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Article ; Online: David Triggle: Research collaborations and scientific exchanges with the China Pharmaceutical University, Nanjing, China.

Dai, De-Zai

2015 Volume 98, Issue 2, Page(s) 303–307

Abstract: Over the period 1995-2012, David Triggle was a frequent visitor to the China Pharmaceutical University in Nanjing, China making many important contributions that enhanced the activities of the Research Division of Pharmacology at the University. In ... ...

Abstract	Over the period 1995-2012, David Triggle was a frequent visitor to the China Pharmaceutical University in Nanjing, China making many important contributions that enhanced the activities of the Research Division of Pharmacology at the University. In addition to providing collegial advice and facilitating interactions with the international pharmacological community, Professor Triggle's international reputation as a thought leader in the field of ion channel research and drug discovery provided important insights into the potential pathophysiological and therapeutic effects of targeting ion channels. This included the L-type calcium channel and the outward delayed rectified potassium currents of rapid (IKr) and slow (IKs) components in the myocardium. The Nanjing research team had been particularly interested in ion channel dysfunction in the context of cardiac arrhythmias, remodeling and drug discovery. With Professor Triggle's assistance, the relationship between an increase in ICa.L and other biological events including an enhancement of IKr and IKr currents, NADPH oxidase and endothelin receptor activation, down regulation of calcium modulating protein FKBP12.6, sarco/endoplasmic reticulum Ca(2+)ATPse (SERCA2A) and calsequens 2 (CASQ2), calcium leak at the diastole and endoplasmic reticulum stress, were evaluated and are discussed. Additionally, the organization of several international symposia was greatly enhanced by input from Professor Triggle as were the published research manuscripts in international pharmacology journals. During his association with the China Pharmaceutical University, Professor Triggle aided in enhancing the scientific standing of the Pharmacology department and was a highly effective ambassador for international research cooperation.
MeSH term(s)	Arrhythmias, Cardiac/etiology ; Arrhythmias, Cardiac/history ; Arrhythmias, Cardiac/physiopathology ; China ; Death, Sudden, Cardiac/etiology ; Drug Discovery/history ; Drug Discovery/methods ; History, 20th Century ; History, 21st Century ; International Educational Exchange/history ; Internationality ; Ion Channels/drug effects ; Ion Channels/history ; Periodicals as Topic/history ; Periodicals as Topic/standards ; Research/history ; United States ; Writing/history ; Writing/standards
Chemical Substances	Ion Channels
Language	English
Publishing date	2015-11-15
Publishing country	England
Document type	Biography ; Historical Article ; Journal Article ; Portraits ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	208787-x
ISSN	1873-2968 ; 0006-2952
ISSN (online)	1873-2968
ISSN	0006-2952
DOI	10.1016/j.bcp.2015.04.023
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Article: CPU86017: a novel Class III antiarrhythmic agent with multiple actions at ion channels.

Dai, De-Zai

Cardiovascular drug reviews

2006 Volume 24, Issue 2, Page(s) 101–115

Abstract: CPU86017 is a novel Class III antiarrhythmic agent derived from berberine and with an improved pharmacological profile, solubility and bioavailability. It is active in suppressing arrhythmias in several animal models. The ED(50) of CPU86017 for ... ...

Abstract	CPU86017 is a novel Class III antiarrhythmic agent derived from berberine and with an improved pharmacological profile, solubility and bioavailability. It is active in suppressing arrhythmias in several animal models. The ED(50) of CPU86017 for suppressing ischemia/reperfusion arrhythmias in rats was 0.22 mg/kg against 2.23 mg/kg for lidocaine. CPU86017 is about 10-fold more potent than lidocaine. It blocks I(K(R.tail)), I(K(S)), and I(Ca(L)) currents with IC(50) values of 25, 14.4, and 11.5 microM, respectively. The plasma t(1/2) of CPU86017, i.v. bolus, in rabbits and dogs is approximately 90 min. The effective plasma levels of CPU86017 in rabbits required to delay the appearance of oubain-induced ventricular arrhythmias is in the range of 0.13-0.31 microg/mL. Higher levels of the drug are required to eliminate ventricular arrhythmias produced by two-stage ligation of the coronary artery in anesthetized dogs. Drug levels in myocardium are much higher than in plasma. CPU80617 has an antioxidant effect that is likely to contribute to its antiarrhythmic activity. The abnormal expression of the ryanodine receptor type 2 (RyR2) and of FKBP12.6 is reduced by CPU80617 during its ventricular tachyarrhythmia-suppressing action. CPU86017 appears to be a promising antiarrhythmic agent with a cardioprotective action. It can be expected to protect from malignant arrhythmias and sudden cardiac death by suppressing molecular events caused by channelopathies.
MeSH term(s)	Animals ; Anti-Arrhythmia Agents/classification ; Anti-Arrhythmia Agents/pharmacology ; Anti-Arrhythmia Agents/therapeutic use ; Arrhythmias, Cardiac/physiopathology ; Arrhythmias, Cardiac/prevention & control ; Berberine/analogs & derivatives ; Berberine/chemistry ; Berberine/therapeutic use ; Death, Sudden, Cardiac/prevention & control ; Humans ; Ion Channels/antagonists & inhibitors ; Ion Channels/physiology ; Molecular Structure ; Ventricular Fibrillation/physiopathology ; Ventricular Fibrillation/prevention & control
Chemical Substances	4-chlorobenzyltetrahydroberberine ; Anti-Arrhythmia Agents ; Ion Channels ; Berberine (0I8Y3P32UF)
Language	English
Publishing date	2006
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	645099-4
ISSN	0897-5957
ISSN	0897-5957
DOI	10.1111/j.1527-3466.2006.00101.x
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Article ; Online: Role of endothelin receptor A and NADPH oxidase in vascular abnormalities

De-Zai Dai / Yin Dai

Vascular Health and Risk Management, Vol 2010, Iss default, Pp 787-

2010 Volume 794

Abstract: De-Zai Dai, Yin DaiResearch Division of Pharmacology, China Pharmaceutical University, Nanjing ...

Abstract	De-Zai Dai, Yin DaiResearch Division of Pharmacology, China Pharmaceutical University, Nanjing, 210009, ChinaAbstract: Vascular dilatation is critically impaired in many diseases and is encountered by an upregulated endothelin receptor A (ETA) in the vasculature in association with a decline in nitric oxide bioavailability. Diabetic vasculopathy is characterized as a compromised vascular dilatation, implicated in many diabetic complications. It appears to be activated ETA and NADPH (nicotinamide adenine dinucleotide phosphate) oxidase in the vasculature. Glucose-lowering agents do not always blunt these changes, as these changes may be progressive leading to the end stage of renal disease. The vascular insults by hypertension, hyperglycemia and aging may share the changes with diabetic vascular beds. Endothelin receptor antagonist CPU0213 and ingredients from plant origins such as CPU86017, p-benzyl-tetra-hydro-berberine are effective in attenuating vascular abnormality by normalizing changes of biomarkers in the vascular wall. The early sign of subclinical atherosclerosis presented as an intima media thickness in the carotid may indicate endothelium dysfunction. The reduced ABI (ankle brachial index) has been taken to predict patients at risk for cardiovascular and cerebrovascular events, and an increased risk of mortality from all causes and cardiovascular disease. An application of agents which suppress the activated ET-NADPH oxidase in the vascular wall is beneficial to attenuate vascular abnormalities. It is worth testing the activity of these agents further for the potential in relieving abnormal vascular activity, reducing the risk of morbidity and mortality in patients at risk.Keywords: diabetes, hypercholesterolemia, ETA, peripheral artery disease, vascular dilatation
Keywords	Diseases of the circulatory (Cardiovascular) system ; RC666-701 ; Specialties of internal medicine ; RC581-951 ; Internal medicine ; RC31-1245 ; Medicine ; R ; DOAJ:Cardiovascular ; DOAJ:Medicine (General) ; DOAJ:Health Sciences
Subject code	610
Language	English
Publishing date	2010-09-01T00:00:00Z
Publisher	Dove Medical Press
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article: Two patterns of ion channelopathy in the myocardium: perspectives for development of anti-arrhythmic agents.

Dai, De-Zai

Current opinion in investigational drugs (London, England : 2000)

2005 Volume 6, Issue 3, Page(s) 289–297

Abstract: Cardiac arrhythmia remains a significant problem, due to the high morbidity and mortality associated with cardiovascular diseases with prominent cardiac remodeling. There is still a lack of effective drugs with which to combat this life-threatening ... ...

Abstract	Cardiac arrhythmia remains a significant problem, due to the high morbidity and mortality associated with cardiovascular diseases with prominent cardiac remodeling. There is still a lack of effective drugs with which to combat this life-threatening disorder. The abnormal electrophysiological properties of the heart can be explained in terms of ion channels and channelopathy and, in recent years, advances have been made in understanding these properties. There are two patterns of ion channelopathies in the diseased heart: Single insufficiency disorder, which is attributed to mutations in genes, and a multiple derangement of channels. Malignant arrhythmias in a diseased heart usually occur when ventricular hypertrophy is evident, and when they are associated with abnormal repolarization. Abnormalities in the ryanodine receptor-calcium release channel complex (RyR)2, FK-506 binding protein (FKBP 12.6), cardiac sarcoplasmic reticulum calcium ATPase (SERCA2a) and phospholamban (PLB) are involved in the initiation of cardiac arrhythmias, and can be identified as targets for therapeutic interventions.
MeSH term(s)	Animals ; Anti-Arrhythmia Agents/chemistry ; Anti-Arrhythmia Agents/therapeutic use ; Calcium Channels/drug effects ; Calcium Channels/metabolism ; Calcium-Transporting ATPases/metabolism ; Cardiomegaly/drug therapy ; Humans ; Ion Channels/drug effects ; Ion Channels/metabolism ; Ion Channels/physiopathology ; Muscle Proteins/metabolism ; Myocardium/metabolism ; Myocardium/pathology ; Ryanodine Receptor Calcium Release Channel/drug effects ; Ryanodine Receptor Calcium Release Channel/metabolism ; Sarcoplasmic Reticulum/drug effects ; Sarcoplasmic Reticulum/metabolism ; Sarcoplasmic Reticulum Calcium-Transporting ATPases ; Tacrolimus Binding Proteins/metabolism
Chemical Substances	Anti-Arrhythmia Agents ; Calcium Channels ; Ion Channels ; Muscle Proteins ; Ryanodine Receptor Calcium Release Channel ; Calcium-Transporting ATPases (EC 3.6.3.8) ; Sarcoplasmic Reticulum Calcium-Transporting ATPases (EC 3.6.3.8) ; Tacrolimus Binding Proteins (EC 5.2.1.-)
Language	English
Publishing date	2005-03
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2027913-9
ISSN	2040-3429 ; 1472-4472 ; 0967-8298
ISSN (online)	2040-3429
ISSN	1472-4472 ; 0967-8298
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Article ; Online: Role of endothelin receptor A and NADPH oxidase in vascular abnormalities.

Dai, De-Zai / Dai, Yin

Vascular health and risk management

2010 Volume 6, Page(s) 787–794

Abstract: Vascular dilatation is critically impaired in many diseases and is encountered by an upregulated endothelin receptor A (ETA) in the vasculature in association with a decline in nitric oxide bioavailability. Diabetic vasculopathy is characterized as a ... ...

Abstract	Vascular dilatation is critically impaired in many diseases and is encountered by an upregulated endothelin receptor A (ETA) in the vasculature in association with a decline in nitric oxide bioavailability. Diabetic vasculopathy is characterized as a compromised vascular dilatation, implicated in many diabetic complications. It appears to be activated ETA and NADPH (nicotinamide adenine dinucleotide phosphate) oxidase in the vasculature. Glucose-lowering agents do not always blunt these changes, as these changes may be progressive leading to the end stage of renal disease. The vascular insults by hypertension, hyperglycemia and aging may share the changes with diabetic vascular beds. Endothelin receptor antagonist CPU0213 and ingredients from plant origins such as CPU86017, p-benzyl-tetra-hydro-berberine are effective in attenuating vascular abnormality by normalizing changes of biomarkers in the vascular wall. The early sign of subclinical atherosclerosis presented as an intima media thickness in the carotid may indicate endothelium dysfunction. The reduced ABI (ankle brachial index) has been taken to predict patients at risk for cardiovascular and cerebrovascular events, and an increased risk of mortality from all causes and cardiovascular disease. An application of agents which suppress the activated ET-NADPH oxidase in the vascular wall is beneficial to attenuate vascular abnormalities. It is worth testing the activity of these agents further for the potential in relieving abnormal vascular activity, reducing the risk of morbidity and mortality in patients at risk.
MeSH term(s)	Animals ; Ankle Brachial Index ; Blood Vessels/metabolism ; Blood Vessels/physiopathology ; Diabetic Angiopathies/metabolism ; Diabetic Angiopathies/physiopathology ; Endothelium, Vascular/metabolism ; Endothelium, Vascular/physiopathology ; Humans ; Hyperlipidemias/metabolism ; Hyperlipidemias/physiopathology ; Hypertension/physiopathology ; NADPH Oxidases/physiology ; Nitric Oxide/metabolism ; Nitric Oxide/physiology ; Obesity/metabolism ; Obesity/physiopathology ; Oxidative Stress/physiology ; Peripheral Arterial Disease/physiopathology ; Receptor, Endothelin A/physiology ; Signal Transduction/physiology
Chemical Substances	Receptor, Endothelin A ; Nitric Oxide (31C4KY9ESH) ; NADPH Oxidases (EC 1.6.3.-)
Language	English
Publishing date	2010-09-07
Publishing country	New Zealand
Document type	Journal Article ; Review
ZDB-ID	2186568-1
ISSN	1178-2048 ; 1176-6344
ISSN (online)	1178-2048
ISSN	1176-6344
DOI	10.2147/vhrm.s6556
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Article ; Online: AQP4 KO exacerbating renal dysfunction is mediated by endoplasmic reticulum stress and p66Shc and is attenuated by apocynin and endothelin antagonist CPU0213.

Cheng, Yu-Si / Dai, De-Zai / Dai, Yin

European journal of pharmacology

2013 Volume 721, Issue 1-3, Page(s) 249–258

Abstract: Aquaporin 4 (AQP4) is essential in normal kidney. We hypothesized that AQP4 knockout (KO) may exacerbate pro-inflammatory factors in the stress induced renal insufficiency. Mechanisms underlying are likely due to activating renal oxidative stress adaptor ...

Abstract	Aquaporin 4 (AQP4) is essential in normal kidney. We hypothesized that AQP4 knockout (KO) may exacerbate pro-inflammatory factors in the stress induced renal insufficiency. Mechanisms underlying are likely due to activating renal oxidative stress adaptor p66Shc and endoplasmic reticulum (ER) stress that could be mediated by endothelin (ET)-NADPH oxidase (NOX) pathway. AQP4 KO and wild type (WT) mice were randomly divided into 4 groups: control, isoproterenol (1mg/kg, s.c., 5d), and interventions in the last 3 days with either apocynin (NADPH oxidase inhibitor, 100mg/kg, p.o.) or CPU0213 (a dual endothelin receptor antagonist 200mg/kg, p.o.). In addition, HK2 cells were cultured in 4 groups: control, isoproterenol (10(-6)M), intervened with apocynin (10(-6)M) or CPU0213 (10(-6)M). In AQP4 KO mice elevated creatinine levels were further increased by isoproterenol compared to AQP4 KO alone. In RT-PCR, western blot and immunohistochemical assay p66Shc and PERK were significantly increased in the kidney of AQP4 KO mice, associated with pro-inflammatory factors CX40, CX43, MMP-9 and ETA compared to the WT mice. Expression of AQP4 was escalated in isoproterenol incubated HK2 cells, and the enhanced protein of PERK and p-PERK/PERK, and p66shc in vivo and in vitro were significantly attenuated by either apocynin or CPU0213. In conclusion, AQP4 KO deteriorates renal dysfunction due to exacerbating ER stress and p66Shc in the kidney. Either endothelin antagonism or NADPH oxidase blockade partly relieves renal dysfunction through suppressing abnormal biomarkers by APQ4 KO and isoproterenol in the kidney.
MeSH term(s)	Acetophenones/antagonists & inhibitors ; Animals ; Aquaporin 4/deficiency ; Aquaporin 4/genetics ; Connexin 43/genetics ; Creatinine/blood ; Down-Regulation/drug effects ; Endoplasmic Reticulum Stress/drug effects ; Endothelins/antagonists & inhibitors ; Female ; Gene Knockout Techniques ; Kidney/pathology ; Kidney/physiopathology ; Male ; Malondialdehyde/blood ; Matrix Metalloproteinase 9/genetics ; Mice ; Pyrazoles/pharmacology ; Shc Signaling Adaptor Proteins/metabolism ; Src Homology 2 Domain-Containing, Transforming Protein 1 ; eIF-2 Kinase/genetics
Chemical Substances	Acetophenones ; Aquaporin 4 ; CPU0213 ; Connexin 43 ; Endothelins ; Pyrazoles ; Shc Signaling Adaptor Proteins ; Shc1 protein, mouse ; Src Homology 2 Domain-Containing, Transforming Protein 1 ; Malondialdehyde (4Y8F71G49Q) ; Creatinine (AYI8EX34EU) ; acetovanillone (B6J7B9UDTR) ; PERK kinase (EC 2.7.11.1) ; eIF-2 Kinase (EC 2.7.11.1) ; Matrix Metalloproteinase 9 (EC 3.4.24.35)
Language	English
Publishing date	2013-12-05
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.2013.09.028
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Article: Induced ion currents and the endothelin pathway as targets for anti-arrhythmic agents.

Dai, De-Zai / Dai, Yin

Current opinion in investigational drugs (London, England : 2000)

2008 Volume 9, Issue 9, Page(s) 1001–1008

Abstract: ... torsades de pointes (Tdp). Ion channelopathy that is involved in mechanisms underlying sudden cardiac death (SCD ...

Abstract	The development of novel anti-arrhythmic drugs is necessary, specifically agents that do not cause torsades de pointes (Tdp). Ion channelopathy that is involved in mechanisms underlying sudden cardiac death (SCD) includes both ion channels in the membrane, and the calcium-releasing channels and the calcium uptake process in the sarcoplasmic reticulum. Advances in the understanding of abnormalities of ion channels in the myocardium caused by congenital defects or by a failing heart and cardiomyopathy offer further insights into the relationship between channelopathy and SCD. Enhanced L-type Ca2+ current (ICa.L) activity has been detected in the hearts of patients with a mutation of the Cav1.2 gene; these patients exhibit a high risk of SCD. Rats with thyroxin-induced cardiomyopathy demonstrate an increase in ICa.L activity that is responsible for exacerbated ventricular fibrillation (VF). This is suppressed by propranolol or CPU-86017, a class III anti-arrhythmic agent with potent antioxidant activity. Interestingly, an increase in rapidly (IKr) and slowly (IKs) activating delayed rectifying K+ currents is caused by gain-of-function mutations of the KCNH2 and KCNQ1 genes, respectively, in patients with short QT syndrome (SQT). Increased IKr and IKs, which are associated with exacerbated VF, are also found in models of thyroxin-induced cardiomyopathy and are suppressed by CPU-86017. ICa.L, IKr and IKs can also be induced in cardiomyocytes when incubated with isoproterenol. A reversal of upstream lesions by an endothelin receptor antagonist CPU-0213 provides suppression of ventricular tachyarrhythmias and upregulates FK506 binding protein 12.6. CPU-86017 and its chiral isomer SR-CPU-86017 relieve upstream lesions, with mild suppression of IKr and moderate suppression of IKs and ICa.L. These agents may be promising as anti-arrhythmic agents that produce less Tdp tachyarrhythmias.
MeSH term(s)	Animals ; Anti-Arrhythmia Agents/pharmacology ; Arrhythmias, Cardiac/physiopathology ; Berberine/analogs & derivatives ; Berberine/pharmacology ; Berberine/therapeutic use ; Death, Sudden, Cardiac ; Endothelins/physiology ; Humans ; Ion Channels/drug effects ; Potassium Channels/drug effects ; Signal Transduction/drug effects ; Signal Transduction/physiology ; Ventricular Fibrillation/physiopathology
Chemical Substances	4-chlorobenzyltetrahydroberberine ; Anti-Arrhythmia Agents ; Endothelins ; Ion Channels ; Potassium Channels ; Berberine (0I8Y3P32UF)
Language	English
Publishing date	2008-09
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2027913-9
ISSN	2040-3429 ; 1472-4472 ; 0967-8298
ISSN (online)	2040-3429
ISSN	1472-4472 ; 0967-8298
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Article: AQP4 KO exacerbating renal dysfunction is mediated by endoplasmic reticulum stress and p66Shc and is attenuated by apocynin and endothelin antagonist CPU0213

Cheng, Yu-Si / Dai, De-Zai / Dai, Yin

European journal of pharmacology. 2013 Dec. 5, v. 721, no. 1-3

2013

Abstract	Aquaporin 4 (AQP4) is essential in normal kidney. We hypothesized that AQP4 knockout (KO) may exacerbate pro-inflammatory factors in the stress induced renal insufficiency. Mechanisms underlying are likely due to activating renal oxidative stress adaptor p66Shc and endoplasmic reticulum (ER) stress that could be mediated by endothelin (ET)—NADPH oxidase (NOX) pathway. AQP4 KO and wild type (WT) mice were randomly divided into 4 groups: control, isoproterenol (1mg/kg, s.c., 5d), and interventions in the last 3 days with either apocynin (NADPH oxidase inhibitor, 100mg/kg, p.o.) or CPU0213 (a dual endothelin receptor antagonist 200mg/kg, p.o.). In addition, HK₂ cells were cultured in 4 groups: control, isoproterenol (10⁻⁶M), intervened with apocynin (10⁻⁶M) or CPU0213 (10⁻⁶M). In AQP4 KO mice elevated creatinine levels were further increased by isoproterenol compared to AQP4 KO alone. In RT-PCR, western blot and immunohistochemical assay p66Shc and PERK were significantly increased in the kidney of AQP4 KO mice, associated with pro-inflammatory factors CX40, CX43, MMP-9 and ETA compared to the WT mice. Expression of AQP4 was escalated in isoproterenol incubated HK₂ cells, and the enhanced protein of PERK and p-PERK/PERK, and p66shc in vivo and in vitro were significantly attenuated by either apocynin or CPU0213. In conclusion, AQP4 KO deteriorates renal dysfunction due to exacerbating ER stress and p66Shc in the kidney. Either endothelin antagonism or NADPH oxidase blockade partly relieves renal dysfunction through suppressing abnormal biomarkers by APQ4 KO and isoproterenol in the kidney.
Keywords	NADP (coenzyme) ; Western blotting ; antagonists ; aquaporins ; biomarkers ; creatinine ; cultured cells ; endoplasmic reticulum ; immunohistochemistry ; kidneys ; mice ; oxidative stress ; pharmacology ; renal failure ; reverse transcriptase polymerase chain reaction
Language	English
Dates of publication	2013-1205
Size	p. 249-258.
Publishing place	Elsevier B.V.
Document type	Article
ZDB-ID	80121-5
ISSN	1879-0712 ; 0014-2999
ISSN (online)	1879-0712
ISSN	0014-2999
DOI	10.1016/j.ejphar.2013.09.028
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Exogenous hydrogen sulphide ameliorates diabetic cardiomyopathy in rats by reversing disordered calcium-handling system in sarcoplasmic reticulum.

Cheng, Yu-Si / Dai, De-Zai / Dai, Yin / Zhu, Dong-Dong / Liu, Bi-Cheng

The Journal of pharmacy and pharmacology

2016 Volume 68, Issue 3, Page(s) 379–388

Abstract: Objectives: Hydrogen sulphide (H2 S) has been found to be involved in cardiovascular diseases, but the exact mechanism has not been clarified. The purpose of this study was to investigate whether sodium hydrogen sulphide (NaHS), the donor of H2 S, can ... ...

Abstract	Objectives: Hydrogen sulphide (H2 S) has been found to be involved in cardiovascular diseases, but the exact mechanism has not been clarified. The purpose of this study was to investigate whether sodium hydrogen sulphide (NaHS), the donor of H2 S, can improve diabetic cardiomyopathy by reversing disordered calcium-handling system in sarcoplasmic reticulum (SR). Methods: Sprague Dawley rats were injected with streptozotocin (STZ, 60 mg/kg, i.p.) to build diabetic model. Treatment groups included: aminoguanidine group (AG, 100 mg/kg, p.o.) and NaHS group (5 mg/kg per day, s.c.). Key findings: Cardiac dysfunction and myocardial hypertrophy were found in diabetic model (DM) group, along with increased ROS levels and upregulated mRNA and protein expressions of NADPH p22(phox) , endothelin A receptor (ETA ) and protein kinase Cε (PKCε). Expressions of calcium-handling proteins in SR including FK506-binding proteins (FKBP12.6), sarcoplasmic reticulum Ca(2+) ATPase (SERCA2a) and calsequestrin 2 (CASQ2) were downregulated in DM group, accompanied by elevated concentration of diastolic free calcium in high glucose-incubated cardiomyocytes, indicating of calcium leak. After treated by NaHS, these abnormalities were attenuated significantly. Conclusions: Exogenous H2 S played a protective role in diabetic cardiomyopathy by inhibiting abnormal calcium-handling system in SR and ET-NADPH oxidase-PKCε pathway.
MeSH term(s)	Animals ; Calcium/metabolism ; Diabetes Mellitus, Experimental/chemically induced ; Diabetes Mellitus, Experimental/drug therapy ; Diabetes Mellitus, Experimental/metabolism ; Diabetic Cardiomyopathies/drug therapy ; Diabetic Cardiomyopathies/metabolism ; Disease Models, Animal ; Down-Regulation/drug effects ; Hydrogen Sulfide/pharmacology ; Male ; Myocardium/metabolism ; Myocytes, Cardiac/drug effects ; Myocytes, Cardiac/metabolism ; RNA, Messenger/metabolism ; Rats ; Rats, Sprague-Dawley ; Reactive Oxygen Species/metabolism ; Sarcoplasmic Reticulum/drug effects ; Sarcoplasmic Reticulum/metabolism ; Signal Transduction/drug effects ; Streptozocin/pharmacology ; Sulfides/pharmacology ; Up-Regulation/drug effects
Chemical Substances	RNA, Messenger ; Reactive Oxygen Species ; Sulfides ; Streptozocin (5W494URQ81) ; Calcium (SY7Q814VUP) ; sodium sulfide (YGR27ZW0Y7) ; Hydrogen Sulfide (YY9FVM7NSN)
Language	English
Publishing date	2016-03
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	3107-0
ISSN	2042-7158 ; 0022-3573 ; 0373-1022
ISSN (online)	2042-7158
ISSN	0022-3573 ; 0373-1022
DOI	10.1111/jphp.12517
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Article ; Online: Apocynin and raisanberine alleviate intermittent hypoxia induced abnormal StAR and 3β-HSD and low testosterone by suppressing endoplasmic reticulum stress and activated p66Shc in rat testes.

Zhang, Guo-Lin / Dai, De-Zai / Zhang, Can / Dai, Yin

Reproductive toxicology (Elmsford, N.Y.)

2013 Volume 36, Page(s) 60–70

Abstract: We hypothesized that hypoxia induced testicular damage is mediated by an activated NADPH oxidase (NOX), therefore, APO (apocynin) an inhibitor of NOX and raisanberine (RS), a calcium influx inhibitor were tested if they could attenuate hypoxic toxicity ... ...

Abstract	We hypothesized that hypoxia induced testicular damage is mediated by an activated NADPH oxidase (NOX), therefore, APO (apocynin) an inhibitor of NOX and raisanberine (RS), a calcium influx inhibitor were tested if they could attenuate hypoxic toxicity to the testis. Male Sprague-Dawley rats were exposed to hypoxia (10±0.5% O₂) for 17d and intervened with APO and RS in the last 6d. Histological changes and expression of pro-inflammation factors were evaluated in vivo. Biomarkers in isolated Leydig cells incubated with H₂O₂ were also assayed in vitro. Hypoxic rats displayed lower serum testosterone and higher LH and FSH. Upregulation of p22/p47(phox), NOX2, MMP9, PERK and p66Shc was associated with downregulation of StAR, 3β-HSD and Cx43 in the hypoxia testis, revealed by Western blot and immunohistochemical assay, respectively. APO and RS at least partially normalize hypoxia caused male hypogonadism by suppressing ER stress, and p66Shc in testes.
MeSH term(s)	3-Hydroxysteroid Dehydrogenases/biosynthesis ; 3-Hydroxysteroid Dehydrogenases/genetics ; 3-Hydroxysteroid Dehydrogenases/metabolism ; Acetophenones/pharmacology ; Acetophenones/therapeutic use ; Animals ; Berberine/analogs & derivatives ; Berberine/pharmacology ; Berberine/therapeutic use ; Biomarkers/blood ; Biomarkers/metabolism ; Calcium Channel Blockers/pharmacology ; Calcium Channel Blockers/therapeutic use ; Cells, Cultured ; Disease Models, Animal ; Endoplasmic Reticulum Stress/drug effects ; Enzyme Inhibitors/pharmacology ; Enzyme Inhibitors/therapeutic use ; Eunuchism/blood ; Eunuchism/drug therapy ; Eunuchism/metabolism ; Gene Expression Regulation/drug effects ; Leydig Cells/drug effects ; Leydig Cells/metabolism ; Leydig Cells/pathology ; Male ; NADPH Oxidases/antagonists & inhibitors ; Phosphoproteins/biosynthesis ; Phosphoproteins/genetics ; Phosphoproteins/metabolism ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Shc Signaling Adaptor Proteins/agonists ; Shc Signaling Adaptor Proteins/antagonists & inhibitors ; Shc Signaling Adaptor Proteins/genetics ; Shc Signaling Adaptor Proteins/metabolism ; Src Homology 2 Domain-Containing, Transforming Protein 1 ; Testis/drug effects ; Testis/metabolism ; Testis/pathology ; Testosterone/blood
Chemical Substances	4-chlorobenzyltetrahydroberberine ; Acetophenones ; Biomarkers ; Calcium Channel Blockers ; Enzyme Inhibitors ; Phosphoproteins ; Shc Signaling Adaptor Proteins ; Shc1 protein, rat ; Src Homology 2 Domain-Containing, Transforming Protein 1 ; steroidogenic acute regulatory protein ; Berberine (0I8Y3P32UF) ; Testosterone (3XMK78S47O) ; acetovanillone (B6J7B9UDTR) ; 3-Hydroxysteroid Dehydrogenases (EC 1.1.-) ; NADPH Oxidases (EC 1.6.3.-)
Language	English
Publishing date	2013-04
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	639342-1
ISSN	1873-1708 ; 0890-6238
ISSN (online)	1873-1708
ISSN	0890-6238
DOI	10.1016/j.reprotox.2012.12.002
Database	MEDical Literature Analysis and Retrieval System OnLINE

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