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Article ; Online: Physiological Benefits of Novel Selenium Delivery via Nanoparticles.

Au, Alice / Mojadadi, Albaraa / Shao, Jia-Ying / Ahmad, Gulfam / Witting, Paul K

International journal of molecular sciences

2023 Volume 24, Issue 7

Abstract: Dietary selenium (Se) intake within the physiological range is critical to maintain various biological functions, including antioxidant defence, redox homeostasis, growth, reproduction, immunity, and thyroid hormone production. Chemical forms of dietary ... ...

Abstract	Dietary selenium (Se) intake within the physiological range is critical to maintain various biological functions, including antioxidant defence, redox homeostasis, growth, reproduction, immunity, and thyroid hormone production. Chemical forms of dietary Se are diverse, including organic Se (selenomethionine, selenocysteine, and selenium-methyl-selenocysteine) and inorganic Se (selenate and selenite). Previous studies have largely investigated and compared the health impacts of dietary Se on agricultural stock and humans, where dietary Se has shown various benefits, including enhanced growth performance, immune functions, and nutritional quality of meats, with reduced oxidative stress and inflammation, and finally enhanced thyroid health and fertility in humans. The emergence of nanoparticles presents a novel and innovative technology. Notably, Se in the form of nanoparticles (SeNPs) has lower toxicity, higher bioavailability, lower excretion in animals, and is linked to more powerful and superior biological activities (at a comparable Se dose) than traditional chemical forms of dietary Se. As a result, the development of tailored SeNPs for their use in intensive agriculture and as candidate for therapeutic drugs for human pathologies is now being actively explored. This review highlights the biological impacts of SeNPs on growth and reproductive performances, their role in modulating heat and oxidative stress and inflammation and the varying modes of synthesis of SeNPs.
MeSH term(s)	Animals ; Humans ; Selenium ; Selenocysteine ; Antioxidants ; Nanoparticles ; Inflammation/drug therapy
Chemical Substances	Selenium (H6241UJ22B) ; Selenocysteine (0CH9049VIS) ; Antioxidants
Language	English
Publishing date	2023-03-23
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms24076068
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Article ; Online: Role for Selenium in Metabolic Homeostasis and Human Reproduction.

Mojadadi, Albaraa / Au, Alice / Salah, Wed / Witting, Paul / Ahmad, Gulfam

Nutrients

2021 Volume 13, Issue 9

Abstract: Selenium (Se) is a micronutrient essential for life. Dietary intake of Se within the physiological range is critical for human health and reproductive functions. Selenium levels outside the recommended range have been implicated in infertility and ... ...

Abstract	Selenium (Se) is a micronutrient essential for life. Dietary intake of Se within the physiological range is critical for human health and reproductive functions. Selenium levels outside the recommended range have been implicated in infertility and variety of other human diseases. However, presently it is not clear how different dietary Se sources are processed in our bodies, and in which form or how much dietary Se is optimum to maintain metabolic homeostasis and boost reproductive health. This uncertainty leads to imprecision in published dietary guidelines and advice for human daily intake of Se and in some cases generating controversies and even adverse outcomes including mortality. The chief aim for this review is to describe the sources of organic and inorganic Se, the metabolic pathways of selenoproteins synthesis, and the critical role of selenprotenis in the thyroid gland homeostasis and reproductive/fertility functions. Controversies on the use of Se in clinical practice and future directions to address these challenges are also described and discussed herein.
MeSH term(s)	Diet ; Female ; Fertility/physiology ; Homeostasis/physiology ; Humans ; Male ; Reproduction/physiology ; Selenium/administration & dosage ; Selenium/deficiency ; Selenium/physiology ; Selenoproteins/biosynthesis ; Selenoproteins/physiology ; Thyroid Gland/physiology
Chemical Substances	Selenoproteins ; Selenium (H6241UJ22B)
Language	English
Publishing date	2021-09-18
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2518386-2
ISSN	2072-6643 ; 2072-6643
ISSN (online)	2072-6643
ISSN	2072-6643
DOI	10.3390/nu13093256
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Article: Role for Selenium in Metabolic Homeostasis and Human Reproduction

Mojadadi, Albaraa / Au, Alice / Salah, Wed / Witting, Paul / Ahmad, Gulfam

Nutrients. 2021 Sept. 18, v. 13, no. 9

2021

Abstract	Selenium (Se) is a micronutrient essential for life. Dietary intake of Se within the physiological range is critical for human health and reproductive functions. Selenium levels outside the recommended range have been implicated in infertility and variety of other human diseases. However, presently it is not clear how different dietary Se sources are processed in our bodies, and in which form or how much dietary Se is optimum to maintain metabolic homeostasis and boost reproductive health. This uncertainty leads to imprecision in published dietary guidelines and advice for human daily intake of Se and in some cases generating controversies and even adverse outcomes including mortality. The chief aim for this review is to describe the sources of organic and inorganic Se, the metabolic pathways of selenoproteins synthesis, and the critical role of selenprotenis in the thyroid gland homeostasis and reproductive/fertility functions. Controversies on the use of Se in clinical practice and future directions to address these challenges are also described and discussed herein.
Keywords	food intake ; homeostasis ; human health ; human reproduction ; humans ; mortality ; selenium ; selenoproteins ; thyroid gland ; uncertainty
Language	English
Dates of publication	2021-0918
Publishing place	Multidisciplinary Digital Publishing Institute
Document type	Article
ZDB-ID	2518386-2
ISSN	2072-6643
ISSN	2072-6643
DOI	10.3390/nu13093256
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Article ; Online: Myeloperoxidase Gene Deletion Causes Drastic Microbiome Shifts in Mice and Does Not Mitigate Dextran Sodium Sulphate-Induced Colitis.

San Gabriel, Patrick T / O'Neil, Thomas R / Au, Alice / Tan, Jian K / Pinget, Gabriela V / Liu, Yuyang / Fong, Genevieve / Ku, Jacqueline / Glaros, Elias / Macia, Laurence / Witting, Paul K / Thomas, Shane R / Chami, Belal

International journal of molecular sciences

2024 Volume 25, Issue 8

Abstract: Neutrophil-myeloperoxidase (MPO) is a heme-containing peroxidase which produces excess amounts of hypochlorous acid during inflammation. While pharmacological MPO inhibition mitigates all indices of experimental colitis, no studies have corroborated the ... ...

Abstract	Neutrophil-myeloperoxidase (MPO) is a heme-containing peroxidase which produces excess amounts of hypochlorous acid during inflammation. While pharmacological MPO inhibition mitigates all indices of experimental colitis, no studies have corroborated the role of MPO using knockout (KO) models. Therefore, we investigated MPO deficient mice in a murine model of colitis. Wild type (Wt) and MPO-deficient mice were treated with dextran sodium sulphate (DSS) in a chronic model of experimental colitis with three acute cycles of DSS-induced colitis over 63 days, emulating IBD relapse and remission cycles. Mice were immunologically profiled at the gut muscoa and the faecal microbiome was assessed via 16S rRNA amplicon sequencing. Contrary to previous pharmacological antagonist studies targeting MPO, MPO-deficient mice showed no protection from experimental colitis during cyclical DSS-challenge. We are the first to report drastic faecal microbiota shifts in MPO-deficient mice, showing a significantly different microbiome profile on Day 1 of treatment, with a similar shift and distinction on Day 29 (half-way point), via qualitative and quantitative descriptions of phylogenetic distances. Herein, we provide the first evidence of substantial microbiome shifts in MPO-deficiency, which may influence disease progression. Our findings have significant implications for the utility of MPO-KO mice in investigating disease models.
MeSH term(s)	Animals ; Dextran Sulfate ; Peroxidase/metabolism ; Peroxidase/genetics ; Mice ; Colitis/microbiology ; Colitis/chemically induced ; Colitis/genetics ; Mice, Knockout ; Gastrointestinal Microbiome ; Disease Models, Animal ; Feces/microbiology ; Gene Deletion ; RNA, Ribosomal, 16S/genetics ; Mice, Inbred C57BL
Chemical Substances	Dextran Sulfate (9042-14-2) ; Peroxidase (EC 1.11.1.7) ; RNA, Ribosomal, 16S
Language	English
Publishing date	2024-04-11
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms25084258
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Article: Modulation of L-type Ca2+ channels by beta3-adrenoceptor activation and the involvement of nitric oxide.

Au, Alice L S / Kwan, Yiu Wa

Journal of cardiac surgery

2003 Volume 17, Issue 5, Page(s) 465–469

Abstract: Background: Both beta1- and beta2-adrenoceptors (AR) in cardiac tissues are responsible for the excitatory effect of catecholamines. Recent evidence demonstrated the presence of another subtype of beta-AR (beta3-AR) in cardiac ventricular preparation. ... ...

Abstract	Background: Both beta1- and beta2-adrenoceptors (AR) in cardiac tissues are responsible for the excitatory effect of catecholamines. Recent evidence demonstrated the presence of another subtype of beta-AR (beta3-AR) in cardiac ventricular preparation. Activation of beta3-AR elicited a depressant response on ventricular contraction. The underlying mechanism(s) for the negative inotropism is relatively unknown. Methods: We investigated the effects of beta3-AR activation on basal voltage-dependent Ca2+ channel (I(CaL)) amplitude of the guinea pig enzyme-dissociated single ventricular myocytes using amphotericin B (200 microg/mL) perforated-patch whole-cell patch-clamp techniques (approximately 22 degrees C). Results: Application of (-)-isoprenaline ((-)-ISO) (100 nM, a nonselective beta-AR agonist) increased the basal I(CaL) amplitude (approximately 210% of control) (n = 8). However, in the presence of nadolol (1 degreesM, a beta1-/beta2-AR antagonist), the stimulatory effect of (-)-ISO on I(CaL )was abolished and a slowly developed inhibition of the basal I(CaL) was recorded (approximately 80% of control) (n = 9). A smaller degree of inhibition was observed with BRL 37344 (100 nM, a selective beta3-AR agonist) (58% of control) (n = 7). The inhibitory effect of (-)-ISO (with nadolol) and BRL 37344 persisted after washout. Pretreating the ventricular myocytes with L-NAME (0.3 microM, a nitric oxide synthase inhibitor), but not D-NAME (0.3 microM), abolished the inhibitory effect of (-)-ISO and BRL 37344 (n = 7-9). Conclusions: The results suggest that beta3-ARs are present in ventricular myocytes. Activation of the beta3-AR resulted in an inhibition of the basal I(CaL) amplitude probably due to the formation of nitric oxide.
MeSH term(s)	Adrenergic beta-Agonists/pharmacology ; Animals ; Calcium Channels, L-Type/metabolism ; Computer Graphics ; Ethanolamines/pharmacology ; Guinea Pigs ; Isoproterenol/pharmacology ; Myocytes, Cardiac/metabolism ; Nitric Oxide/metabolism ; Receptors, Adrenergic, beta-3/drug effects
Chemical Substances	Adrenergic beta-Agonists ; Calcium Channels, L-Type ; Ethanolamines ; Receptors, Adrenergic, beta-3 ; Nitric Oxide (31C4KY9ESH) ; BRL 37344 (5DZZ1926YW) ; Isoproterenol (L628TT009W)
Language	English
Publishing date	2003-01-22
Publishing country	United States
Document type	Journal Article
ZDB-ID	639059-6
ISSN	1540-8191 ; 0886-0440
ISSN (online)	1540-8191
ISSN	0886-0440
DOI	10.1111/j.1540-8191.2001.tb01179.x
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Article: Contribution of glibenclamide-sensitive, ATP-dependent K+ channel activation to acetophenone analogues-mediated in vitro pulmonary artery relaxation of rat.

Seto, Sai Wang / Ho, Yick Yan / Hui, Hung Ngai / Au, Alice Lai Shan / Kwan, Yiu Wa

Life sciences

2006 Volume 78, Issue 6, Page(s) 631–639

Abstract: Compared to the currently available therapeutic drugs for peripheral vascular diseases, agents that are selective for relaxing pulmonary circulation are scarce. The present study was undertaken, using isometric tension change measurement and whole-cell ... ...

Abstract	Compared to the currently available therapeutic drugs for peripheral vascular diseases, agents that are selective for relaxing pulmonary circulation are scarce. The present study was undertaken, using isometric tension change measurement and whole-cell patch-clamp electrophysiology methods, to evaluate the vascular relaxation effect and the underlying mechanisms involved of two naturally found alkaloids: paeonol (2-hydroxy-4-methoxy-acetophenone), acetovanillone (4-hydroxy-3-methoxy-acetophenone) and the non-substituted analogue acetophenone on pulmonary artery of Sprague-Dawley rats. Cumulative administration (3 microM-1 mM) of acetophenone analogues resulted in a concentration-dependent relaxation of phenylephrine (1 microM) pre-contracted pulmonary artery. A relative order of inhibitory potency, estimated by comparing the concentration at which a 50% relaxation of phenylephrine-induced contraction observed was: acetovanillone > paeonol > acetophenone. Endothelial denudation and inhibition of nitric oxide synthase (with 20 microM N(G)-nitro-L-arginine methyl-ester) only moderately suppressed (17.6 +/- 4.2%) acetovanillone- but not paeonol- or acetophenone-mediated maximum relaxation. Glibenclamide (3 microM, an ATP-sensitive K(+) (IK(ATP)) channel blocker) markedly attenuated all acetophenone analogues-mediated endothelium-independent relaxation. Neither cis-N-(2-phenylcyclopentyl)azacyclotridec-1-en-2-amine (MDL 12330A, 10 microM), iberiotoxin (300 nM), 4-aminopyridine (3 mM), (+/-)-propranolol (1 microM, a non-selective beta-adrenoceptor blocker) nor 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ) (3 microM, a guanylate cyclase inhibitor) altered endothelium-independent relaxation. In electrophysiological experiments using single pulmonary artery smooth muscle cells, acetovanillone, paeonol, acetophenone and cromakalim activated glibenclamide-sensitive, IK(ATP) channels. In conclusion, our results demonstrate that acetophenone analogues caused pulmonary artery relaxation through opening of IK(ATP) channels. In addition, acetovanillone-mediated pulmonary artery relaxation is partly depended on nitric oxide released from endothelium.
MeSH term(s)	Acetophenones/pharmacology ; Adenosine Triphosphate/pharmacology ; Animals ; Dose-Response Relationship, Drug ; Endothelium, Vascular/physiology ; Glyburide/pharmacology ; In Vitro Techniques ; Male ; Nitric Oxide/physiology ; Potassium Channels/drug effects ; Pulmonary Artery/drug effects ; Pulmonary Artery/physiology ; Rats ; Rats, Sprague-Dawley ; Vasodilation/drug effects
Chemical Substances	Acetophenones ; Potassium Channels ; Nitric Oxide (31C4KY9ESH) ; paeonol (3R834EPI82) ; Adenosine Triphosphate (8L70Q75FXE) ; acetovanillone (B6J7B9UDTR) ; acetophenone (RK493WHV10) ; Glyburide (SX6K58TVWC)
Language	English
Publishing date	2006-01-02
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	3378-9
ISSN	1879-0631 ; 0024-3205
ISSN (online)	1879-0631
ISSN	0024-3205
DOI	10.1016/j.lfs.2005.05.063
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Article: Modulation by homocysteine of the iberiotoxin-sensitive, Ca2+ -activated K+ channels of porcine coronary artery smooth muscle cells.

Au, Alice L S / Seto, S W / Chan, S W / Chan, M S / Kwan, Y W

European journal of pharmacology

2006 Volume 546, Issue 1-3, Page(s) 109–119

Abstract: We evaluated the acute effect of homocysteine on the iberiotoxin-sensitive, Ca(2+)-activated K(+) (BK(Ca)) channels of the porcine coronary artery smooth muscle cells. NS 1619 (1 to 30 microM) caused a concentration-dependent enhancement of the BK(Ca) ... ...

Abstract	We evaluated the acute effect of homocysteine on the iberiotoxin-sensitive, Ca(2+)-activated K(+) (BK(Ca)) channels of the porcine coronary artery smooth muscle cells. NS 1619 (1 to 30 microM) caused a concentration-dependent enhancement of the BK(Ca) amplitude (recorded using the whole-cell, membrane-rupture configuration) only with an elevated [Ca(2+)](i) of approximately 444 nM, but not with [Ca(2+)](i) of approximately 100 nM. Homocysteine (30 microM) caused a small inhibition ( approximately 16%) of the BK(Ca) amplitude ([Ca(2+)](i)= approximately 444 nM), and a greater inhibition ( approximately 77%) was observed with 100 microM NADH present in the pipette solution. The inhibition persisted after washing. With NADPH (100 microM), a smaller magnitude of inhibition ( approximately 34%) of the BK(Ca) amplitude was recorded. The NS 1619-mediated enhancement of the BK(Ca) amplitude (with elevated [Ca(2+)](i) plus NADH in the pipette) was attenuated by homocysteine. The homocysteine-mediated inhibition of the BK(Ca) amplitude was suppressed by Tiron (10 mM) or diphenylene iodonium (30 nM), applied alone, but not by superoxide dismutase (500 U/ml) and catalase (500 U/ml). Generation of superoxide (O(2)(-)) of the smooth muscle cells (with NADH presence), measured using the lucigenin-enhanced chemiluminescence, was markedly increased by angiotensin II (100 nM) and homocysteine (30 microM). The chemiluminescence signal was sensitive to apocynin (300 microM) or Tiron, applied alone, but not to superoxide dismutase and catalase. In conclusion, our results demonstrate that acute homocysteine application inhibits the iberiotoxin-sensitive BK(Ca) channels (with elevated [Ca(2+)](i) and NADH present) which is probably caused by the NADH oxidase activation and the concomitant generation of intracellular superoxide.
MeSH term(s)	1,2-Dihydroxybenzene-3,5-Disulfonic Acid Disodium Salt/pharmacology ; Acetophenones/pharmacology ; Angiotensin II/pharmacology ; Animals ; Benzimidazoles/pharmacology ; Calcium/metabolism ; Coronary Vessels/cytology ; Coronary Vessels/drug effects ; Coronary Vessels/metabolism ; Dose-Response Relationship, Drug ; Enzyme Activation/drug effects ; Enzyme Inhibitors/pharmacology ; Homocysteine/analogs & derivatives ; Homocysteine/pharmacology ; In Vitro Techniques ; Ion Channel Gating/drug effects ; Membrane Potentials/drug effects ; Muscle, Smooth, Vascular/cytology ; Muscle, Smooth, Vascular/drug effects ; Muscle, Smooth, Vascular/metabolism ; NAD/metabolism ; NADPH Oxidases/antagonists & inhibitors ; NADPH Oxidases/metabolism ; Patch-Clamp Techniques ; Peptides/pharmacology ; Potassium Channel Blockers/pharmacology ; Potassium Channels, Calcium-Activated/drug effects ; Potassium Channels, Calcium-Activated/metabolism ; Superoxides/metabolism ; Swine ; Vasoconstrictor Agents/pharmacology
Chemical Substances	Acetophenones ; Benzimidazoles ; Enzyme Inhibitors ; Peptides ; Potassium Channel Blockers ; Potassium Channels, Calcium-Activated ; Vasoconstrictor Agents ; Homocysteine (0LVT1QZ0BA) ; NAD (0U46U6E8UK) ; Superoxides (11062-77-4) ; Angiotensin II (11128-99-7) ; NS 1619 (153587-01-0) ; 1,2-Dihydroxybenzene-3,5-Disulfonic Acid Disodium Salt (4X87R5T106) ; iberiotoxin (773HER9B6T) ; acetovanillone (B6J7B9UDTR) ; homocysteine thiolactone (D5H88XF24X) ; NADPH Oxidases (EC 1.6.3.-) ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2006-09-28
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.2006.06.073
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Article: An in vitro study of histamine on the pulmonary artery of the Wistar-Kyoto and spontaneously hypertensive rats.

Lau, Wing Hung / Kwan, Yiu Wa / Au, Alice Lai Shan / Cheung, Wui Hang

European journal of pharmacology

2003 Volume 470, Issue 1-2, Page(s) 45–55

Abstract: The vascular response to most neurotransmitters of different vascular beds is altered under hypertensive condition. The modulatory effect of genetic pulmonary arterial hypertension on histamine responses is not known. The present study was undertaken to ... ...

Abstract	The vascular response to most neurotransmitters of different vascular beds is altered under hypertensive condition. The modulatory effect of genetic pulmonary arterial hypertension on histamine responses is not known. The present study was undertaken to evaluate the modulatory effect of enzymatic degradation (via histamine N-methyl-transferase and diamine oxidase) on the vascular response of histamine, and the subtype(s) of histamine receptor present in the pulmonary artery (first branch, O.D. approximately 800 microm) of the normotensive Wistar-Kyoto (WKY) and spontaneously hypertensive rats (SHR) (male, 22-26 weeks old). In phenylephrine (1 microM) pre-contracted preparations, histamine and 6-[2-(4-imidazolyl)ethylamino]-N-(4-trifluoromethylphenyl) heptanecarboxamide (HTMT, a histamine H(1) receptor agonist) elicited a concentration-dependent relaxation, with a smaller magnitude recorded in SHR. Application of 10 microM S-[4-(N,N-dimethylamino)-butyl]isothiourea (SKF 91488, a selective histamine N-methyl-transferase inhibitor), but not aminoguanidine (100 microM, a diamine oxidase inhibitor), significantly attenuated histamine-induced relaxation. Clobenpropit (1 nM, a potent histamine H(3) receptor antagonist) "antagonised" the suppressive effect of SKF 91488 and histamine-evoked relaxation was restored. Endothelial denudation reduced histamine- and abolished HTMT-elicited relaxation. Dimaprit (a histamine H(2) receptor agonist) caused an endothelium-independent, cis-N-(2-phenylcyclopentyl)azacyclotridec-1-en-2-amine (MDL 12330A, 10 microM, an adenylate cyclase inhibitor)-sensitive, concentration-dependent relaxation, with a similar magnitude in both strains of rat. Histamine-evoked relaxation was reversed into a further contraction (clobenpropit (10 nM)-sensitive) (with a greater magnitude occurred in the WKY rat) after blocking the histamine H(1) and H(2) receptors with diphenhydramine plus cimetidine (30 microM each). A similar further contraction (clobenpropit-sensitive) was observed with imetit (a histamine H(3)/H(4) receptor agonist) (> or =3 microM). Under resting tension, imetit (> or =0.3 microM) caused a clobenpropit (10 nM)- and prazosin (1 microM)-sensitive, concentration-dependent contraction, with a greater contraction in the WKY rats. Our results suggest that inhibition of histamine catabolism using SKF 91488 (histamine N-methyl-transferase inhibitor) resulted in a reduction of histamine-mediated relaxation that was due to the activation of the clobenpropit-sensitive, histamine H(3)/H(4) receptor and the release of catecholamine. In addition, activation of histamine H(1) and H(2) receptors resulted in relaxation whereas histamine H(3)/H(4) receptor activation by imetit yielded a prazosin-sensitive contraction of the pulmonary artery.
MeSH term(s)	Animals ; Dose-Response Relationship, Drug ; Histamine/metabolism ; Histamine/pharmacology ; Hypertension/metabolism ; In Vitro Techniques ; Male ; Pulmonary Artery/drug effects ; Pulmonary Artery/metabolism ; Rats ; Rats, Inbred SHR ; Rats, Inbred WKY ; Receptors, Histamine/metabolism ; Vasoconstriction/drug effects ; Vasoconstriction/physiology ; Vasodilation/drug effects ; Vasodilation/physiology
Chemical Substances	Receptors, Histamine ; Histamine (820484N8I3)
Language	English
Publishing date	2003-05-30
Publishing country	Netherlands
Document type	Comparative Study ; 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/s0014-2999(03)01759-x
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Article: Mechanisms responsible for the in vitro relaxation of ligustrazine on porcine left anterior descending coronary artery.

Shan Au, Alice Lai / Kwan, Yiu Wa / Kwok, Ching Chi / Zhang, Rong-Zhen / He, Guo-Wei

European journal of pharmacology

2003 Volume 468, Issue 3, Page(s) 199–207

Abstract: In this study, we have evaluated the underlying mechanisms responsible for the relaxation response of ligustrazine (2,3,5,6-tetra-methyl-pyrazine; 2,3,5,6-MP) and its structural analogues (2-methyl-pyrazine (2-MP); ethyl-pyrazine (EP); 2,3-di-methyl- ... ...

Abstract	In this study, we have evaluated the underlying mechanisms responsible for the relaxation response of ligustrazine (2,3,5,6-tetra-methyl-pyrazine; 2,3,5,6-MP) and its structural analogues (2-methyl-pyrazine (2-MP); ethyl-pyrazine (EP); 2,3-di-methyl-pyrazine (2,3-MP); 2,5-di-methyl-pyrazine (2,5-MP); 2,6-di-methyl-pyrazine (2,6-MP) and 2,3,5-tri-methyl-pyrazine (2,3,5-MP)) in porcine left anterior descending coronary artery (tertiary branch, O.D. </=1 mm). In 5-hydroxytryptamine (3 microM) precontracted preparations, cumulative administration (0.1-300 microM) of all pyrazine analogues caused an endothelium-independent, concentration-dependent relaxation. The relative inhibitory potency, as compared at concentration with which 50% relaxation occurred, was 2,3,5,6-MP>2,3,5-MP>EP>2,5-MP>/=2,6-MP>/=2,3-MP>2-MP. Besides, salbutamol and forskolin caused an endothelium-independent relaxation. The relaxation response of ligustrazine, salbutamol and forskolin was blunted in the presence of cis-N-(2-phenylcyclopentyl) azacyclotridec-1-en-2-amine (MDL 12330A) (10 microM, an adenylate cyclase inhibitor) and N-[2-((bromocinnamyl)amino)ethyl]-5-isoquinoline-sulphonamide (H-89, a protein kinase A inhibitor, 3 microM). Patch-clamp, whole-cell electrophysiological studies using single smooth muscle cells of the left anterior descending coronary artery revealed that ligustrazine (300 microM), salbutamol (30 microM) and forskolin (1 microM) inhibited the nifedipine-sensitive L-type Ca(2+) channels, and the inhibitory effect was eradicated by MDL 12330A (10 microM) and H-89 (1 microM). However, neither the Ca(2+)-dependent K(+) channel nor the ATP-dependent K(+) channel was modified by ligustrazine (300 microM). In conclusion, our results indicate that ligustrazine-mediated left anterior descending coronary artery relaxation is due to the activation of adenylate cyclase/protein kinase A cascade and the subsequent inhibition of nifedipine-sensitive, voltage-dependent L-type Ca(2+) channels. However, opening of K(+) channels seems to play no role in mediating the relaxation effect of ligustrazine.
MeSH term(s)	Animals ; Calcium/physiology ; Calcium Channels, L-Type/drug effects ; Coronary Vessels/drug effects ; Cyclic AMP-Dependent Protein Kinases/metabolism ; Dose-Response Relationship, Drug ; Endothelium, Vascular/drug effects ; Endothelium, Vascular/metabolism ; Female ; Male ; Muscle Relaxation/drug effects ; Muscle Relaxation/physiology ; Muscle, Smooth, Vascular/drug effects ; Muscle, Smooth, Vascular/metabolism ; Myocytes, Smooth Muscle/drug effects ; Myocytes, Smooth Muscle/metabolism ; Patch-Clamp Techniques ; Pyrazines/administration & dosage ; Pyrazines/pharmacology ; Signal Transduction/drug effects ; Structure-Activity Relationship ; Swine
Chemical Substances	Calcium Channels, L-Type ; Pyrazines ; Cyclic AMP-Dependent Protein Kinases (EC 2.7.11.11) ; Calcium (SY7Q814VUP) ; tetramethylpyrazine (V80F4IA5XG)
Language	English
Publishing date	2003-05-16
Publishing country	Netherlands
Document type	Evaluation Studies ; 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/s0014-2999(03)01691-1
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Article: Comparison of vascular relaxation, lipolysis and glucose uptake by peroxisome proliferator-activated receptor-gamma activation in +db/+m and +db/+db mice.

Seto, Sai Wang / Lam, Tsz Yan / Leung, George P H / Au, Alice L S / Ngai, Sai Ming / Chan, Shun Wan / Kwan, Yiu Wa

European journal of pharmacology

2007 Volume 572, Issue 1, Page(s) 40–48

Abstract: In this study, we determined the in vitro effect of peroxisome proliferator-activated receptor-gamma (PPAR-gamma) activation on the aortic relaxation, lipolysis and insulin-induced [(3)H]-glucose uptake of the abdominal (omental) adipocytes of the non- ... ...

Abstract	In this study, we determined the in vitro effect of peroxisome proliferator-activated receptor-gamma (PPAR-gamma) activation on the aortic relaxation, lipolysis and insulin-induced [(3)H]-glucose uptake of the abdominal (omental) adipocytes of the non-diabetic (+db/+m) and obese/diabetic (+db/+db) mice. The expression of PPAR-gamma (mRNA and protein) in aorta and adipose tissues was evaluated and compared. Cumulative application of ciglitazone, pioglitazone and troglitazone (PPAR-gamma agonists) caused a concentration-dependent aortic relaxation (sensitive to 2-chloro-5-nitro-N-phenylbenzamide (GW9662) (1 microM, a selective PPAR-gamma antagonist) and N(omega)-nitro-l-arginine methyl ester (l-NAME) (20 microM, a nitric oxide synthase inhibitor)) with a maximum relaxation of approximately 30% (3 microM) in +db/+m mice, whereas no relaxation was observed in +db/+db mice. All PPAR-gamma agonists examined did not alter the basal lipolysis of both species, but forskolin caused a concentration-dependent lipolysis, with a greater magnitude observed in +db/+m mice. Insulin (0.1 and 1 microM) caused an enhancement of [(3)H]-glucose uptake into adipocytes with a greater magnitude in +db/+m mice. In contrast, none of the PPAR-gamma agonists tested (0.1, 1 and 10 microM) altered the basal and the insulin (0.1 microM)-induced [(3)H]-glucose uptake into adipocytes of both species. In addition, there was no difference in PPAR-gamma expression (mRNA and protein) in the aorta and adipose tissues between the species. In conclusion, our results demonstrate that PPAR-gamma is present in the abdominal (omental) adipose tissue and thoracic aorta. An acute activation of PPAR-gamma produced a small ( approximately 30%) aortic relaxation (nitric oxide/endothelium-dependent) of +db/+m mice. However, all PPAR-gamma agonists examined have no acute effect on lipolysis and the insulin-induced glucose uptake into adipocytes of both +db/+m and +db/+db mice.
MeSH term(s)	Abdominal Fat/metabolism ; Adipocytes/drug effects ; Adipocytes/metabolism ; Animals ; Aorta, Thoracic/drug effects ; Aorta, Thoracic/physiopathology ; Carbohydrate Metabolism/drug effects ; Chromans/pharmacology ; Diabetes Mellitus, Type 2/metabolism ; Diabetes Mellitus, Type 2/physiopathology ; Endothelium, Vascular/drug effects ; Endothelium, Vascular/physiopathology ; Female ; Glucose/metabolism ; Hypoglycemic Agents/pharmacology ; In Vitro Techniques ; Insulin/pharmacology ; Lipid Metabolism ; Lipolysis/drug effects ; Mice ; Mice, Inbred C57BL ; Mice, Mutant Strains ; Obesity/metabolism ; Obesity/physiopathology ; PPAR gamma/agonists ; PPAR gamma/biosynthesis ; RNA, Messenger/agonists ; RNA, Messenger/biosynthesis ; Thiazolidinediones/pharmacology ; Vasodilation/drug effects
Chemical Substances	Chromans ; Hypoglycemic Agents ; Insulin ; PPAR gamma ; RNA, Messenger ; Thiazolidinediones ; troglitazone (I66ZZ0ZN0E) ; Glucose (IY9XDZ35W2) ; ciglitazone (U8QXS1WU8G) ; pioglitazone (X4OV71U42S)
Language	English
Publishing date	2007-10-15
Publishing country	Netherlands
Document type	Comparative Study ; 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.2007.05.070
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