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Fulltext Histological changes in the heart and the proximal aorta in experimental diabetic rats fed with Piper sarmentsoum

Thent ZC, Lin TS, Das S, Zakaria Z

Afr J Tradit Complement Altern Med, 2012;9(3):396-404.
PMID: 23983373

Cardiovascular complications are one of the major causes of death in diabetes mellitus. Piper sarmentosum (P.s) is an herb that possesses antihyperglycaemic effects. The main aim of the study was to observe the histological changes in the heart and the proximal aorta of streptozotocin-induced diabetic rats following P.s administration. Twenty-four male Sprague-Dawley rats (n=24) were equally randomized into four groups: control group supplemented with normal saline (C); control group supplemented with P.s (CTx) ; diabetic group supplemented with normal saline (D) and, diabetic group supplemented with P.s (DTx). Diabetes was induced by STZ (50mg/kg body weight) intramuscularly. P.s extract (0.125g/kg) was administered orally for 28 days, following four weeks of STZ induction. The cardiac and aortic tissues were collected and processed under different stains: Haematoxylin and Eosin (H & E), Verhoeff-Van Gieson (VVG), Masson's Trichome (MT) and Periodic Acid- Schiff (PAS). There were abnormal cardiomyocytes nuclei, disarray of myofibres and increase in connective tissue deposits in cardiac tissues of the diabetic untreated group. The thickness of tunica media and ratio of tunica intima to media were found to be significantly increased in the aorta of diabetic untreated group (P < 0.05) compared to the control group. There were degenerative changes in the proximal aorta in diabetic untreated groups. All the histological damages of cardiac and aortic tissues were found to be lesser in the diabetic treated groups. Supplementation with P.s extract prevented the oxidative damage arising from diabetes mellitus, and reduced its complications.

Matched MeSH terms: Myocardium/pathology*
Fulltext The impacts of intrauterine Bisphenol A exposure on pregnancy and expression of miRNAs related to heart development and diseases in animal model

Rasdi Z, Kamaludin R, Ab Rahim S, Syed Ahmad Fuad SB, Othman MHD, Siran R, et al.

Sci Rep, 2020 Apr 03;10(1):5882.
PMID: 32246001 DOI: 10.1038/s41598-020-62420-1

This study aimed to examine the impact of BPA exposure on pregnancy and foetuses on cardiac tissues and the expression of cardiac microRNAs (miRNAs) related to heart development and diseases. Pregnancy is known to be the "critical windows" in determining the offspring physical and cells development in their life after birth. The increment of the risk of cardiovascular disease (CVD) in a later stage of life has been reported by few studies demonstrated from prenatal exposure of BPA. BPA has been shown to alter miRNAs expression profiles for organ development, regeneration and metabolic functions. These alterations have been associated with the risk of CVDs. However, the associations between pregnancy outcomes and miRNAs expression in cardiac of mother- and foetuses-exposed to BPA are still not entirely explored. In BPA-exposed pregnant rat groups, a significant weight gained was observed in comparison to control (p

Matched MeSH terms: Myocardium/pathology
Fulltext A Biochemical and Pharmacological Characterization of Phospholipase A2 and Metalloproteinase Fractions from Eastern Russell's Viper (Daboia siamensis) Venom: Two Major Components Associated with Acute Kidney Injury

Chaisakul J, Khow O, Wiwatwarayos K, Rusmili MRA, Prasert W, Othman I, et al.

Toxins (Basel), 2021 Jul 26;13(8).
PMID: 34437392 DOI: 10.3390/toxins13080521

Acute kidney injury (AKI) following Eastern Russell's viper (Daboia siamensis) envenoming is a significant symptom in systemically envenomed victims. A number of venom components have been identified as causing the nephrotoxicity which leads to AKI. However, the precise mechanism of nephrotoxicity caused by these toxins is still unclear. In the present study, we purified two proteins from D. siamensis venom, namely RvPLA2 and RvMP. Protein identification using LCMS/MS confirmed the identity of RvPLA2 to be snake venom phospholipase A2 (SVPLA2) from Thai D. siamensis venom, whereas RvMP exhibited the presence of a factor X activator with two subunits. In vitro and in vivo pharmacological studies demonstrated myotoxicity and histopathological changes of kidney, heart, and spleen. RvPLA2 (3-10 µg/mL) caused inhibition of direct twitches of the chick biventer cervicis muscle preparation. After administration of RvPLA2 or RvMP (300 µg/kg, i.p.) for 24 h, diffuse glomerular congestion and tubular injury with minor loss of brush border were detected in envenomed mice. RvPLA2 and RvMP (300 µg/kg; i.p.) also induced congestion and tissue inflammation of heart muscle as well as diffuse congestion of mouse spleen. This study showed the significant roles of PLA2 and SVMP in snake bite envenoming caused by Thai D. siamensis and their similarities with observed clinical manifestations in envenomed victims. This study also indicated that there is a need to reevaluate the current treatment strategies for Thai D. siamensis envenoming, given the potential for irreversible nephrotoxicity.

Matched MeSH terms: Myocardium/pathology
Quantitative autoradiographic studies of relaxin binding in rat atria, uterus and cerebral cortex: characterization and effects of oestrogen treatment

Tan YY, Wade JD, Tregear GW, Summers RJ

Br J Pharmacol, 1999 May;127(1):91-8.
PMID: 10369460

The binding characteristics of the relaxin receptor in rat atria, uterus and cortex were studied using a [33P]-labelled human gene 2 relaxin (B33) and quantitative receptor autoradiography. The binding kinetics of [33P]-human gene 2 relaxin (B33) were investigated in slide-mounted rat atrial sections. The binding achieved equilibrium after 60 min incubation at room temperature (23+/-1 degrees C) and dissociated slowly. The association and dissociation rate constants were 4.31+/-0.34x10(8) M(-1) x min(-1) and 1.55+/-0.38x10(-3) min(-1) respectively. Thus, the kinetic dissociation constant was 3.46+/-0.59 pM. Binding was saturable to a single population of non-interacting sites throughout atria, in uterine myometrium and the 5th layer of cerebral cortex. The binding affinities (pK(D)) of [33P]-human gene 2 relaxin (B33) were 8.92+/-0.09 in atrial myocardium and 8.79+/-0.04 in cerebral cortex of male rats, and 8.79+/-0.10 in uterine myometrium. Receptor densities in the cerebral cortex and atria were higher than in uterine myometrium, indicating that relaxin also has important roles in non-reproductive tissues. In male rats, treatment with 17beta-oestradiol (20 microg in 0.1 ml sesame oil s.c., 18-24 h) significantly decreased the density of relaxin receptors in atria and cerebral cortex. Identical treatment in female rats had no significant effect in atria and cerebral cortex, but it significantly increased the density of relaxin receptors in uterine myometrium. Relaxin binding was competitively displaced by porcine and rat native relaxins. Porcine native relaxin binds to the relaxin receptor in male rat atria (8.90+/-0.02), and cerebral cortex (8.90+/-0.03) and uterine myometrium (8.89+/-0.03) with affinities not significantly different from human gene 2 (B33) relaxin. Nevertheless, rat relaxin binds to the receptors with affinities (8.35+/-0.09 in atria, 8.22+/-0.07 in cerebral cortex and 8.48+/-0.06 in uterine myometrium) significantly less than human gene 2 (B33) and porcine relaxins. Quantitative receptor autoradiography is the method of choice for measurement of affinities and densities of relaxin receptor in atria, uterine myometrium and cerebral cortex. High densities were found in all these tissues. 17beta-oestradiol treatment produced complex effects where it increased the densities of relaxin receptors in uterus but decreased those in atria and cerebral cortex of the male rats, and had no effect on the atria and cerebral cortex of the female rats.

Matched MeSH terms: Myocardium/metabolism*
Fulltext Mediation of Cardiac Macrophage Activity via Auricular Vagal Nerve Stimulation Ameliorates Cardiac Ischemia/Reperfusion Injury

Chung CH, Bretherton B, Zainalabidin S, Deuchars SA, Deuchars J, Mahadi MK

Front Neurosci, 2020;14:906.
PMID: 33013299 DOI: 10.3389/fnins.2020.00906

Background: Myocardial infarction (MI) reperfusion therapy causes paradoxical cardiac complications. Following restoration of blood flow to infarcted regions, a multitude of inflammatory cells are recruited to the site of injury for tissue repair. Continual progression of cardiac inflammatory responses does, however, lead to adverse cardiac remodeling, inevitably causing heart failure.
Main Body: Increasing evidence of the cardioprotective effects of both invasive and non-invasive vagal nerve stimulation (VNS) suggests that these may be feasible methods to treat myocardial ischemia/reperfusion injury via anti-inflammatory regulation. The mechanisms through which auricular VNS controls inflammation are yet to be explored. In this review, we discuss the potential of autonomic nervous system modulation, particularly via the parasympathetic branch, in ameliorating MI. Novel insights are provided about the activation of the cholinergic anti-inflammatory pathway on cardiac macrophages. Acetylcholine binding to the α7 nicotinic acetylcholine receptor (α7nAChR) expressed on macrophages polarizes the pro-inflammatory into anti-inflammatory subtypes. Activation of the α7nAChR stimulates the signal transducer and activator of transcription 3 (STAT3) signaling pathway. This inhibits the secretion of pro-inflammatory cytokines, limiting ischemic injury in the myocardium and initiating efficient reparative mechanisms. We highlight recent developments in the controversial auricular vagal neuro-circuitry and how they may relate to activation of the cholinergic anti-inflammatory pathway.
Conclusion: Emerging published data suggest that auricular VNS is an inexpensive healthcare modality, mediating the dynamic balance between pro- and anti-inflammatory responses in cardiac macrophages and ameliorating cardiac ischemia/reperfusion injury.

Matched MeSH terms: Myocardium
Protective effects of melatonin and N-acetyl cysteine against oxidative stress induced by microcystin-LR on cardiac muscle tissue

Ait Abderrahim L, Taïbi K, Abderrahim NA, Alomery AM, Abdellah F, Alhazmi AS, et al.

Toxicon, 2019 Aug 26;169:38-44.
PMID: 31465783 DOI: 10.1016/j.toxicon.2019.08.005

Microcystin Leucine-Arginine (MC-LR) is a toxin produced by the cyanobacteria Microcystis aeruginosa. It is the most encountered and toxic type of cyanotoxins. Oxidative stress was shown to play a role in the pathogenesis of microcystin LR by the induction of intracellular reactive oxygen species (ROS) formation that oxidize and damage cellular macromolecules. In the present study we examined the effect of acute MC-LR dose on the cardiac muscle of BALB/c mice. Afterwards, melatonin and N-acetyl cysteine (NAC) were assayed and evaluated as potential protective and antioxidant agents against damages generated by MC-LR. For this purpose, thirty mice were assigned into six groups of five mice each. The effect of MC-LR was first compared to the control group supplied with distilled water, then compared to the other groups supplied with melatonin and NAC. The experiment lasted 10 days after which animals were euthanized. Biomarkers of toxicity such as alkaline phosphatase activity, lipid peroxidation, protein carbonyl content, reduced glutathione content, serum lactate dehydrogenase and serum sorbitol dehydrogenase were assayed. Results showed that toxin treated mice have experienced significant oxidative damage in their myocardial tissue as revealed by noticeable levels of oxidative stress biomarkers and by the reduction in alkaline phosphatase activity. Whereas, melatonin and NAC treated mice manifested lesser oxidative damages. Our findings suggest a potential therapeutic use of melatonin and N-acetyl cysteine as antioxidant protective agents against oxidative damage induced by MC-LR.

Matched MeSH terms: Myocardium
Therapeutic effects of Schistosoma mansoni soluble egg antigen in high fat diet induced dyslipidemia, hepatic and cardiovascular pathology in mice

Toulah FH, El-Aswad BEW, Harba NM, Naguib YM

Trop Biomed, 2018 Dec 01;35(4):893-907.
PMID: 33601839

High-fat diet (HFD) can cause hyperlipidemia, fatty liver and cardiovascular disorders. Herein, we evaluated therapeutic effects and possible underlying mechanisms of actions of Schistosoma mansoni soluble egg antigen (SEA) against experimental HFD induced dyslipidemia, hepatic and cardiovascular pathology. Forty Swiss albino mice were divided into four groups (10 each); mice fed standard diet (SD), mice fed HFD, mice fed HFD for 8 weeks then infected by S. mansoni cercaria (HFD+I) and mice fed HFD for 8 weeks then treated with SEA (HFD+SEA), all mice were euthanized 16 weeks after starting the experiment. HFD+SEA mice showed significantly (p<0.001) reduced total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C) and triglycerides (TG), and significantly (p<0.05) increased high-density lipoprotein cholesterol (HDL-C) comparing to HFD mice with non-significant difference with HFD+I mice group. Doppler flowmetry showed significantly (p<0.01) lower arterial resistance and significantly (p<0.05) higher blood flow velocity in HFD+SEA and HFD+I mice groups than HFD mice. HFD+SEA mice revealed improving in liver and aortic pathology and these were better than HFD+I mice group. HFD+SEA and HFD+I mice groups had less myocardium lipid deposits, but still showing some congested blood vessels. HFD myocardium revealed strong CD34+ expression on immunohistochemistry study, while that of HFD+SEA showed weak and HFD+I mice had moderate expressions. HFD+SEA mice had significantly (p<0.01) lower serum IL-1β and vascular endothelial growth factor (VEGF) and significantly (p<0.001) higher serum transforming growth factor beta 1 (TGF-β1) and IL-10 than HFD mice with non-significant difference with HFD+I mice. In conclusion, SEA lowered serum lipids, improved aortic function, decreased liver and cardiovascular pathology in HFD mice, so, it is recommended to purify active molecules from SEA to develop anti-dyslipidemic treatment.

Matched MeSH terms: Myocardium
Fulltext Anterior penetrating chest injury with left ventricular thrombus

Ruth Sabrina, S., Nik Azlan, N.M., Adi, O.

Medicine & Health, 2013;8(1):28-32.
MyJurnal

Urban cities are synonym with a high incidence of penetrating chest injuries either from accidents or interpersonal violence. The outcome of penetrating chest wound can vary from immediate death to a prolonged morbidity. We here report a case of 39-year-gentleman who presented to Emergency Department Hospital Raja Permaisuri Bainun, Ipoh, Perak after being stabbed to the chest. His anterior penetrating chest wound was located at the 5th intercostal space medial to the midclavicular line. The stab wound penetrated the myocardium, causing minimal myocardial rupture. He also suffered from left haemothorax and hemopericardium. The haemothorax was drained with insertion of 32 French chest tube. The patient was admitted under the cardiothoracic team and discharged five days later without surgical intervention. He presented again to the Emergency Department with complains of shortness of breath and pleuritic pain. A left ventricular thrombus was detected via echocardiography. Unfortunately, he took his own discharge. Five days later he came again to Emergency Department with sporadic of loss of vision. The mural thrombus dislodged and embolized to the retinal artery causing amaurosis fugax. The patient was treated with aspirin 150mg and his symptoms subsequently resolved.

Matched MeSH terms: Myocardium
Fulltext Angiotensin II Type I Receptor Antagonism Attenuates Nicotine-Induced Cardiac Remodeling, Dysfunction, and Aggravation of Myocardial Ischemia-Reperfusion Injury in Rats

Ramalingam A, Budin SB, Mohd Fauzi N, Ritchie RH, Zainalabidin S

Front Pharmacol, 2019;10:1493.
PMID: 31920673 DOI: 10.3389/fphar.2019.01493

Increased exposure to nicotine contributes to the development of cardiac dysfunction by promoting oxidative stress, fibrosis, and inflammation. These deleterious events altogether render cardiac myocytes more susceptible to acute cardiac insults such as ischemia-reperfusion (I/R) injury. This study sought to elucidate the role of angiotensin II type I (AT1) receptors in cardiac injury resulting from prolonged nicotine administration in a rat model. Male Sprague-Dawley rats were given nicotine (0.6 mg/kg ip) for 28 days to induce cardiac dysfunction, alone or in combination with the AT1 receptor antagonist, irbesartan (10 mg/kg, po). Vehicle-treated rats were used as controls. Rat hearts isolated from each experimental group at study endpoint were examined for changes in function, histology, gene expression, and susceptibility against acute I/R injury determined ex vivo. Rats administered nicotine alone exhibited significantly increased cardiac expression of angiotensin II and angiotensin-converting enzyme (ACE) in addition to elevated systolic blood pressure (SBP) and heart rate. Furthermore, nicotine administration markedly reduced left ventricular (LV) performance with concomitant increases in myocardial oxidative stress, fibrosis, and inflammation. Concomitant treatment with irbesartan attenuated these effects, lowering blood pressure, heart rate, oxidative stress, and expression of fibrotic and inflammatory genes. Importantly, the irbesartan-treated group also manifested reduced susceptibility to I/R injury ex vivo. These findings suggest that AT1 receptors play an important role in nicotine-induced cardiac dysfunction, and pharmacological approaches targeting cardiac AT1 receptors may thus benefit patients with sustained exposure to nicotine.

Matched MeSH terms: Myocardium
Potential protective effect of sunitinib after administration of diclofenac: biochemical and histopathological drug-drug interaction assessment in a mouse model

Tan JR, Chakravarthi S, Judson JP, Haleagrahara N, Segarra I

Naunyn Schmiedebergs Arch Pharmacol, 2013 Jul;386(7):619-33.
PMID: 23552887 DOI: 10.1007/s00210-013-0861-4

Sunitinib is a tyrosine kinase inhibitor for GIST and advanced renal cell carcinoma. Diclofenac is used in cancer pain management. Coadministration may mediate P450 toxicity. We evaluate their interaction, assessing biomarkers ALT, AST, BUN, creatinine, and histopathological changes in the liver, kidney, heart, brain, and spleen. ICR mice (male, n = 6 per group/dose) were administered saline (group A) or 30 mg/kg diclofenac ip (group B), or sunitinib po at 25, 50, 80, 100, 140 mg/kg (group C) or combination of diclofenac (30 mg/kg, ip) and sunitinib (25, 50, 80, 100, 140 mg/kg po). Diclofenac was administered 15 min before sunitinib, mice were euthanized 4 h post-sunitinib dose, and biomarkers and tissue histopathology were assessed. AST was 92.2 ± 8.0 U/L in group A and 159.7 ± 14.6 U/L in group B (p < 0.05); in group C, it the range was 105.1-152.6 U/L, and in group D, it was 156.0-209.5 U/L (p < 0.05). ALT was 48.9 ± 1.6 U/L (group A), 95.1 ± 4.5 U/L (p < 0.05) in group B, and 50.5-77.5 U/L in group C and 82.3-115.6 U/L after coadministration (p < 0.05). Renal function biomarker BUN was 16.3 ± 0.6 mg/dl (group A) and increased to 29.9 ± 2.6 mg/dl in group B (p < 0.05) and it the range was 19.1-33.3 mg/dl (p < 0.05) and 26.9-40.8 mg/dl in groups C and D, respectively. Creatinine was 5.9 pmol/ml in group A; 6.2 pmol/ml in group B (p < 0.01), and the range was 6.0-6.2 and 6.2-6.4 pmol/ml in groups C and D, respectively (p < 0.05 for D). Histopathological assessment (vascular and inflammation damages) showed toxicity in group B (p < 0.05) and mild toxicity in group C. Damage was significantly lesser in group D than group B (p < 0.05). Spleen only showed toxicity after coadministration. These results suggest vascular and inflammation protective effects of sunitinib, not shown after biomarker analysis.

Matched MeSH terms: Myocardium/pathology
Clinical and pathological manifestations of human henipavirus infection

Wong KT, Tan CT

Curr. Top. Microbiol. Immunol., 2012;359:95-104.
PMID: 22427144 DOI: 10.1007/82_2012_205

The clinicopathological features of human Nipah virus and Hendra virus infections appear to be similar. The clinical manifestations may be mild, but if severe, includes acute encephalitic and pulmonary syndromes with a high mortality. The pathological features in human acute henipavirus infections comprise vasculopathy (vasculitis, endothelial multinucleated syncytia, thrombosis), microinfarcts and parenchymal cell infection in the central nervous system, lung, kidney and other major organs. Viral inclusions, antigens, nucleocapsids and RNA are readily demonstrated in blood vessel wall and numerous types of parenchymal cells. Relapsing henipavirus encephalitis is a rare complication reported in less than 10% of survivors of the acute infection and appears to be distinct from the acute encephalitic syndrome. Pathological evidence suggests viral recrudescence confined to the central nervous system as the cause.

Matched MeSH terms: Myocardium/pathology*
Evaluating the toxic and beneficial effects of jering beans (Archidendron jiringa) in normal and diabetic rats

Shukri R, Mohamed S, Mustapha NM, Hamid AA

J Sci Food Agric, 2011 Nov;91(14):2697-706.
PMID: 21744354 DOI: 10.1002/jsfa.4516

Jering (Archidendron jiringa) is eaten in the tropics and traditionally extolled for treating diabetes, high blood pressure and eliminating bladder stones. Jering contains an unusual amino acid-djenkolic acid (S,S'-methylenebiscysteine)-which may form sharp crystals in the urinary tract, causing pain and haematuria. This study evaluates the beneficial and toxic effects of dietary jering on tissues and organs in normal and diabetic rats.

Matched MeSH terms: Myocardium/pathology
Fulltext Efficacy of a bacteriophage isolated from chickens as a therapeutic agent for colibacillosis in broiler chickens

Lau GL, Sieo CC, Tan WS, Hair-Bejo M, Jalila A, Ho YW

Poult Sci, 2010 Dec;89(12):2589-96.
PMID: 21076096 DOI: 10.3382/ps.2010-00904

The efficacy of bacteriophage EC1, a lytic bacteriophage, against Escherichia coli O78:K80, which causes colibacillosis in poultry, was determined in the present study. A total of 480 one-day-old birds were randomly assigned to 4 treatments groups, each with 4 pens of 30 birds. Birds from the control groups (groups I and II) received PBS (pH 7.4) or 10(10) pfu of bacteriophage EC1, respectively. Group III consisted of birds challenged with 10(8) cfu of E. coli O78:K80 and treated with 10(10) pfu of bacteriophage EC1 at 2 h postinfection, whereas birds from group IV were challenged with 10(8) cfu of E. coli O78:K80 only. All the materials were introduced into the birds by intratracheal inoculation. Based on the results of the present study, the infection was found to be less severe in the treated E. coli-challenged group. Mean total viable cell counts of E. coli identified on eosin methylene blue agar (designated EMB + E. coli) in the lungs were significantly lower in treated, E. coli-challenged birds than in untreated, E. coli-challenged birds on d 1 and 2 postinfection. The EMB + E. coli isolation frequency was also lower in treated birds; no E. coli was detectable in blood samples on any sampling day, and E. coli were isolated only in the liver, heart, and spleen of treated chickens at a ratio of 2/6, 1/6, and 3/6, respectively, at d 1 postinfection. The BW of birds from the E. coli-challenged group treated with bacteriophage EC1 were not significantly different from those of birds from both control groups but were 15.4% higher than those of the untreated, E. coli-challenged group on d 21 postinfection. The total mortality rate of birds during the 3-wk experimental period decreased from 83.3% in the untreated, E. coli-challenged birds (group IV) to 13.3% in birds treated with bacteriophage EC1 (group III). These results suggest that bacteriophage EC1 is effective in vivo and could be used to treat colibacillosis in chickens.

Matched MeSH terms: Myocardium/pathology
Human Hendra virus infection causes acute and relapsing encephalitis

Wong KT, Robertson T, Ong BB, Chong JW, Yaiw KC, Wang LF, et al.

Neuropathol. Appl. Neurobiol., 2009 Jun;35(3):296-305.
PMID: 19473296 DOI: 10.1111/j.1365-2990.2008.00991.x

To study the pathology of two cases of human Hendra virus infection, one with no clinical encephalitis and one with relapsing encephalitis.

Matched MeSH terms: Myocardium/pathology
Guided evaluation and standardisation of mesenchymal stem cell culture conditions to generate conditioned medium favourable to cardiac c-kit cell growth

Ng WH, Umar Fuaad MZ, Azmi SM, Leong YY, Yong YK, Ng AMH, et al.

Cell Tissue Res, 2019 Feb;375(2):383-396.
PMID: 30232595 DOI: 10.1007/s00441-018-2918-7

Mesenchymal stem cells (MSCs) are known to secrete cardioprotective paracrine factors that can potentially activate endogenous cardiac c-kit cells (CCs). This study aims to optimise MSC growth conditions and medium formulation for generating the conditioned medium (CdM) to facilitate CC growth and expansion in vitro. The quality of MSC-CdM after optimisation of seeding density during MSC stabilisation and medium formulation used during MSC stimulation including glucose, ascorbic acid, serum and oxygen levels and the effects of treatment concentration and repeated CdM harvesting were assessed based on CC viability in vitro under growth factor- and serum-deprived condition. Our data showed that functional CdM can be produced from MSCs with a density of 20,000 cells/cm2, which were stimulated using high glucose (25 mM), ascorbic acid supplemented, serum-free medium under normoxic condition. The generated CdM, when applied to growth factor- and serum-deprived medium at 1:1 ratio, improved CC viability, migration and proliferation in vitro. Such an effect could further be augmented by generating CdM concentrates without compromising CC gene and protein expressions, while retaining its capability to undergo differentiation to form endothelial, smooth muscle and cardiomyocytes. Nevertheless, CdM could not be repeatedly harvested from the same MSC culture, as the protein content and its effect on CC viability deteriorated after the first harvest. In conclusion, this study provides a proof-of-concept strategy to standardise the production of CdM from MSCs based on rapid, stepwise assessment of CC viability, thus enabling production of CdM favourable to CC growth for in vitro or clinical applications.

Matched MeSH terms: Myocardium/cytology*
Crocodiles and alligators: Antiamoebic and antitumor compounds of crocodiles

Siddiqui R, Jeyamogan S, Ali SM, Abbas F, Sagathevan KA, Khan NA

Exp Parasitol, 2017 Dec;183:194-200.
PMID: 28917711 DOI: 10.1016/j.exppara.2017.09.008

Crocodiles exist in unsanitary environments, feed on rotten meat, are often exposed to heavy metals such as arsenic, cadmium, cobalt, chromium, mercury, nickel, lead, selenium, tolerate high levels of radiation, and are amid the very few species to survive the catastrophic Cretaceous-Tertiary extinction event, nonetheless they can live for up to a 100 years. Moreover, as they live in unhygienic conditions, they regularly come across pathogens. Logically, we postulate that crocodiles possess mechanisms to defend themselves from noxious agents as well as protecting themselves from pathogens. To test this hypothesis, various organ lysates and serum of Crocodylus palustris were prepared. Amoebicidal assays were performed using Acanthamoeba castellanii belonging to the T4 genotype. Cytotoxicity assays were performed using Prostate cancer cells culture by measuring lactate dehydrogenase release as a marker for cell death. Growth inhibition assays were performed to determine the growth inhibitory effects of various organ lysates. Serum and heart lysates of Crocodylus palustris exhibited powerful anti-tumor activity exhibiting more than 70% Prostate cancer cell death (P

Matched MeSH terms: Myocardium/chemistry
Fulltext Lipoprotein lipase expression, serum lipid and tissue lipid deposition in orally-administered glycyrrhizic acid-treated rats

Lim WY, Chia YY, Liong SY, Ton SH, Kadir KA, Husain SN

Lipids Health Dis, 2009;8:31.
PMID: 19638239 DOI: 10.1186/1476-511X-8-31

The metabolic syndrome (MetS) is a cluster of metabolic abnormalities comprising visceral obesity, dyslipidaemia and insulin resistance (IR). With the onset of IR, the expression of lipoprotein lipase (LPL), a key regulator of lipoprotein metabolism, is reduced. Increased activation of glucocorticoid receptors results in MetS symptoms and is thus speculated to have a role in the pathophysiology of the MetS. Glycyrrhizic acid (GA), the bioactive constituent of licorice roots (Glycyrrhiza glabra) inhibits 11beta-hydroxysteroid dehydrogenase type 1 that catalyzes the activation of glucocorticoids. Thus, oral administration of GA is postulated to ameliorate the MetS.

Matched MeSH terms: Myocardium/enzymology; Myocardium/pathology

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