Displaying publications 1 - 20 of 58 in total

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  1. Khan A, Ab Ghani S
    Biosens Bioelectron, 2012 Jan 15;31(1):433-8.
    PMID: 22154168 DOI: 10.1016/j.bios.2011.11.007
    The electrochemical biosensors based on poly(o-phenylenediamine) (PoPD) and acetylcholinesterase (AChE) and choline oxidase (ChO) enzymes were fabricated on carbon fibre (CF) substrate. The electropolymerized PoPD was used to reduce the interfering substances. The electrode assembly was completed by depositing functionalized carbon nano tubes (FCNTs) and Nafion (Naf). Amperometric detection of acetylcholine (ACh) and choline (Ch) were realized at an applied potential of +750 mV vs Ag/AgCl (saturated KCl). At pH 7.4, the final assembly, Naf-FCNTs/AChE-ChO((10:1))/PoPD/CF(Elip), was observed to have high sensitivity towards Ch (6.3±0.3 μA mM(-1)) and ACh (5.8±0.3 μA mM(-1)), linear range for Ch (K(M)=0.52±0.03 mM) and ACh (K(M)=0.59±0.07 mM), and for Ch the highest ascorbic acid blocking capacity (97.2±2 1mM AA). It had a response time of <5s and with 0.045 μM limit of detection. Studies on different ratio (ACh/Ch) revealed that 10:1, gave best overall response.
    Matched MeSH terms: Acetylcholine/analysis*; Acetylcholine/chemistry; Acetylcholinesterase/chemistry*
  2. Muthuraju, S., Abdullah, J.M.
    Orient Neuron Nexus, 2011;2(1):10-14.
    MyJurnal
    Neuronal cell death results from various circumstances such as hypoxia, ischemic and neurodegenerative diseases (NDs). In these events, the resulting modification of neurotransmitters, either excitatory or inhibitory, mediate much of the neuronal damage. However, this consequence depends upon their pre and post synaptic receptor activities which are the key mechanism for signal regulation. Among these, acetylcholine (ACh) is a well known neurotransmitter which is predominantly involved in neuroprotection as well as cognitive functions through its receptors activity, particularly the nicotinic subtypes. Several lines of evidence suggest that among these subtypes, a7 nicotinic acetylcholine receptor (a7nAChR) offers much promise for neuroprotective role in relation to the central nervous system (CNS) disorders like schizophrenia and Alzheimer's disease (AD). Several lines of evidence exist to show the potential mechanisms in which this nAChR subtype and its agonists such as nicotine, that trigger the a7nAChR-mediated suppression of neuronal cell death. This review focuses on the potential role of a7nAChR in neuroprotection by examining recent experimental data, both in vitro and in vivo, that argue for the neuroprotective role of a7nAChR in the CNS.
    Matched MeSH terms: Acetylcholine
  3. Mudassar Imran Bukhari S, Yew KK, Thambiraja R, Sulong S, Ghulam Rasool AH, Ahmad Tajudin LS
    Ther Adv Ophthalmol, 2019 08 22;11:2515841419868100.
    PMID: 31489400 DOI: 10.1177/2515841419868100
    Purpose: To determine the role of microvascular endothelial dysfunction as risk factor for primary open angle glaucoma.

    Methods: A cross-sectional study was conducted involving 114 Malay patients with POAG seen at the eye clinic of Hospital Universiti Sains Malaysia. Patients aged between 40 and 80 years who were diagnosed with other types of glaucoma, previous glaucoma filtering surgery or other surgeries except uncomplicated cataract surgery and pterygium surgery were excluded. A total of 101 patients who were followed up for dry eyes, age-related cataracts or post cataracts extraction surgery were recruited as control subjects. Those with family history of glaucoma or glaucoma suspect were excluded. Microvascular endothelial function was assessed using laser Doppler fluximetry and the process of iontophoresis. Iontophoresis with acetylcholine (ACh) and sodium nitroprusside (SNP) was used to measure microvascular endothelium-dependent and endothelium-independent vasodilatations, respectively.

    Results: In general, POAG patients demonstrated lower ACh% and AChmax values compared with controls. There was significant difference in microvascular endothelial function [ACh%: mean, 95% confidence interval = 503.1 (378.0, 628.3), and AChmax: mean, 95% confidence interval = 36.8 (30.2, 43.5)] between primary open angle glaucoma cases (p 

    Matched MeSH terms: Acetylcholine
  4. Ahmed F, Ghalib RM, Sasikala P, Ahmed KK
    Pharmacogn Rev, 2013 Jul;7(14):121-30.
    PMID: 24347920 DOI: 10.4103/0973-7847.120511
    Alzheimer's disease (AD) is a progressive neurodegenerative disease, wherein a progressive loss of cholinergic synapses occurs in hippocampus and neocortex. Decreased concentration of the neurotransmitter, acetylcholine (ACh), appears to be critical element in the development of dementia, and the most appropriate therapeutic approach to treat AD and other form of dementia is to restore acetylcholine levels by inhibiting both major form of cholinesterase: Acetylcholinesterase (AChE) and butyrylcholinesterase (BChE). Consequently, researches have focused their attention towards finding cholinesterase inhibitors from natural products. A large number of such inhibitors have been isolated from medicinal plants. This review presents a comprehensive account of the advances in field of cholinesterase inhibitor phytoconstituents. The structures of some important phytoconstituents (collected through www.Chemspider.com) are also presented and the scope for future research is discussed.
    Matched MeSH terms: Acetylcholine; Acetylcholinesterase
  5. Belqes Abdullah, A. T., Yvonne, T. G. B., Ahmad, S. H., Abdul Aziz, A. S. I., Aida, H. G. R.
    MyJurnal
    Introduction: Iontophoresis of vasoactive substances such as acetylcholine (ACh) and sodium nitroprusside (SNP) combined with Laser Doppler fluximetry (LDF) is a non-invasive tool used to determine microvascular endothelial function. This study aims to test the effect of sodium chloride on
    non-specific vasodilatation when used as a vehicle in the process of iontophoresis. This study also aims to define the number of current pulses needed to get the maximum effect during iontophoresis with ACh and SNP using low current strength. Methods: The experiment was conducted in five healthy females. Baseline skin perfusion was taken before administration of seven current pulses. Current strength of 0.007 mA and current density of 0.01 mA/cm2 were used. Acetylcholine was used to assess endothelial dependent vasodilatation, while SNP was used to assess endothelial independent vasodilatation. The mean skin perfusion (AU) responses to the iontophoresis of ACh at the anodal and SNP at the cathode leads were recorded. Sodium chloride (0.9%) was used as a vehicle to obtain concentration of 1% for both ACh and SNP. Iontophoresis of pure vehicle (NaCl) was conducted on a separate day to observe the effect of vehicle only on the iontophoresis process at both anode and cathode. Results: Iontophoresis of NaCl showed no significant increase in perfusion compared to baseline at both anode and cathode. Significant increases in skin perfusion were observed with SNP and ACh; a plateau of ACh was reached from the 3rd pulse onwards; while the plateau of SNP was reached from the 4th pulse onwards. Conclusion: NaCl could be used as a vehicle for Ach and SNP during iontophoresis as it did not cause non-specific vasodilatation. Using five current pulses are adequate for iontophoresis of ACh and SNP to assess microvascular endothelial function.
    Matched MeSH terms: Acetylcholine
  6. Thevathasan OI, Archdeacon JW
    Med J Malaya, 1966 Jun;20(4):306-15.
    PMID: 4224339
    Matched MeSH terms: Acetylcholine/pharmacology*
  7. Kiyooka T, Ohanyan V, Yin L, Pung YF, Chen YR, Chen CL, et al.
    Basic Res Cardiol, 2022 Jan 17;117(1):3.
    PMID: 35039940 DOI: 10.1007/s00395-021-00908-1
    Endothelial dysfunction in diabetes is generally attributed to oxidative stress, but this view is challenged by observations showing antioxidants do not eliminate diabetic vasculopathy. As an alternative to oxidative stress-induced dysfunction, we interrogated if impaired mitochondrial function in endothelial cells is central to endothelial dysfunction in the metabolic syndrome. We observed reduced coronary arteriolar vasodilation to the endothelium-dependent dilator, acetylcholine (Ach), in Zucker Obese Fatty rats (ZOF, 34 ± 15% [mean ± standard deviation] 10-3 M) compared to Zucker Lean rats (ZLN, 98 ± 11%). This reduction in dilation occurred concomitantly with mitochondrial DNA (mtDNA) strand lesions and reduced mitochondrial complex activities in the endothelium of ZOF versus ZLN. To demonstrate endothelial dysfunction is linked to impaired mitochondrial function, administration of a cell-permeable, mitochondria-directed endonuclease (mt-tat-EndoIII), to repair oxidatively modified DNA in ZOF, restored mitochondrial function and vasodilation to Ach (94 ± 13%). Conversely, administration of a cell-permeable, mitochondria-directed exonuclease (mt-tat-ExoIII) produced mtDNA strand breaks in ZLN, reduced mitochondrial complex activities and vasodilation to Ach in ZLN (42 ± 16%). To demonstrate that mitochondrial function is central to endothelium-dependent vasodilation, we introduced (via electroporation) liver mitochondria (from ZLN) into the endothelium of a mesenteric vessel from ZOF and restored endothelium-dependent dilation to vasoactive intestinal peptide (VIP at 10-5 M, 4 ± 3% vasodilation before mitochondrial transfer and 48 ± 36% after transfer). Finally, to demonstrate mitochondrial function is key to endothelium-dependent dilation, we administered oligomycin (mitochondrial ATP synthase inhibitor) and observed a reduction in endothelium-dependent dilation. We conclude that mitochondrial function is critical for endothelium-dependent vasodilation.
    Matched MeSH terms: Acetylcholine/metabolism; Acetylcholine/pharmacology
  8. Akyuz E, Doganyigit Z, Paudel YN, Koklu B, Kaymak E, Villa C, et al.
    Life (Basel), 2021 Mar 26;11(4).
    PMID: 33810231 DOI: 10.3390/life11040276
    Epilepsy is characterized by an imbalance in neurotransmitter activity; an increased excitatory to an inhibitory activity. Acetylcholine (ACh), serotonin, and norepinephrine (NE) may modulate neural activity via several mechanisms, mainly through its receptors/transporter activity and alterations in the extracellular potassium (K+) concentration via K+ ion channels. Seizures may disrupt the regulation of inwardly rectifying K+ (Kir) channels and alter the receptor/transporter activity. However, there are limited data present on the immunoreactivity pattern of these neurotransmitter receptors/transporters and K+ channels in chronic models of epilepsy, which therefore was the aim of this study. Changes in the immunoreactivity of epileptogenesis-related neurotransmitter receptors/transporters (M2, 5-HT2B, and NE transporter) as well as Kir channels (Kir3.1 and Kir6.2) were determined in the cortex, hippocampus and medulla of adult Wistar rats by utilizing a Pentylenetetrazol (PTZ)-kindling chronic epilepsy model. Increased immunoreactivity of the NE transporter, M2, and 5-HT2B receptors was witnessed in the cortex and medulla. While the immunoreactivity of the 5-HT2B receptor was found increased in the cortex and medulla, it was decreased in the hippocampus, with no changes observed in the M2 receptor in this region. Kir3.1 and Kir6.2 staining showed increase immunoreactivity in the cerebral cortex, but channel contrasting findings in the hippocampus and medulla. Our results suggest that seizure kindling may result in significant changes in the neurotransmitter system which may contribute or propagate to future epileptogenesis, brain damage and potentially towards sudden unexpected death in epilepsy (SUDEP). Further studies on the pathogenic role of these changes in neurotransmitter receptors/transporters and K+ channel immunoreactivity may identify newer possible targets to treat seizures or prevent epilepsy-related comorbidities.
    Matched MeSH terms: Acetylcholine
  9. Muthukumaravel K, Kanagavalli V, Pradhoshini KP, Vasanthi N, Santhanabharathi B, Alam L, et al.
    PMID: 36283648 DOI: 10.1016/j.cbpc.2022.109492
    In this modern industrialized era of large-scale production of agrochemicals, various emerging contaminants form the main components of waste water and sludge in most of the developing countries of the world. In this concern, phenol- an inevitable and alarming chemical pollutant in aquatic ecosystem, gains a speedy access into the water bodies as an industrial by-product. Though the detrimental effects of phenol have been studied in various aspects of aquatic life, current study is an initiative to unravel the toxic effects of phenol at molecular level in Cirrhinus mrigala. Plasma cortisol level and acetylcholine esterase activity in fish was estimated by Chemiluminescent immunoassay technique and Ellman assay respectively. Scanning electron microscopic studies were carried out to unravel the gill histopathological alterations in exposed fish. It was observed that phenol (22.32 mg/l) inhibits 50 % of acetylcholine esterase activity in brain thereby affecting the locomotion of the targeted carp. Cortisol elevated during the 7th day in exposed fish, but declined progressively on the forthcoming 21st and 28th days. Manifestations in gill encompass curling, fusion, aberrations, sloughing of gill epithelium, wider inter filamentary space and mucus coating in the primary gill filament. It concludes that the discernable deviations produced in both biochemical parameters and key organ gill can be used as a biomarker and bio-indicator respectively for assessing the existence of emerging toxicants in aquatic ecosystem.
    Matched MeSH terms: Acetylcholine/pharmacology; Acetylcholinesterase
  10. Sellke FW, Armstrong ML, Harrison DG
    Circulation, 1990 May;81(5):1586-93.
    PMID: 2110036
    Atherosclerosis impairs endothelium-dependent relaxation of large conduit arteries. Because coronary resistance vessels are spared from the development of overt atherosclerosis, endothelium-dependent responses were examined in these vascular segments. Malaysian cynomolgus monkeys (n = 6) were made atherosclerotic by being fed a 0.7% cholesterol diet for 18 months. Control monkeys (n = 6) were fed a standard diet. Coronary microvessels (122-220 microns) were studied in a pressurized (20 mm Hg), no-flow state using a video-imaging apparatus. Relaxations of microvessels, preconstricted with the thromboxane analogue U46619, were determined in response to acetylcholine, bradykinin, the calcium ionophore A23187, adenosine, and sodium nitroprusside. Microvascular relaxations to bradykinin and A23187 were reduced in atherosclerotic monkeys compared with controls, whereas acetylcholine produced additional contraction in atherosclerotic monkeys. Responses of preconstricted microvessels to adenosine and sodium nitroprusside were identical in atherosclerotic and control animals. Indomethacin did not alter responses in control or atherosclerotic animals. Histologic examination revealed neither intimal thickening nor plaque formation in microvessels of this size class despite marked changes in conduit arteries. Electron microscopy showed minor alterations of endothelial cell morphology in microvessels of atherosclerotic animals. In conclusion, long-term hypercholesterolemia markedly impairs endothelium-dependent vascular relaxation in the coronary microcirculation where overt atherosclerosis does not develop. These changes in endothelial cell function may significantly alter regulation of myocardial perfusion by neurohumoral stimuli.
    Matched MeSH terms: Acetylcholine/pharmacology
  11. Damodaran T, Müller CP, Hassan Z
    Pharmacol Rep, 2019 Jun;71(3):443-448.
    PMID: 31003155 DOI: 10.1016/j.pharep.2019.01.012
    BACKGROUND: Chronic cerebral hypoperfusion (CCH) can induce the accumulation of reactive oxygen species, which leads to oxidative damage, neuronal injury, and central cholinergic dysfunction in vulnerable regions of the brain, such as the hippocampus and cerebral cortex. These effects can lead to significant cognitive impairments in clinical populations of vascular dementia (VaD). The present studies aimed to investigate the role of the cholinergic system in memory functions and hippocampal long-term potentiation (LTP) impairments induced by CCH in rats.

    METHODS: Male Sprague Dawley rats were subjected to permanent bilateral occlusion of common carotid arteries (PBOCCA) or sham surgery. Then, PBOCCA rats received ip injections with, either vehicle (control group), the muscarinic receptor agonist oxotremorine (0.1 mg/kg), or the acetylcholinesterase inhibitor physostigmine (0.1 mg/kg). Cognitive functions were evaluated using a passive avoidance task and the Morris water maze test. In addition, hippocampal LTP was recorded in vivo under anaesthesia.

    RESULTS: The PBOCCA rats exhibited significant deficits in passive avoidance retention and spatial learning and memory tests. They also showed a suppression of LTP formation in the hippocampus. Oxotremorine and physostigmine significantly improved the learning and memory deficits as well as the suppression of LTP in PBOCCA rats.

    CONCLUSIONS: The present data suggest that the cholinergic system plays an important role in CCH-induced cognitive deficits and could be an effective therapeutic target for the treatment of VaD.

    Matched MeSH terms: Acetylcholine/pharmacology
  12. Silva A, Kuruppu S, Othman I, Goode RJ, Hodgson WC, Isbister GK
    Neurotox Res, 2017 01;31(1):11-19.
    PMID: 27401825 DOI: 10.1007/s12640-016-9650-4
    Russell's vipers are snakes of major medical importance in Asia. Russell's viper (Daboia russelii) envenoming in Sri Lanka and South India leads to a unique, mild neuromuscular paralysis, not seen in other parts of the world where the snake is found. This study aimed to identify and pharmacologically characterise the major neurotoxic components of Sri Lankan Russell's viper venom. Venom was fractionated using size exclusion chromatography and reverse-phase high-performance liquid chromatography (RP-HPLC). In vitro neurotoxicities of the venoms, fractions and isolated toxins were measured using chick biventer and rat hemidiaphragm preparations. A phospholipase A2 (PLA2) toxin, U1-viperitoxin-Dr1a (13.6 kDa), which constitutes 19.2 % of the crude venom, was isolated and purified using HPLC. U1-viperitoxin-Dr1a produced concentration-dependent in vitro neurotoxicity abolishing indirect twitches in the chick biventer nerve-muscle preparation, with a t 90 of 55 ± 7 min only at 1 μM. The toxin did not abolish responses to acetylcholine and carbachol indicating pre-synaptic neurotoxicity. Venom, in the absence of U1-viperitoxin-Dr1a, did not induce in vitro neurotoxicity. Indian polyvalent antivenom, at the recommended concentration, only partially prevented the neurotoxic effects of U1-viperitoxin-Dr1a. Liquid chromatography mass spectrometry analysis confirmed that U1-viperitoxin-Dr1a was the basic S-type PLA2 toxin previously identified from this venom (NCBI-GI: 298351762; SwissProt: P86368). The present study demonstrates that neurotoxicity following Sri Lankan Russell's viper envenoming is primarily due to the pre-synaptic neurotoxin U1-viperitoxin-Dr1a. Mild neurotoxicity observed in severely envenomed Sri Lankan Russell's viper bites is most likely due to the low potency of U1-viperitoxin-Dr1a, despite its high relative abundance in the venom.
    Matched MeSH terms: Acetylcholine/pharmacology
  13. Leong XF, Najib MN, Das S, Mustafa MR, Jaarin K
    Tohoku J. Exp. Med., 2009 Sep;219(1):71-8.
    PMID: 19713687
    Oxidization of dietary cooking oil increases the risk of cardiovascular diseases such as hypertension by increasing the formation oxidative oxygen radicals. The aim of study was to investigate the effects of repeatedly heated palm oil on blood pressure, plasma nitrites, and vascular reactivity. Nitrites were measured, as an indirect marker for nitric oxide production. Male Sprague-Dawley rats were divided into four groups: control group fed with basal diet and other three groups fortified with 15% weight/weight fresh palm oil (FPO), palm oil heated five times (5HPO) or palm oil heated ten times (10HPO) for 24 weeks. The oil was heated to 180 degrees C for 10 min. Blood pressure was measured at baseline and at intervals of four weeks for 24 weeks using non-invasive tail-cuff method. Following 24 weeks, the rats were sacrificed and thoracic aortas were dissected for measurement of vascular reactivity. Blood pressure was elevated significantly (p < 0.05) in 5HPO and 10HPO groups, with the 10HPO group showing higher values. Aortic rings from animals fed with heated oil showed diminished relaxation in response to acetylcholine or sodium nitroprusside, and greater contraction to phenylephrine. Acetylcholine and sodium nitroprusside cause endothelium-dependent and endothelium-independent relaxation, respectively. Relaxation responses remained unaltered in the FPO group, with the attenuated contractile response to phenylephrine, compared to control group. FPO increased plasma nitrites by 28%, whereas 5HPO and 10HPO reduced them by 25% and 33%, respectively. Intake of repeatedly heated palm oil causes an increase in blood pressure, which may be accounted for by the attenuated endothelium-dependent vasorelaxant response.
    Matched MeSH terms: Acetylcholine/pharmacology
  14. Nabishah BM, Morat PB, Khalid BA, Kadir BA
    Clin Exp Pharmacol Physiol, 1990 Dec;17(12):841-7.
    PMID: 2092952
    1. The effects of corticosteroid pretreatment on acetylcholine (ACH)-induced contraction of bronchial smooth muscle (BSM) were studied. 2. ACH dose-response curves for dexamethasone (DM)- and corticosterone (B)-treated but not deoxycorticosterone (DOC)-treated BSM were significantly shifted to the right; this provides evidence that glucocorticoid treatment reduced the sensitivity of BSM to ACH. 3. Morphine enhanced BSM contraction in response to ACH by 20%. DM suppressed this enhancement. 4. These findings correlated well with the reduction of muscarinic receptor numbers in BSM by glucocorticoids in our previous study. In addition, glucocorticoids reduced the sensitivity of BSM to opioids.
    Matched MeSH terms: Acetylcholine/pharmacology*
  15. Chidambaram SB, Pandian A, Sekar S, Haridass S, Vijayan R, Thiyagarajan LK, et al.
    Environ Toxicol, 2016 Dec;31(12):1955-1963.
    PMID: 26434561 DOI: 10.1002/tox.22196
    PURPOSE: Present study was undertaken to evaluate the antiamnesic effect of Sesamum indicum (S. indicum) seeds (standardized for sesamin, a lignan, content) in scopolamine, a muscarinic antagonist intoxicated mice.

    METHODS: Male Swiss albino mice (18-22 g bw) were pretreated with methanolic extract of sesame seeds (MSSE) (100 and 200 mg/kg/day, p.o) for a period of 14 days. Scopolamine (0.3 mg/kg, i.p.) was injected on day 14, 45 ± 10 min after MSSE administration. Antiamnesic effect of MSSE was evaluated using step-down latency (SDL) on passive avoidance apparatus and transfer latency (TL) on an elevated plus maze. To unravel the mechanism of action, we examined the effects of MSSE on the genes such as acetyl cholinesterase (AChE), muscarinic receptor M1 subtype (mAChRM1 ), and brain derived neurotrophic factor (BDNF) expression within hippocampus of experimental mice. Further, its effects on bax and bcl-2 were also evaluated. Histopathological examination of hippocampal CA1 region was performed using cresyl violet staining.

    RESULTS: MSSE treatment produced a significant and dose dependent increase in step down latency in passive avoidance test and decrease in transfer latency in elevated plus maze in scopolamine intoxicated injected mice. MSSE down-regulated AChE and mAChRM1 and up-regulated BDNF mRNA expression. Further, it significantly down-regulated the bax and caspase 3 and up-regulated bcl-2 expression in scopolamine intoxicated mice brains. Mice treated with MSSE showed increased neuronal counts in hippocampal CA1 region when compared with scopolamine-vehicle treated mice.

    CONCLUSION: Sesame seeds have the ability to interact with cholinergic components involved in memory function/restoration and also an interesting candidate to be considered for future cognitive research. © 2015 Wiley Periodicals, Inc. Environ Toxicol 31: 1955-1963, 2016.

    Matched MeSH terms: Acetylcholine/metabolism; Acetylcholinesterase/metabolism
  16. Vijayapandi P, Annabathina V, SivaNagaSrikanth B, Manjunath V, Boggavarapu P, Mohammed P AK, et al.
    PMID: 24082330
    The present investigation was aimed at determining the effects of hexane, acetone, methanol and aqueous extracts of Acorus calamus leaves (ACHE, ACAE, ACME and ACAQE) on cholinergic and histaminic system using isolated frog rectus abdominis muscle and guinea pig ileum. A dose dependent potentiation of Ach response (anticholinesterase like effect) was found with ACAE and ACME at 0.25, 0.5, 0.75 and 1 mg/ml, but at higher dose of ACAE, ACME, ACAQE and ACHE (5, 20 mg/ml) inhibit the Ach response (antinicotinic effect). These results revealed biphasic effect of Acorus calamus leaves extracts on acetylcholine induced contractile response in isolated frog rectus abdominis muscle preparation (i.e. potentiation effect at lower dose and inhibitory effect at higher dose). Studies on isolated guinea pig ileum demonstrated antihistaminic effect in a dose dependent manner (100-1000 µg/ml) with ACAE, ACME and ACAQE. In addition, the dose dependent inhibition of Ach response (antimuscarinic effect) was observed with ACAE and ACME. In conclusion, Acorus calamus leaves extracts exerts antinicotinic, anticholinesterase like activities in isolated frog rectus abdominis muscle and antihistaminic, antimuscarinic effect in guinea pig ileum. It has been suggested that these observed activities can be further studied for therapeutic potential of Acorus calamus leaves in the treatment of cognitive disorders and asthma.
    Matched MeSH terms: Acetylcholine/metabolism; Acetylcholine/pharmacology; Acetylcholinesterase/metabolism
  17. Jaarin K, Mustafa MR, Leong XF
    Clinics (Sao Paulo), 2011;66(12):2125-32.
    PMID: 22189740
    OBJECTIVES: The goal of this study was to determine the possible mechanism that is involved in the blood pressure-raising effect of heated vegetable oils.

    METHODS: Adult male Sprague-Dawley rats were divided into 11 groups; the control group was fed with rat chow, and the other groups were fed with chow that was mixed with 15% weight/weight palm or soy oils, which were either in a fresh form or heated once, twice, five, or ten times. Blood pressures were measured at the baseline and throughout the 24-week study. Plasma nitric oxide levels were assessed prior to treatment and at the end of the study. Following 24 weeks, the rats were sacrificed to investigate their vascular reactivity using the thoracic aorta.

    RESULTS: Palm and soy oils had no detrimental effects on blood pressure, and they significantly elevated the nitric oxide contents and reduced the contractile responses to phenylephrine. However, trials using palm and soy oils that were repeatedly heated showed an increase in blood pressure, enhanced phenylephrine-induced contractions, reduced acetylcholine- and sodium nitroprusside-induced relaxations relative to the control and rats that were fed fresh vegetable oils.

    CONCLUSIONS: The blood pressure-raising effect of the heated vegetable cooking oils is associated with increased vascular reactivity and a reduction in nitric oxide levels. The chronic consumption of heated vegetable oils leads to disturbances in endogenous vascular regulatory substances, such as nitric oxide. The thermal oxidation of the cooking oils promotes the generation of free radicals and may play an important contributory role in the pathogenesis of hypertension in rats.

    Matched MeSH terms: Acetylcholine/pharmacology
  18. Muthuraman A, Ramesh M, Mustaffa F, Nadeem A, Nishat S, Paramakrishnan N, et al.
    Molecules, 2023 May 26;28(11).
    PMID: 37298835 DOI: 10.3390/molecules28114358
    Molecular docking is widely used in the assessment of the therapeutic potential of pharmaceutical agents. The binding properties of beta-carotene (BC) to acetylcholine esterase (AChE) proteins were characterized using the molecular docking method. The mechanism of AChE inhibition was assessed by an experimental in vitro kinetic study. In addition, the role of BC action was tested by the zebrafish embryo toxicity test (ZFET). The results of the docking ability of BC to AChE showed significant ligand binding mode. The kinetic parameter, i.e., the low AICc value shown as the compound was the competitive type of inhibition of AChE. Further, BC also showed mild toxicity at a higher dose (2200 mg/L) in ZFET assessment with changes in biomarkers. The LC50 value of BC is 1811.94 mg/L. Acetylcholine esterase (AChE) plays a pivotal role in the hydrolysis of acetylcholine, which leads to the development of cognitive dysfunction. BC possesses the regulation of acetylcholine esterase (AChE) and acid phosphatase (AP) activity to prevent neurovascular dysfunction. Therefore, the characterization of BC could be used as a pharmaceutical agent for the treatment of cholinergic neurotoxicity-associated neurovascular disorders such as developmental toxicity, vascular dementia, and Alzheimer's disease due to its AChE and AP inhibitory actions.
    Matched MeSH terms: Acetylcholine; Acetylcholinesterase/metabolism
  19. Lutterodt GD
    Pharmacol Res, 1995 Jul-Aug;32(1-2):89-94.
    PMID: 8668653 DOI: 10.1016/S1043-6618(95)80014-X
    Sidaverin, a crystalline compound extracted from a polar fraction of Sida veronicaefolia (Lam), elicited oxytocin-like contractions in the non-gravid rat isolated uterus preparation with a concentration-response relationship. Equipotent concentrations of oxytocin and sidaverin, using matched responses, were approximately 0.16 U and 0.4 micrograms ml-1, respectively. Sidaverin-induced contractile response was atropine reversible. The concentration-response curves for sidaverin and oxytocin were parallel, and both responses were inhibited by the specific oxytocin antagonist, Atosiban, indicating possible involvement of oxytocin receptors in the action of sidaverin. There were potentiation of action of one drug to that of the other, irrespective of the order of administration and even after washing off the first before introducing the second drug. In the gravid uterus, sidaverin produced contractions in preparations from day 1 to day 6 or 7, caused relaxation in days 7-11, and elicited contractions in day 11 through term, the sensitivity of the preparations increasing exponentially toward term with strong sustained contractions. With the exception of days 7-11, when sidaverin antagonized oxytocin action, it potentiated action of oxytocin on the gravid uterus.
    Matched MeSH terms: Acetylcholine/pharmacology
  20. Lutterodt GD
    J Ethnopharmacol, 1989 May;25(3):235-47.
    PMID: 2747259
    The electrically stimulated guinea-pig ileum and spontaneously contracting guinea-pig ileum preparations were employed in studies on the effects of an alcoholic extract and two flavonoid compounds, quercetin and quercetin-3-arabinoside, extracted from the leaves of Psidium guajava. The extract showed a morphine-like inhibition of acetylcholine release in the coaxially stimulated ileum, together with an initial increase in muscular tone, followed by a gradual decrease. The morphine-like inhibition was found to be due to quercetin, starting at concentrations of 1.6 micrograms/ml. The glycoside did not show any such action at concentrations of up to 1.28 mg/ml. The extract inhibited spontaneous contractions in the unstimulated ileum with a concentration-response relationship.
    Matched MeSH terms: Acetylcholine/metabolism
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