-7770
ISSN (online)	1423-0127
ISSN	1021-7770
DOI	10.1007/s11373-007-9214-y
Database	MEDical Literature Analysis and Retrieval System OnLINE

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