Displaying publications 1 - 20 of 58 in total

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  1. Si LY, Kamisah Y, Ramalingam A, Lim YC, Budin SB, Zainalabidin S
    Appl Physiol Nutr Metab, 2017 Jul;42(7):765-772.
    PMID: 28249121 DOI: 10.1139/apnm-2016-0506
    Vascular endothelial dysfunction (VED) plays an important role in the initiation of cardiovascular diseases. Roselle, enriched with antioxidants, demonstrates high potential in alleviating hypertension. This study was undertaken to investigate the effects of roselle supplementation of VED and remodelling in a rodent model with prolonged nicotine administration. Male Sprague-Dawley rats (n = 6 per group) were administered with 0.6 mg/kg nicotine for 28 days to induce VED. The rats were given either aqueous roselle (100 mg/kg) or normal saline orally 30 min prior to nicotine injection daily. One additional group of rats served as control. Thoracic aorta was isolated from rats to measure vascular reactivity, vascular remodelling and oxidative stress. Roselle significantly lowered aortic sensitivity to phenylephrine-induced vasoconstriction (Endo-(+) Cmax = 234.5 ± 3.9%, Endo-(-) Cmax = 247.6 ± 5.2%) compared with untreated nicotine group (Endo-(+) Cmax = 264.5 ± 6.9%, Endo-(-) Cmax = 276.5 ± 6.8%). Roselle also improved aortic response to endothelium-dependent vasodilator, acetylcholine (Endo-(+) Rmax = 73.2 ± 2.1%, Endo-(-) Rmax = 26.2 ± 0.8%) compared to nicotine group (Endo-(+) Rmax = 57.8 ± 1.7%, Endo-(-) Rmax = 20.9 ± 0.8%). In addition, roselle prevented an increase in intimal media thickness and elastic lamellae proliferation to preserve vascular architecture. Moreover, we also observed a significantly lowered degree of oxidative stress in parallel with increased antioxidant enzymes in aortic tissues of the roselle-treated group. This study demonstrated that roselle prevents VED and remodelling, and as such it has high nutraceutical value as supplement to prevent cardiovascular diseases.
    Matched MeSH terms: Acetylcholine/pharmacology
  2. Sanip Z, Hanaffi SH, Ahmad I, Yusoff SS, Rasool AH, Yusoff HM
    Tob Induc Dis, 2015;13(1):32.
    PMID: 26346914 DOI: 10.1186/s12971-015-0052-9
    BACKGROUND: Studies have demonstrated that secondhand smoke (SHS) exposure could impair endothelial function. However, the effect of SHS exposure specifically on microvascular endothelial function is not well understood. This study aimed to determine the effects of SHS exposure on microvascular endothelial function among non-smoking, generally healthy women.

    FINDINGS: We studied 127 women; and based on their hair nicotine levels measured using gas chromatography-mass spectrometry, 25 of them were categorized as having higher hair nicotine levels, 25 were grouped as having lower hair nicotine and 77 women were grouped into the non-detected group. The non-detected group did not have detectable levels of hair nicotine. Anthropometry, blood pressure (BP), lipid profile and high-sensitivity C-reactive protein (hsCRP) were measured accordingly. Microvascular endothelial function was assessed non-invasively using laser Doppler fluximetry and the process of iontophoresis involving acetylcholine and sodium nitroprusside as endothelium-dependent and endothelium-independent vasodilators respectively. The mean hair nicotine levels for higher and lower hair nicotine groups were 0.74 (1.04) and 0.05 (0.01) ng/mg respectively. There were no significant differences in anthropometry, BP, lipid profile and hsCRP between these groups. There were also no significant differences in the microvascular perfusion and endothelial function between these groups.

    CONCLUSION: In this study, generally healthy non-smoking women who have higher, lower and non-detected hair nicotine levels did not show significant differences in their microvascular endothelial function. Low levels of SHS exposure among generally healthy non-smoking women may not significantly impair their microvascular endothelial function.

    Matched MeSH terms: Acetylcholine
  3. Ha ZY, Mathew S, Yeong KY
    Curr Protein Pept Sci, 2020;21(1):99-109.
    PMID: 31702488 DOI: 10.2174/1389203720666191107094949
    Butyrylcholinesterase is a serine hydrolase that catalyzes the hydrolysis of esters in the body. Unlike its sister enzyme acetylcholinesterase, butyrylcholinesterase has a broad substrate scope and lower acetylcholine catalytic efficiency. The difference in tissue distribution and inhibitor sensitivity also points to its involvement external to cholinergic neurotransmission. Initial studies on butyrylcholinesterase showed that the inhibition of the enzyme led to the increment of brain acetylcholine levels. Further gene knockout studies suggested its involvement in the regulation of amyloid-beta, a brain pathogenic protein. Thus, it is an interesting target for neurological disorders such as Alzheimer's disease. The substrate scope of butyrylcholinesterase was recently found to include cocaine, as well as ghrelin, the "hunger hormone". These findings led to the development of recombinant butyrylcholinesterase mutants and viral gene therapy to combat cocaine addiction, along with in-depth studies on the significance of butyrylcholinesterase in obesity. It is observed that the pharmacological impact of butyrylcholinesterase increased in tandem with each reported finding. Not only is the enzyme now considered an important pharmacological target, it is also becoming an important tool to study the biological pathways in various diseases. Here, we review and summarize the biochemical properties of butyrylcholinesterase and its roles, as a cholinergic neurotransmitter, in various diseases, particularly neurodegenerative disorders.
    Matched MeSH terms: Acetylcholine/metabolism; Acetylcholinesterase/genetics; Acetylcholinesterase/metabolism
  4. Zulkifli MH, Viswenaden P, Jasamai M, Azmi N, Yaakob NS
    Biomed Pharmacother, 2019 Feb 20;112:108630.
    PMID: 30797147 DOI: 10.1016/j.biopha.2019.108630
    5-HT3R antagonists such as ondansetron, granisetron and tropisetron have been clinically used to treat nausea and vomiting in chemotherapy patients. However, current study and research revealed novel potentials of these ligands in other diseases like inflammation, Alzheimer's, and drug abuse. Towards utilising these drugs as anti-smoking agents to treat nicotine dependence problem, there are conflicting reports regarding the potential of these ligands in modulating the effects of nicotine in both human and animal behavioural studies. This is complicated by the heterogeneity of 5-HT3R itself, cross regulation between nicotinic acetylcholinergic receptor (nAChR) and distinct pharmacological profiles of 5-HT3R antagonists. This review gathered existing studies conducted investigating the potential of "-setron" class of 5-HT3R antagonists in modulating nicotine effects. We proposed that the mechanism where 5-HT3R antagonists mediate the effects of nicotine could be attributed by both direct at 5-HT3R and indirect mechanism in nicotine addiction downstream regulation. The indirect mechanism mediated by the 5-HT3R antagonist could be through α7 nAChR, 5-HT1B receptor (5-HT1BR), 5-HT1C receptor (5-HT1CR), calcineurin activity, p38 MAPK level, PPAR-γ and NF-κβ. Our review suggested that future studies should focus on newer 5-HT3R antagonist with superior pharmacological profile or the one with multitarget action rather than high selectivity at single receptor.
    Matched MeSH terms: alpha7 Nicotinic Acetylcholine Receptor
  5. Hisyam Jamari, Mohd Salleh Rofiee, Richard James Johari, Mohd Zaki Salleh, Teh, Lay Kek
    MyJurnal
    The potential of Moringa oleifera Lam. (Moringaceae) and Centella asiatica (L.) Urban (Apiaceae) extracts (TGT-PRIMAAGE) in slowing the decline of memory and learning activity was investigated using D-galactose-induced ageing rat model. The extracts were profiled and standardised based on markers identified using LC/MS-QTOF. Toxicity study of the extract was done, and the rat did not show any sign of toxicity. The extract was orally administered to the rat and dose dependent (100, 500 and 1000 mg/kg) efficacy were investigated. The rats were subjected to Morris Water Maze whereby 3 parameters were studied (number of entry to platform, latency and novel object recognition). Plasma was collected for the determination of catalase (CAT) activity and levels of malondialdehyde (MDA) and advanced glycation end products (AGEs). The activity of acetylcholinesterase (AChE), level of acetylcholine (ACh) and lipid peroxidation (LPO) were measured using the brain lysates. Significant improvement (p < 0.05) was seen in the memory and learning abilities in the aged rats that received medium and high dose of TGT-PRIMAAGE, and tocotrienol. Rats treated with TGT-PRIMAAGE had also shown improved CAT activity and resulted in reduced LPO. The level of ACh was found increased in parallel with the reduced AChE activity. The capabilities of learning and memory of the TGT-PRIMAAGE treated rats were enhanced via inhibition of AChE activity and subsequently increased level of ACh.
    Matched MeSH terms: Acetylcholine; Acetylcholinesterase
  6. Kwa, Siew Kim, Zainab Abdul Majeed, Tan, Kah Nian
    MyJurnal
    Myasthenia gravis (MG) is a rare autoimmune disorder
    characterised by fluctuating and variable combination
    of muscle weakness and fatigue. Most cases are due to
    T-cell mediated autoantibodies against post-synaptic
    acetylcholine receptors (AChR-Ab), thus preventing
    acetylcholine from binding and signalling skeletal
    muscle to contract.1
    The annual incidence is 7-23 new cases per million.1
    It can occur at any age but with two peaks; an earlyonset
    (20-40 years) female-predominant and a late-onset
    (60-80 years) male-predominant peak. MG is classified
    into ocular and generalised (80%). More than half the
    patients initially present with ptosis and diplopia but half
    will progress to generalised disease with involvement of
    bulbar, limb and respiratory weakness. Those presenting
    as generalised MG can also develop eye signs later.1
    It is important to recognise MG early because it is
    highly treatable. Untreated disease leads to permanent
    weakness.2 Treatment reduces mortality from lifethreatening
    myasthenic crisis.1,3 Misdiagnosis leads to
    potentially harmful interventions and inappropriate
    management.4,5 Diagnosis in late-onset MG is easily
    missed2,3,4,5 because of overlapping symptoms with
    other diseases common in the elderly. We report a case
    of delay and misdiagnosis in an elderly patient with
    co-morbidities. (Copied from article).
    Matched MeSH terms: Acetylcholine
  7. Chen S, Lin Z, Tan KL, Chen R, Su W, Zhao H, et al.
    Front Psychiatry, 2020;11:564843.
    PMID: 33061920 DOI: 10.3389/fpsyt.2020.564843
    Butyrylcholinesterase (BChE) efficiently hydrolyzes acetylcholine (ACh) at high concentrations when acetylcholinesterase (AChE) is substrate-inhibited. Recent studies have shown that BChE also has a function that is independent of ACh, but it has not been fully explored. Low BChE expression is accompanied with higher stress-induced aggression and ghrelin levels in stress models, and BChE knockout mice exhibit cognitive and memory impairments. However, the role of BChE in posttraumatic stress disorder (PTSD) remains unclear. In the present study, we investigated the role of BChE in contextual fear memory and its regulatory effect on the expression of factors related to the glutamate (Glu)-glutamine (Gln) cycle via knockdown studies. We used AAVs and lentiviruses to knockdown BChE expression in the mouse hippocampal CA1 region and C8D1A astrocytes. Our behavioral data from those mice injected with AAV-shBChE in the hippocampal CA1 region showed strengthened fear memory and increased dendritic spine density. Elevated Glu levels and glutamine synthetase (GS) enzyme activity were detected in contextual fear conditioned-BChE knockdown animals and astrocytes. We observed that an AAV-shBChE induced lowering of BChE expression in the hippocampus CA1 region enhanced contextual fear memory expression and promoted the astrocytic Glu-Gln cycle but did not elevate ACh-hydrolyzing activity. This study provides new insight into the regulatory role of BChE in cognition and suggests potential target for stress-related psychiatric disorder such as PTSD where patients experience fear after exposure to severe life-threatening traumatic events.
    Matched MeSH terms: Acetylcholine; Acetylcholinesterase
  8. Akbar A, Sharma JN
    Pharmacol Res, 1992 Apr;25(3):279-86.
    PMID: 1518772
    We have investigated the effect of indomethacin on histamine- and acetylcholine (ACh)-induced responses in the intact and denuded epithelium of guinea pig isolated tracheal smooth muscle. Epithelium removal resulted in increased responsiveness to ACh and histamine. Indomethacin (2.8 microM) enhanced the sensitivity of both intact and denuded preparations to histamine and ACh. These findings suggest that the tracheal epithelium of guinea pig plays a protective role against bronchoconstrictors, such as ACh and histamine. Furthermore, indomethacin-mediated hyperresponsiveness caused by these agonists in epithelium denuded preparations might be a reflection of removal of prostaglandin (PG) biosynthesis. A similar process of interaction in indomethacin-treated asthmatic patients (with damaged airway epithelium) might take place. The significance of these findings is discussed.
    Matched MeSH terms: Acetylcholine/pharmacology*
  9. Kundap UP, Paudel YN, Kumari Y, Othman I, Shaikh MF
    Front Pharmacol, 2019;10:315.
    PMID: 31057394 DOI: 10.3389/fphar.2019.00315
    Epilepsy is a neuronal disorder associated with several neurological and behavioral alterations characterized by recurrent spontaneous epileptic seizures. Despite having more than 20 anti-epileptic drugs (AEDs), they only provide a symptomatic treatment. As well as, currently available AEDs also displayed cognitive alterations in addition to retarding seizure. This leads to the need for exploring new molecules that not only retard seizure but also improve cognitive impairment. Embelin (EMB) is a benzoquinone derivative which has already demonstrated its pharmacological potentials against arrays of neurological conditions. The current study developed a chronic kindling model in adult zebrafish by using repeated administration of small doses of pentylenetetrazole (PTZ) and a single dose of Kainic acid (KA) to investigate the associated memory impairment. This has been done by using the three-axis maze which is a conventional method to test the learning ability and egocentric memory in zebrafish. As well as, the ameliorative potential of EMB has been evaluated against chronic epilepsy-related memory alterations. Moreover the expression level of pro-inflammatory genes such as C-C motif ligand 2 (CCL2), toll-like receptor-4 (TLR4), tumor necrosis factor-α (TNF-α), interleukin-1 (IL-1) and interferon-γ (IFN-γ) were evaluated. The level of several neurotransmitters such as γ-aminobutyric acid (GABA), acetylcholine (Ach) and glutamate (Glu) was evaluated by liquid chromatography-mass spectrometry (LC-MS). The results showed that daily dose of PTZ 80 mg/kg for 10 days successfully induces a kindling effect in zebrafish, whereas the single dose of KA did not. As compared to control, the PTZ and KA group demonstrates impairment in memory as demonstrated by the three-axis maze. The PTZ group treated with a series of EMB doses (ranging from 0.156 to 0.625 mg/kg) was found to have retarded seizure as well as significantly reduces epilepsy-induced memory alteration. In addition, EMB treatment reduces the expression of inflammatory markers implicating its anti-inflammatory potential. Moreover, levels of GABA, Ach, and glutamate are increased in EMB administered group as compared to the PTZ administered group. Overall, findings demonstrate that EMB might be a potential candidate against chronic epilepsy-related cognitive dysfunction as EMB prevents the seizures, so we expect it to prevent the associated neuroinflammation and learning deficit.
    Matched MeSH terms: Acetylcholine
  10. Choo BKM, Kundap UP, Johan Arief MFB, Kumari Y, Yap JL, Wong CP, et al.
    PMID: 30844417 DOI: 10.1016/j.pnpbp.2019.02.014
    Epilepsy is marked by seizures that are a manifestation of excessive brain activity and is symptomatically treatable by anti-epileptic drugs (AEDs). Unfortunately, the older AEDs have many side effects, with cognitive impairment being a major side effect that affects the daily lives of people with epilepsy. Thus, this study aimed to determine if newer AEDs (Zonisamide, Levetiracetam, Perampanel, Lamotrigine and Valproic Acid) also cause cognitive impairment, using a zebrafish model. Acute seizures were induced in zebrafish using pentylenetetrazol (PTZ) and cognitive function was assessed using the T-maze test of learning and memory. Neurotransmitter and gene expression levels related to epilepsy as well as learning and memory were also studied to provide a better understanding of the underlying processes. Ultimately, impaired cognitive function was seen in AED treated zebrafish, regardless of whether seizures were induced. A highly significant decrease in γ-Aminobutyric Acid (GABA) and glutamate levels was also discovered, although acetylcholine levels were more variable. The gene expression levels of Brain-Derived Neurotrophic Factor (BDNF), Neuropeptide Y (NPY) and Cyclic Adenosine Monophosphate (CAMP) Responsive Element Binding Protein 1 (CREB-1) were not found to be significantly different in AED treated zebrafish. Based on the experimental results, a decrease in brain glutamate levels due to AED treatment appears to be at least one of the major factors behind the observed cognitive impairment in the treated zebrafish.
    Matched MeSH terms: Acetylcholine/metabolism
  11. Kundap UP, Kumari Y, Othman I, Shaikh MF
    Front Pharmacol, 2017;8:515.
    PMID: 28824436 DOI: 10.3389/fphar.2017.00515
    Epilepsy is a neuronal disorder allied with distinct neurological and behavioral alterations characterized by recurrent spontaneous epileptic seizures. Impairment of the cognitive performances such as learning and memory is frequently observed in epileptic patients. Anti-epileptic drugs (AEDs) are efficient to the majority of patients. However, 30% of this population seems to be refractory to the drug treatment. These patients are not seizure-free and frequently they show impaired cognitive functions. Unfortunately, as a side effect, some AEDs could contribute to such impairment. The major problem associated with conducting studies on epilepsy-related cognitive function is the lack of easy, rapid, specific and sensitive in vivo testing models. However, by using a number of different techniques and parameters in the zebrafish, we can incorporate the unique feature of specific disorder to study the molecular and behavior basis of this disease. In the view of current literature, the goal of the study was to develop a zebrafish model of epilepsy induced cognitive dysfunction. In this study, the effect of AEDs on locomotor activity and seizure-like behavior was tested against the pentylenetetrazole (PTZ) induced seizures in zebrafish and epilepsy associated cognitive dysfunction was determined using T-maze test followed by neurotransmitter estimation and gene expression analysis. It was observed that all the AEDs significantly reversed PTZ induced seizure in zebrafish, but had a negative impact on cognitive functions of zebrafish. AEDs were found to modulate neurotransmitter levels, especially GABA, glutamate, and acetylcholine and gene expression in the drug treated zebrafish brains. Therefore, combination of behavioral, neurochemical and genenetic information, makes this model a useful tool for future research and discovery of newer and safer AEDs.
    Matched MeSH terms: Acetylcholine
  12. Said S. E. H. Elnashaie
    MyJurnal
    Bifurcation and chaos are important phenomena affecting many physical and chemical systems. They are also related to the stability/instability and multiplicity phenomena associated with these systems. The phenomena are not only of theoretical/mathematical interest but are also important for laboratory, pilot plant and commercial units. This paper concentrates on 3 systems:

    1. The novel auto-thermic Circulating Fluidized Membrane Steam Reformer (CFBMSR) for the efficient production of the clean fuel hydrogen and which shows multiplicity of the steady state (static bifurcation)

    2. A novel fermentor for the efficient production of bio-ethanol that shows static/dynamic bifurcation as well as chaotic behaviour

    3. The neurocycle of the acetylcholine transmitter in the brain using diffusion-reaction models in order to gain insight into their possible connection to Alzheimer and Parkinson Diseases (AD/PD); these are preliminary efforts to investigate the bifurcation and chaotic behaviour of this neurocycle.
    Matched MeSH terms: Acetylcholine
  13. Azemi AK, Mokhtar SS, Rasool AHG
    Oxid Med Cell Longev, 2020;2020:7572892.
    PMID: 32879653 DOI: 10.1155/2020/7572892
    Diabetes mellitus is associated with endothelial dysfunction; it causes progressive vascular damage resulting from an impaired endothelium-dependent vasorelaxation. In the diabetes state, presence of hyperglycemia and insulin resistance predisposes to endothelial dysfunction. Clinacanthus nutans, widely used as a traditional medicine for diabetes is reported to have hypoglycemic, hypolipidemic, antioxidant, and anti-inflammatory properties. However, the possibility of C. nutans affecting the vascular endothelial function in diabetes remains unclear. This study was aimed at evaluating the effects of C. nutans methanolic leaves extract (CNME) on endothelial function in a type 2 diabetes (T2DM) rat model. Sixty male Sprague-Dawley rats were divided into five groups (n = 12 per group): nondiabetic control, nondiabetic treated with four weeks of CNME (500 mg/kg/daily), untreated diabetic rats, diabetic treated with metformin (300 mg/kg/daily), and diabetic treated with CNME (500 mg/kg/daily). T2DM was induced by a single intraperitoneal injection of low-dose streptozotocin (STZ) to rats fed with high-fat diet (HFD). Endothelial-dependent and endothelial-independent relaxations and contractions of the thoracic aorta were determined using the organ bath. Aortic endothelial nitric oxide synthase (eNOS) expression was determined using Western blotting. Endothelial-dependent relaxation was reduced in diabetic rats. Both diabetic groups treated with CNME or metformin significantly improved the impairment in endothelium-dependent vasorelaxation; this was associated with increased expression of aortic eNOS protein. CNME- and metformin-treated groups also reduced aortic endothelium-dependent and aortic endothelium-independent contractions in diabetics. Both of these diabetic-treated groups also reduced blood glucose levels and increased body weight compared to the untreated diabetic group. In conclusion, C. nutans improves endothelial-dependent vasodilatation and reduces endothelial-dependent contraction, thus ameliorating endothelial dysfunction in diabetic rats. This may occur due to its effect on increasing eNOS protein expression.
    Matched MeSH terms: Acetylcholine/pharmacology
  14. Al-Tahami BA, Yvonne-Tee GB, Halim AS, Ismail AA, Rasool AH
    Methods Find Exp Clin Pharmacol, 2010 Apr;32(3):181-5.
    PMID: 20448860 DOI: 10.1358/mf.2010.32.3.1423887
    Iontophoresis of acetylcholine (ACh) and sodium nitroprusside (SNP) combined with laser Doppler fluximetry (LDF) is a tool used to determine microvascular endothelial function. Our aim was to study the reproducibility of different parameters of this technique using iontophoresis with low current strength on the forearm skin of healthy subjects. Baseline skin perfusion was done before application of five current pulses with 1 min of current-free interval. Current strength of 0.007 mA, current density of 0.01 mA/cm(2) and charge density of 6 mC/cm(2) were used, along with 1% ACh and 1% SNP. The absolute maximum change in perfusion (max), percent change in perfusion (% change), peak change in perfusion (peak) and area under the curve during iontophoresis (AUC) at the anodal and cathodal leads were recorded. Measurements were performed in three sessions for 2 days. The coefficient of variation (CV) was calculated for each parameter. Among the parameters studied, maximum change in perfusion and peak flux were the most reproducible parameters.
    Matched MeSH terms: Acetylcholine/pharmacokinetics
  15. Rahim NS, Lim SM, Mani V, Hazalin NAMN, Majeed ABA, Ramasamy K
    J Diet Suppl, 2020 Oct 14.
    PMID: 33962540 DOI: 10.1080/19390211.2020.1830223
    Neuroinflammation is associated with neuronal cell death and could lead to chronic neurodegeneration. This study investigated the neuroprotective potential of virgin coconut oil (VCO) against lipopolysaccharide (LPS)-induced cytotoxicity of neuroblastoma SK-N-SH cells. The findings were validated using Wistar rats, which were fed with 1-10 g/kg VCO for 31 days, exposed to LPS (0.25 mg/kg) and subjected to the Morris Water Maze Test. Brain homogenate was subjected to biochemical analyses and gene expression studies. α-Tocopherol (α-T; 150 mg/kg) served as the positive control. VCO (100 µg/mL) significantly (p 
    Matched MeSH terms: Acetylcholine; Acetylcholinesterase
  16. Rahim NS, Lim SM, Mani V, Abdul Majeed AB, Ramasamy K
    Pharm Biol, 2017 Dec;55(1):825-832.
    PMID: 28118770 DOI: 10.1080/13880209.2017.1280688
    CONTEXT: Virgin coconut oil (VCO) has been reported to possess antioxidative, anti-inflammatory and anti-stress properties.

    OBJECTIVE: Capitalizing on these therapeutic effects, this study investigated for the first time the potential of VCO on memory improvement in vivo.

    MATERIALS AND METHODS: Thirty male Wistar rats (7-8 weeks old) were randomly assigned to five groups (n = six per group). Treatment groups were administered with 1, 5 and 10 g/kg VCO for 31 days by oral gavages. The cognitive function of treated-rats were assessed using the Morris Water Maze Test. Brains were removed, homogenized and subjected to biochemical analyses of acetylcholine (ACh) and acetylcholinesterase (AChE), antioxidants [superoxide dismutase (SOD), catalase (CAT), glutathione (GSH), glutathione peroxidase (GPx) and glutathione reductase (GRx)], lipid peroxidase [malondialdehyde (MDA)] as well as nitric oxide (NO). α-Tocopherol (αT; 150 mg/kg) was also included for comparison purposes.

    RESULTS: VCO-fed Wistar rats exhibited significant (p  33%) and NO (≥ 34%). Overall, memory improvement by VCO was comparable to αT.

    DISCUSSION AND CONCLUSION: VCO has the potential to be used as a memory enhancer, the effect of which was mediated, at least in part, through enhanced cholinergic activity, increased antioxidants level and reduced oxidative stress.

    Matched MeSH terms: Acetylcholine/analysis
  17. David SR, Lai PPN, Chellian J, Chakravarthi S, Rajabalaya R
    Sci Rep, 2023 Aug 01;13(1):12423.
    PMID: 37528147 DOI: 10.1038/s41598-023-39442-6
    The present work examined the effect of oral administration of rutin and its combination with metformin, an antidiabetic drug on blood glucose, total cholesterol and triglycerides level and vascular function in streptozotocin (STZ) -induced diabetic rats. Male Sprague Dawley rats were rendered diabetic by a single intraperitoneal injection of STZ (50 mg/kg). Rutin and metformin were orally administered to diabetic rats at a dose of 100 mg/kg and 300 mg/kg body weight/day, respectively, for 4 weeks. Plasma analysis was conducted to determine changes in the plasma glucose and lipid levels. Rat aortic ring reactivity in response to endothelium-dependent (acetylcholine, ACh) and endothelium-independent (sodium nitroprusside, SNP) relaxants, and to the α1-adrenergic agonist phenylephrine (PE) were recorded. Histology of pancreas, liver and kidney were evaluated. In results, rutin and metformin alone and in combination has led to significant improvements in blood glucose, cholesterol and triglyceride levels compared to diabetic group. Diabetic aortic rings showed significantly greater contraction in response to PE, and less relaxation in response to ACh and SNP. Treatment with rutin and metformin in combination significantly reduced PE-induced contraction and increased ACh-induced and SNP-induced relaxation in diabetes when compared to rutin or metformin alone. Significant histological improvements were seen with combination therapy. In conclusion, rutin and metformin combination therapy has the most potentiality for restoring blood glucose and lipid level as well as vascular function.
    Matched MeSH terms: Acetylcholine/pharmacology
  18. Nurul-Iman BS, Kamisah Y, Jaarin K, Qodriyah HM
    PMID: 23861707 DOI: 10.1155/2013/629329
    This study was performed to explore the effects of virgin coconut oil (VCO) in male rats that were fed with repeatedly heated palm oil on blood pressure, plasma nitric oxide level, and vascular reactivity. Thirty-two male Sprague-Dawley rats were divided into four groups: (i) control (basal diet), (ii) VCO (1.42 mL/kg, oral), (iii) five-times-heated palm oil (15%) (5HPO), and (iv) five-times-heated palm oil (15%) and VCO (1.42 mL/kg, oral) (5HPO + VCO). Blood pressure was significantly increased in the group that was given the 5HPO diet compared to the control group. Blood pressure in the 5HPO + VCO group was significantly lower than the 5HPO group. Plasma nitric oxide (NO) level in the 5HPO group was significantly lower compared to the control group, whereas in the 5HPO + VCO group, the plasma NO level was significantly higher compared to the 5HPO group. Aortic rings from the 5HPO group exhibited attenuated relaxation in response to acetylcholine and sodium nitroprusside as well as increased vasoconstriction to phenylephrine compared to the control group. Aortic rings from the 5HPO + VCO group showed only attenuated vasoconstriction to phenylephrine compared to the 5HPO group. In conclusion, VCO prevents blood pressure elevation and improves endothelial functions in rats fed with repeatedly heated palm oil.
    Matched MeSH terms: Acetylcholine
  19. Wong FC, Ahmad M, Heng LY, Peng LB
    Talanta, 2006 Jun 15;69(4):888-93.
    PMID: 18970653 DOI: 10.1016/j.talanta.2005.11.034
    An optical biosensor consisting of a chromoionophore (ETH5294) (CM) doped sol-gel film interfaced with another sol-gel film immobilized with acetylcholinesterase (AChE) was employed to detect the insecticide dichlorvos. The main advantage of this optical biosensor is the use of a sol-gel layer with immobilized CM that possesses lipophilic property. The highly lipophilic nature of the CM and its compatibility with the sol-gel matrix has prevented leaching, which is frequently a problem in optical sensor construction based on pH indicator dyes. The immobilization of the indicator and enzyme was simple and need no chemical modification. The CM layer is pH sensitive and detects the pH changes of the acetylcholine chloride (AChCl) substrate when hydrolyzed by AChE layer deposited above. In the absence of the AChE layer, the pH response of the CM layer is linear from pH 6 to 8 (R(2)=0.98, n=3) and it showed no leaching of the lipophilic chromoionophore. When the AChE layer is deposited on top, the optical biosensor responds to AChCl with a linear dynamic range of 40-90mM AChCl (R(2)=0.984, n=6). The response time of the biosensor is 12min. Based on the optimum incubation time of 15min, a linear calibration curve of dichlorvos against the percentage inhibition of AChE was obtained from 0.5 to 7mg/L of dichlorvos (17-85% inhibition, R(2)=0.991, n=9). The detection limit for dichlorvos was 0.5mg/L. The results of the analysis of 1.7-6.0mg/L of dichlorvos using this optical biosensor agreed well with a gas chromatography-mass spectrometry detection method.
    Matched MeSH terms: Acetylcholine; Acetylcholinesterase
  20. Akyuz E, Polat AK, Eroglu E, Kullu I, Angelopoulou E, Paudel YN
    Life Sci, 2021 Jan 15;265:118826.
    PMID: 33259863 DOI: 10.1016/j.lfs.2020.118826
    Epilepsy is a neurologicaldisorder characterized by persistent predisposition to recurrent seizurescaused by abnormal neuronal activity in the brain. Epileptic seizures maydevelop due to a relative imbalance of excitatory and inhibitory neurotransmitters. Expressional alterations of receptors and ion channelsactivated by neurotransmitters can lead to epilepsy pathogenesis.

    AIMS: In this updated comprehensive review, we discuss the emerging implication of mutations in neurotransmitter-mediated receptors and ion channels. We aim to provide critical findings of the current literature about the role of neurotransmitters in epilepsy.

    MATERIALS AND METHODS: A comprehensive literature review was conducted to identify and critically evaluate studies analyzing the possible relationship between epilepsy and neurotransmitters. The PubMed database was searched for related research articles.

    KEY FINDINGS: Glutamate and gamma-aminobutyric acid (GABA) are the main neurotransmitters playing a critical role in the pathophysiology of this balance, and irreversible neuronal damage may occur as a result of abnormal changes in these molecules. Acetylcholine (ACh), the main stimulant of the autonomic nervous system, mediates signal transmission through cholinergic and nicotinic receptors. Accumulating evidence indicates that dysfunction of nicotinic ACh receptors, which are widely expressed in hippocampal and cortical neurons, may be significantly implicated in the pathogenesis of epilepsy. The dopamine-norepinephrine-epinephrine cycle activates hormonal and neuronal pathways; serotonin, norepinephrine, histamine, and melatonin can act as both hormones and neurotransmitters. Recent reports have demonstrated that nitric oxide mediates cognitive and memory-related functions via stimulating neuronal transmission.

    SIGNIFICANCE: The elucidation of the role of the main mediators and receptors in epilepsy is crucial for developing new diagnostic and therapeutic approaches.

    Matched MeSH terms: Acetylcholine/metabolism
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