Displaying publications 1 - 20 of 134 in total

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  1. Edwin N
    Med J Malaysia, 1978 Dec;33(2):184-5.
    PMID: 755173
    Matched MeSH terms: Endothelium/ultrastructure
  2. Appanna R, Wang SM, Ponnampalavanar SA, Lum LC, Sekaran SD
    Am J Trop Med Hyg, 2012 Nov;87(5):936-42.
    PMID: 22987650 DOI: 10.4269/ajtmh.2012.11-0606
    Plasma leakage in severe dengue has been postulated to be associated with skewed cytokine immune responses. In this study, the association of cytokines with vascular permeability in dengue patients was investigated. Human serum samples collected from 48 persons (13 with dengue fever, 29 with dengue hemorrhagic fever, and 6 healthy) were subjected to cytokines analysis by using Luminex Multiplex Technology. Selected serum samples from patients with dengue hemorrhagic fever sera and recombinant human cytokines were then tested for roles on inducing vascular permeability by treatment of human umbilical vein endothelial cells. Confocal immunofluorescence staining indicated morphologic alteration of human umbilical vein endothelial cells treated with serum samples from patients with dengue hemorrhagic fever compared with serum samples from healthy persons. The findings suggest that cytokines produced during dengue hemorrhagic infections could induce alterations in the vascular endothelium, which may play a fundamental role in the pathophysiology of dengue.
    Matched MeSH terms: Endothelium, Vascular/metabolism*
  3. Mohammad-Salih PA
    Med J Malaysia, 2011 Oct;66(4):300-3.
    PMID: 22299546 MyJurnal
    This study was conducted to describe corneal endothelial cell density and morphology in Malay eyes. Non-contact specular microscopy was performed in 125 eyes of 125 Malay volunteers, aged 20-87 years. Studied parameters included endothelial cell density (CD), mean cell area (MCA), coefficient of variation (CV) in cell area, as well as hexagonal appearance of the cells. Mean endothelial cell density in the study population was 2648 +/- 310 cell/mm(2). Mean CA, CV and percentage of hexagonal cells were 382.8 +/- 47.7microm(2), 58.1 +/- 22.6, 44.3% +/- 11.5% respectively. There was a statistically significant decrease in endothelial cell density (correlation - 0.300, P = 0.001) and CV in cell size (correlation - 0.208, P = 0.02) with age. There was a statistically significant increase in mean cell area (correlation 0.300, P = 0.001) with increasing age. The correlation between age and percentage of hexagonal cells was insignificant (correlation 0.074, P = 0.41). In conclusion, a consistent decrease was noted in the endothelial cell density with increasing age. The differences in endothelial cell density between genders were statistically insignificant.
    Matched MeSH terms: Endothelium, Corneal/cytology*
  4. Bastion ML, Zahidin AZ
    BMJ Case Rep, 2010;2010.
    PMID: 22750927 DOI: 10.1136/bcr.11.2009.2497
    An unusual case of disciform keratitis developing in a patient with silicone oil-filled eye following vitrectomies for posterior globe rupture.
    Matched MeSH terms: Endothelium/virology
  5. Jaais F, Dutton GN
    Ophthalmic Surg, 1992 Mar;23(3):210-4.
    PMID: 1574293
    We studied by scanning electron microscopy the effects of the repeated use of a newly-designed, disposable, suction trephine (Microsurgical, Ltd, Bedfordshire, England) on the nature of the cut of successive corneal buttons from sheep eyes. After the trephine was used more than nine times, the cut edge became more irregular as successive buttons were produced. Also, progressively greater degrees of endothelial cells adjacent to the cut edge were lost. Although the corneal buttons initially were circular, those produced after the 20th cut became more oval. These results suggest that a disposable corneal trephine should be reused no more than nine times.
    Matched MeSH terms: Endothelium, Corneal/ultrastructure
  6. Loh YC, Tan CS, Ch'ng YS, Yeap ZQ, Ng CH, Yam MF
    Int J Mol Sci, 2018 Jan 02;19(1).
    PMID: 29301280 DOI: 10.3390/ijms19010120
    Hypertension is asymptomatic and a well-known "silent killer", which can cause various concomitant diseases in human population after years of adherence. Although there are varieties of synthetic antihypertensive drugs available in current market, their relatively low efficacies and major application in only single drug therapy, as well as the undesired chronic adverse effects associated, has drawn the attention of worldwide scientists. According to the trend of antihypertensive drug evolution, the antihypertensive drugs used as primary treatment often change from time-to-time with the purpose of achieving the targeted blood pressure range. One of the major concerns that need to be accounted for here is that the signaling mechanism pathways involved in the vasculature during the vascular tone regulation should be clearly understood during the pharmacological research of antihypertensive drugs, either in vitro or in vivo. There are plenty of articles that discussed the signaling mechanism pathways mediated in vascular tone in isolated fragments instead of a whole comprehensive image. Therefore, the present review aims to summarize previous published vasculature-related studies and provide an overall depiction of each pathway including endothelium-derived relaxing factors, G-protein-coupled, enzyme-linked, and channel-linked receptors that occurred in the microenvironment of vasculature with a full schematic diagram on the ways their signals interact. Furthermore, the crucial vasodilative receptors that should be included in the mechanisms of actions study on vasodilatory effects of test compounds were suggested in the present review as well.
    Matched MeSH terms: Endothelium, Vascular/physiology
  7. Chellian J, Mak KK, Chellappan DK, Krishnappa P, Pichika MR
    Sci Rep, 2022 Dec 10;12(1):21393.
    PMID: 36496468 DOI: 10.1038/s41598-022-25739-5
    The antidiabetic effects of quercetin and metformin are well known. However, their synergistic effect in reversing the symptoms of diabetes-induced endothelial dysfunction remains unknown. In this study, we have investigated their synergistic effect in streptozotocin (STZ)-nicotinamide induced diabetic rats. Seventy-five rats were divided into five groups; normal control, diabetic control, treatment groups (10 mg/kg quercetin, 180 mg/kg metformin, and combined). The plasma glucose and lipid levels, liver enzymes, ex-vivo studies on aortic rings, histology of liver, kidney, pancreas, abdominal aorta and thoracic aorta, and immunohistochemical studies were carried out. The findings revealed that the combination of quercetin and metformin showed a greater antidiabetic effect than either drug, and rendered protection to the endothelium. The combination effectively reversed the hyperglycemia-induced endothelial dysfunction in diabetic rats. Furthermore, it also reversed the dysregulated expression of eNOS, 3-nitrotyrosine, VCAM-1, CD31 and SIRT-1. Overall, the present study's findings demonstrate that quercetin potentiates the activity of metformin to control the complications associated with diabetes.
    Matched MeSH terms: Endothelium, Vascular/metabolism
  8. Khaw LT, Ball HJ, Mitchell AJ, Grau GE, Stocker R, Golenser J, et al.
    Exp Parasitol, 2014 Oct;145:34-41.
    PMID: 25045850 DOI: 10.1016/j.exppara.2014.07.002
    We here describe the novel finding that brain endothelial cells in vitro can stimulate the growth of Plasmodium falciparum through the production of low molecular weight growth factors. By using a conditioned medium approach, we show that the brain endothelial cells continued to release these factors over time. If this mirrors the in vivo situation, these growth factors potentially would provide an advantage, in terms of enhanced growth, for sequestered parasitised red blood cells in the brain microvasculature. We observed this phenomenon with brain endothelial cells from several sources as well as a second P. falciparum strain. The characteristics of the growth factors included: <3 kDa molecular weight, heat stable, and in part chloroform soluble. Future efforts should be directed at identifying these growth factors, since blocking their production or actions might be of benefit for reducing parasite load and, hence, malaria pathology.
    Matched MeSH terms: Endothelium/cytology; Endothelium/metabolism; Endothelium/parasitology
  9. Yeh-Siang L, Subramaniam G, Hadi AH, Murugan D, Mustafa MR
    Molecules, 2011 Apr 06;16(4):2990-3000.
    PMID: 21471938 DOI: 10.3390/molecules16042990
    Generation of reactive oxygen species plays a pivotal role in the development of cardiovascular diseases. The present study describes the effects of the methanolic extract of Phoebe grandis (MPG) stem bark on reactive oxygen species-induced endothelial dysfunction in vitro. Endothelium-dependent (acetylcholine, ACh) and -independent relaxation (sodium nitroprusside, SNP) was investigated from isolated rat aorta of Sprague-Dawley (SD) in the presence of the β-NADH (enzymatic superoxide inducer) and MPG extract. Superoxide anion production in aortic vessels was measured by lucigen chemiluminesence. Thirty minutes incubation of the rat aorta in vitro with β-NADH increased superoxide radical production and significantly inhibited ACh-induced relaxations. Pretreatment with MPG (0.5, 5 and 50 μg/mL) restored the ACh-induced relaxations (R(max): 92.29% ± 2.93, 91.02% ± 4.54 and 88.31 ± 2.36, respectively) in the presence of β-NADH. MPG was ineffective in reversing the impaired ACh-induced relaxations caused by pyrogallol, a non-enzymatic superoxide generator. Superoxide dismutase (a superoxide scavenger), however, reversed the impaired ACh relaxations induced by both β-NADH and pyrogallol. MPG also markedly inhibited the β-NADH-induced generation of the superoxide radicals. Furthermore, MPG scavenging peroxyl radicals generated by tBuOOH (10⁻⁴ M).These results indicate that MPG may improve the endothelium dependent relaxations to ACh through its scavenging activity as well as by inhibiting the NADH/NADPH oxidase induced generation of superoxide anions.
    Matched MeSH terms: Endothelium, Vascular/drug effects*; Endothelium, Vascular/metabolism; Endothelium, Vascular/physiology
  10. Ling WC, Mustafa MR, Murugan DD
    J Cardiovasc Pharmacol, 2020 02;75(2):123-134.
    PMID: 31651673 DOI: 10.1097/FJC.0000000000000771
    Nitrite, an anion produced from the oxidative breakdown of nitric oxide (NO), has traditionally been viewed as an inert molecule. However, this dogma has been challenged with the findings that nitrite can be readily reduced to NO under pathological conditions, hence representing a physiologically relevant storage reservoir of NO either in the blood or tissues. Nitrite administration has been demonstrated to improve myocardial function in subjects with heart failure and to lower the blood pressure in hypertensive subjects. Thus, extensive amount of work has since been carried out to investigate the therapeutic potential of nitrite in treating cardiovascular diseases, especially hypertension. Studies done on several animal models of hypertension have demonstrated the efficacy of nitrite in preventing and ameliorating the pathological changes associated with the disease. This brief review of the current findings aims to re-evaluate the use of nitrite for the treatment of hypertension and in particular to highlight its role in improving endothelial function.
    Matched MeSH terms: Endothelium, Vascular/drug effects*; Endothelium, Vascular/metabolism; Endothelium, Vascular/physiopathology
  11. Andrea, B.K., Safinaz, M.K., Umi Kalthum, M.N., Mushawiahti, M.
    MyJurnal
    Traumatic injury to the eye can occur due to various causes, most of which are avoidable. Here we report three cases of intrastromal corneal foreign bodies (FB) which required surgical removal. Most corneal FBs are removed easily at the slit lamp, however, these cases required surgical intervention due to the mechanism of which the FB penetrated into the stroma. Although the mechanism of injury was similar, with all three cases occurring at high velocity, we observed that the entry and level of penetration differed in each case. In the first case, the corneal FB penetrated the cornea and was embedded in the anterior stroma, whereas in the second case, the FB was embedded in the posterior stroma, but with an intact endothelium. In the third case, the FB caused a full thickness, self-sealed laceration wound but remained embedded in the stroma. Through further evaluation, we noted that several factors contribute towards the severity of the injury, namely, anatomy of the cornea, area affected, shape, size, mass and velocity of the object. We speak in depth about the mechanism of injury and physics associated with these injuries and why the penetration differed in each case.
    Matched MeSH terms: Endothelium
  12. Hussin AM, Ashor AW, Schoenmakers I, Hill T, Mathers JC, Siervo M
    Eur J Nutr, 2017 Apr;56(3):1095-1104.
    PMID: 26848580 DOI: 10.1007/s00394-016-1159-3
    BACKGROUND: In addition to regulating calcium homoeostasis and bone health, vitamin D influences vascular and metabolic processes including endothelial function (EF) and insulin signalling. This systematic review and meta-analysis of randomised clinical trials (RCTs) were conducted to investigate the effect of vitamin D supplementation on EF and to examine whether the effect size was modified by health status, study duration, dose, route of vitamin D administration, vitamin D status (baseline and post-intervention), body mass index (BMI), age and type of vitamin D.

    METHODS: We searched the Medline, Embase, Cochrane Library and Scopus databases from inception until March 2015 for studies meeting the following criteria: (1) RCT with adult participants, (2) vitamin D administration alone, (3) studies that quantified EF using commonly applied methods including ultrasound, plethysmography, applanation tonometry and laser Doppler.

    RESULTS: Sixteen articles reporting data for 1177 participants were included. Study duration ranged from 4 to 52 weeks. The effect of vitamin D on EF was not significant (SMD: 0.08, 95 % CI -0.06, 0.22, p = 0.28). Subgroup analysis showed a significant improvement of EF in diabetic subjects (SMD: 0.31, 95 % CI 0.05, 0.57, p = 0.02). A non-significant trend was found for diastolic blood pressure (β = 0.02; p = 0.07) and BMI (β = 0.05; p = 0.06).

    CONCLUSIONS: Vitamin D supplementation did not improve EF. The significant effect of vitamin D in diabetics and a tendency for an association with BMI may indicate a role of excess adiposity and insulin resistance in modulating the effects of vitamin D on vascular function. This remains to be tested in future studies.

    Matched MeSH terms: Endothelium/drug effects*; Endothelium/metabolism
  13. Zhang CY, Tan BK
    Phytother Res, 1999 Mar;13(2):157-9.
    PMID: 10190192
    14-deoxyandrographolide (DA) and 14-deoxy-11,12-didehydroandrographolide (DDA) are two diterpenoids isolated from A. paniculata, a popular folk medicine used as an antihypertensive drug in Malaysia. We have previously reported that DDA exhibited a greater hypotensive effect in anaesthetized rats and a vasorelaxant activity in isolated rat aorta, compared with DA. Their vasorelaxant activities were mediated through the activation of the enzymes, nitric oxide synthase (NOS) and guanylyl cyclase. The present study demonstrated that both DA and DDA stimulated nitric oxide (NO) release from human endothelial cells. DDA compared with DA caused a greater production of NO; this is in line with the finding of the earlier study that the vasorelaxant effect of DDA was more dependent on endothelium than DA.
    Matched MeSH terms: Endothelium, Vascular/drug effects*; Endothelium, Vascular/metabolism
  14. Lee NT, Ong LK, Gyawali P, Nassir CMNCM, Mustapha M, Nandurkar HH, et al.
    Biomolecules, 2021 07 06;11(7).
    PMID: 34356618 DOI: 10.3390/biom11070994
    The cerebral endothelium is an active interface between blood and the central nervous system. In addition to being a physical barrier between the blood and the brain, the endothelium also actively regulates metabolic homeostasis, vascular tone and permeability, coagulation, and movement of immune cells. Being part of the blood-brain barrier, endothelial cells of the brain have specialized morphology, physiology, and phenotypes due to their unique microenvironment. Known cardiovascular risk factors facilitate cerebral endothelial dysfunction, leading to impaired vasodilation, an aggravated inflammatory response, as well as increased oxidative stress and vascular proliferation. This culminates in the thrombo-inflammatory response, an underlying cause of ischemic stroke and cerebral small vessel disease (CSVD). These events are further exacerbated when blood flow is returned to the brain after a period of ischemia, a phenomenon termed ischemia-reperfusion injury. Purinergic signaling is an endogenous molecular pathway in which the enzymes CD39 and CD73 catabolize extracellular adenosine triphosphate (eATP) to adenosine. After ischemia and CSVD, eATP is released from dying neurons as a damage molecule, triggering thrombosis and inflammation. In contrast, adenosine is anti-thrombotic, protects against oxidative stress, and suppresses the immune response. Evidently, therapies that promote adenosine generation or boost CD39 activity at the site of endothelial injury have promising benefits in the context of atherothrombotic stroke and can be extended to current CSVD known pathomechanisms. Here, we have reviewed the rationale and benefits of CD39 and CD39 therapies to treat endothelial dysfunction in the brain.
    Matched MeSH terms: Endothelium, Vascular/metabolism*; Endothelium, Vascular/pathology
  15. Ibrahim NN, Rasool AH, Wong AR, Rahman AR
    Clin Chim Acta, 2009 Nov;409(1-2):62-6.
    PMID: 19723516 DOI: 10.1016/j.cca.2009.08.018
    Pulse wave analysis (PWA) combined with beta(2)-agonist challenge has recently been used to assess endothelial function. beta-2 adrenergic receptor (beta(2)AR) polymorphisms may affect response to beta(2)-agonist. We determined whether beta(2)AR polymorphisms influence endothelial response in our model using PWA and salbutamol.
    Matched MeSH terms: Endothelium/drug effects; Endothelium/physiology*
  16. Kharitonova M, Iezhitsa I, Zheltova A, Ozerov A, Spasov A, Skalny A
    J Trace Elem Med Biol, 2015 Jan;29:227-34.
    PMID: 25127069 DOI: 10.1016/j.jtemb.2014.06.026
    Magnesium (Mg) deficiency is implicated in the development of numerous disorders of the cardiovascular system. Moreover, the data regarding the efficacy of different magnesium compounds in the correction of impaired functions due to low magnesium intake are often fragmentary and inconsistent. The aim of this study was to compare the effects of the most bioavailable Mg compounds (Mg l-aspartate, Mg N-acetyltaurate, Mg chloride, Mg sulphate and Mg oxybutyrate) on systemic inflammation and endothelial dysfunction in rats fed a low Mg diet for 74 days. A low Mg diet decreased the Mg concentration in the plasma and erythrocytes, which was accompanied by a reduced concentration of eNOs and increased levels of endothelin-1 level in the serum and impaired endothelium-dependent vasodilatation. These effects increased the concentration of proinflammatory molecules, such as VCAM-1, TNF-α, IL-6 and CRP, indicating the development of systemic inflammation and endothelial dysfunction. The increased total NO level, which estimated from the sum of the nitrate and nitrite concentrations in the serum, may also be considered to be a proinflammatory marker. Two weeks of Mg supplementation partially or fully normalised the ability of the vascular wall to effect adequate endothelium-dependent vasodilatation and reversed the levels of most endothelial dysfunction and inflammatory markers (except CRP) to the mean values of the control group. Mg sulphate had the smallest effect on the endothelin-1, TNF-α and VCAM-1 levels. Mg N-acetyltaurate was significantly more effective in restoring the level of eNOS compared to all other studied compounds, except for Mg oxybutyrate. Taken together, the present findings demonstrate that all Mg compounds equally alleviate endothelial dysfunction and inflammation caused by Mg deficiency. Mg sulphate tended to be the least effective compound.
    Matched MeSH terms: Endothelium, Vascular/drug effects*; Endothelium, Vascular/physiopathology*
  17. Sharma AK, Khanna D, Balakumar P
    Int J Cardiol, 2014 Mar 15;172(2):530-2.
    PMID: 24495652 DOI: 10.1016/j.ijcard.2014.01.053
    Matched MeSH terms: Endothelium, Vascular/drug effects*; Endothelium, Vascular/pathology
  18. Ghani RA, Bin Yaakob I, Wahab NA, Zainudin S, Mustafa N, Sukor N, et al.
    J Clin Lipidol, 2013 Sep-Oct;7(5):446-53.
    PMID: 24079286 DOI: 10.1016/j.jacl.2013.04.004
    BACKGROUND: Type 2 diabetes is associated with early development of endothelial dysfunction. Patients present with typical dyslipidemia (predominantly high levels of triglycerides [TG] and low levels of high-density lipoprotein cholesterol [HDL-C]) or mixed hypercholesterolemia (high levels of low-density lipoprotein cholesterol [LDL-C] and TG with low HDL-C). Normal levels include LDL-C < 100 mg/dL, TG < 135 mg/dL, and HDL-C > 40 mg/dL for men and >50 mg/dL for women.
    OBJECTIVE: To determine the effects of 8 weeks' administration of fenofibrate on inflammatory markers, metabolic parameters, and endothelial dysfunction.
    METHODS: We administered micronized fenofibrate (Laboratories Fourneir S.A Dijon, France) daily for 8 weeks to 40 dyslipidemic, type 2 diabetes patients with equal numbers in each arm of the typical or mixed dyslipidemia groups. Noninvasive endothelial function assessments were performed and serum inflammatory markers obtained before and after treatment.
    RESULTS: The typical group demonstrated significantly greater TG reduction and HDL-C increment, ie, 56% vs, 21.3% (P < .005) and 21% vs. 7.6% (P = .001), respectively, compared with the mixed group. There was greater LDL-C reduction within the mixed group compared with the typical group 21.0% vs. 2.2% (P < .05). Endothelial dysfunction was present in both groups at baseline. After treatment, the typical group demonstrated significant improvement in resting brachial diameter (3.9 mm [interquartile range {IQR} 3.3-4.7] to 4.2 mm [IQR 3.4-4.8], P = .001) compared with no change within the mixed group (3.6 mm [IQR 3.1-5.4] to 3.7 mm [IQR 3.1-5.3], P = .26). Flow-mediated diameter improved significantly in both groups. The mixed group had significantly greater levels of hs-CRP at baseline but no changes throughout the study. The mixed group demonstrated an increase in vascular adhesion molecule-1 from 706 ng/mL (IQR 566-1195) to 845 ng/mL (637-1653; P = .01), a reduction of tumor necrosis factor-α from 7.0 pg/mL (IQR 1.0-43.5) to 2.5 pg/mL (IQR 1.5-13.5; P = .04) throughout the study.
    CONCLUSIONS: We effectively compared 8 weeks of fenofibrate therapy in type 2 diabetics with contrasting lipid abnormalities. The typical dyslipidemia group showed significantly greater lipid improvements compared with the mixed dyslipidemia group. Both groups had improvements in endothelial functions that were independent of the lipid levels. We concluded that fibrate therapy in type 2 diabetics is beneficial, especially those with typical dyslipidemia and extends beyond its lipid lowering properties.
    KEYWORDS: Endothelial dysfunction; Fenofibrate; High-density lipoprotein cholesterol; Low density lipoprotein; Noninvasive endothelial function assessments; Triglyceride; Vascular cell adhesion molecule-1; hsCRP
    Matched MeSH terms: Endothelium/drug effects; Endothelium/pathology
  19. Tan CS, Tew WY, Jingying C, Yam MF
    Chem Biol Interact, 2021 Oct 01;348:109620.
    PMID: 34411564 DOI: 10.1016/j.cbi.2021.109620
    Naringenin is a naturally occurring flavanone (flavonoid) known to have bioactive effects on human health. It has been reported to show cardiovascular effects. This study aimed to investigate the possible vasorelaxant effect of naringenin and the mechanism behind it by using a Sprague Dawley rat aortic ring assay model. Naringenin caused significant vasorelaxation of endothelium-intact aortic rings precontracted with phenylephrine (pD2 = 4.27 ± 0.05; Rmax = 121.70 ± 4.04%) or potassium chloride (pD2 = 4.00 ± 0.04; Rmax = 103.40 ± 3.82%). The vasorelaxant effect decreased in the absence of an endothelium (pD2 = 3.34 ± 0.10; Rmax = 62.29 ± 2.73%). The mechanisms of the vasorelaxant effect of naringenin in the presence of antagonists were also investigated. Indomethacin, 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one, atropine, 4-aminopyridine, Nω-nitro-l-arginine methyl ester, glibenclamide and propranolol significantly reduced the relaxation stimulated by naringenin in the presence of endothelium. Besides that, the effect of naringenin on the voltage-operated calcium channel (VOCC) in the endothelium-intact aortic ring was studied, as was intracellular Ca2+ release from the sarcoplasmic reticulum (SR) in the endothelium-denuded aortic ring. The results showed that naringenin also significantly blocked the entry of Ca2+ via the VOCC, SERCA/SOCC and suppressed the release of Ca2+ from the SR. Thus, the vasorelaxant effect shown by naringenin mostly involve the COX pathway, the endothelium-dependent pathway via NO/sGC/prostaglandin, calcium and potassium channels.
    Matched MeSH terms: Endothelium, Vascular/drug effects*; Endothelium, Vascular/metabolism*
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